Tag: forskning

Mangan, forskningsreferencer

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Januar 1999

1. Baly DL, Curry DL, Keen CL, Hurley LS. Effect of manganese deficiency on insulin secretion and homeostasis in rats. J Nutr 1984; 114: 1438-1446.
2. Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982; 35: 456.
3. Bertinchamps AJ, Miller ST, Cotzias GC. Interdependence of routes excreting manganese. Am J Physiol 1966 211: 217-224.
4. Britton AA, Cotzias GC. Dependence of manganese turnover on intake. Am J Physiol 1966; 221: 203-206.
5. Cotzias GC et al. Slow turnover of manganese in active rheumatoid arthritis and acceleration by prednisone. J Clin Invest 47:992, 1968.
6. Davidsson L, Almgren A, Juillerat MA et al. Manganese absorption in humans. The effect of phytic acid and ascorbic acid in soy formula. Am J Clin Nutr 1995; 62: 984-987.
7. Engel RW, Price NO, Miller RF Copper, manganese, cobalt, and molybdenum balance in pre-adolescent girls. J Nutr 1967; 92: 197-204.
8. Greger JL, Baligar P, Abernathy RP et al. Calcium, magnesium, phosphorus, coppcr, and manganese balance in adolescent females. Am J Clin Nutr 1978; 31: 117-121.
9. Gribauskas P et al. Manganese levels in hair as an additional indicator for early diagnosis of ischemic disease of the heart. Lab Delo ;10:629, 1985.
10. Gruden N. Suppression of transduodenal manganese transport by milk diet supplemented with iron. Nutr Metabol 1977; 21: 305-309.
11. Guthrie BE, Robinson MF. Daily intakes of manganese, copper, zinc and cadmium by New Zealand women. Br J Nutr 1977; 38: 55-63.
12. Keen, CL, Zidenberg-Cherr, S. Present knowledge in nutrition. 6th edn. Washington, DC: Nutrition Foundation. 1990: p 279-286.
13. Keen, CL, Zidenberg-Cherr, S. Manganese. In: Present knowledge in nutrition. 7th edn. Washington, DC: Nutrition Fo~ndation.1996: p 334-343.
14. Kies C, ed. Nutritional bioavailability of manganese. Washington, DC: American Chemical Society. 1982.
15. McLeod BE, Robinson MF. Metabolic balance of manganese in young women. Br J Nutr 1972; 27: 221-227.
16. Schlage C, Wortberg B. Manganese in the diet of healthy preschool and school children. Acta Paediatr Scand 1972, 61: 648-652.
17. Spencer H, Asmussen CR, Holtzman RB et al. Metabolic balances of cadmium, copper, manganese, and zinc in man. Am J Clin Nutr 1979; 32: 1867-1875.
18. Wenlock RW, Buss DH, Dixon EJ. Manganese in British food. Br J Nutr 1979; 41: 253-261.

Kilder:
Joseph E. Pizzorno Jr., Michael T. Murrey & Melvyn R. Werbach.

Selen, forskningsreferencer

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Januar 1999

  1. Bruce A et al. The effect of selenium and vitamin E on glutathione peroxidase levels and subjective symptoms in patients with arthrosis and rheumatoid arthritis, in Proc N Z Workshop on Trace Elements in N Z. Dunedin, U. of Otago, 1981: 92.
  2. Chen X, Xiaoshu, Chen X et al. Selenium in biology and medicine. New York: AVI/Van Nostrand Reinhold. 1987: p 589-607.
  3. Clark LC. The epidemiology of selenium and cancer. Fed Proc 1985; 44: 2584-2589.
  4. Clark L, Combs GF Jr, Turnbull BW et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. JAMA 1996.
  5. Constans J, Pellegrin JL, Sergeant C, et al. Serum selenium predicts outcome in HIV infection. J AIDS Human Retrovirol 10:392, 1995.
  6. Delmas-Beauvieux M-C, Peuchant E, Couchouron A, et al. The enzymatic antioxidant system in blood and glutathione status in human immunodeficiency virus (HIV)-infected patients: Effects of supplementation with selenium or carotene. Am J Clin Nutr 64:101-7, 1996.
  7. Fletcher MP, Gershwin ME, Keen CL et al. Trace element deficiences and immune responsiveness in humans and animal models. In: Chandra RK, ed. Nutrition and immunology. New York: Alan R, Liss. p 215-239, 1988.
  8. Gebre-Medhin M et al. Selenium supplementation in X-linked muscular dystrophy. Effects on erythrocyte and serum selenium and on erythrocyte glutathione peroxidase activity. Acta Paediatr Scand 74;6:886-90, 1985.
  9. Glover JR. Proceedings of the symposium on selenium-tellurium environments. Pittsburgh: Industrial Health Foundation. 1976: p 279-292.
  10. Hinks LJ, Inwards KD, Lloyd B, Clayton BE. Body content of selenium in coeliac disease. Br Med J Clin Res 288:1862-3, 1984.
  11. Jackson ML. Selenium. Present status and perspectives in biology and medicine. Clifton, NJ: Humana Press. 1988: p 13-21.
  12. James S et al. Effekter av selenvitamin E-behandling till kvinnor med lång variga arbetsrelaterade nack-och skuldersmärtor. En dubbelblindstudie. Läkaresällskapets Riksstämma, 1985.
  13. Jameson S et al. Pain relief and selenium balance in patients with connective tissue disease and osteoarthrosis: A double-blind selenium tocopherol supplementation study. Nutr Res Suppl 1: 391-7, 1985.
  14. Juhlin L et al. Blood glutathione-peroxidase levels in skin diseases: Effect of selenium and vitamin E treatment. Acta Derm Venereal (Stockh) 62; 3: 211-4, 1982.
  15. Karakucuk S et al. Selenium concentrations in serum, lens and aqueous humor of patients with senile cataract. Acta Ophthalmol Scand 73:323-32, 1995.
  16. Kok FJ et al. Decreased selenium levels in acute myocardial infarction. JAMA 261;8:1161-4, 1989.
  17. Korpela H et al. Effect of selenium supplementation after acute myocardial infarction. Res Commun Chem Pathol Pharmacol 65:249-52, 1989.
  18. Kose K et al. Plasma selenium levels in rheumatoid arthritis. Biol Trace Elem Res 53: 51-6, 1996.
  19. L’Abbe M, Fischer W, Trick K et al. Dietary Se and tumor glutathione peroxidase and superoxide dismutase activities. J Nutr Biochem 1991; 2: 430-436.
  20. Levander OA. A global review of human selenium nutrition. Ann Rev Nutr 1987; 7: 227-250.
  21. Levander OA. Trace substances in environmental health – 23. Springfield: University of Missouri. 1990: p 11-19.
  22. Levander, OA, Burk, RF. Selenium. In. Present knowledge in nutrition. 7th edn. Washington, DC: Nutrition Foundation. 1996: p 320-328.
  23. Longnecker GF. Nutrition and cancer prevention: investigating the role of micronutrients. New York: Marcel Dekker. 1989: p 389-420.
  24. Macpherson A, Scott R, Yates R. The Effect of Selenium Supplementation in Sub-Fertile Males. (Abstract), 8th International Conference on Trace Element Metabolism in Man and Animals, 1993.
  25. Moore JA et al. Selenium concentrations in plasma of patients with arteriographically defined coronary atherosclerosis. Clin Chem 30:1171, 1984
  26. Munthe E, Aaseth J. Treatment of Rheumatoid Arthritis with Selenium and Vitamin E. Scan J of Rheumatol 53 (suppl.): 103, 1984.
  27. Oster O et al. The serum selenium concentration of patients with acute myocardial infarction. Ann Clin Res 18;1:36-42, 1986.
  28. Overad K, Thorling EB, Bjerring P, Ebbesen P. Selenium inhibits W-light-induced skin caronogenesis in hairless mice. Cancer Lett 1985; 27: 163-170.
  29. Peretz A, Nève J, Famaey J. Selenium in rheumatic diseases. Semin Arthritis Rheum 20: 305-16, 1991.
  30. Peretz A, Nève J, Duchateau J, Famaey JP. Adjuvant treatment of recent onset rheumatoid arthritis by selenium supplementation: Preliminary observations. Br J Rheumatol 31: 281-6, 1992.
  31. Robinson MF et al. Effect of daily supplements of selenium on patients with muscular complaints in Otago and Canterbury. N Z Med J 93:289-292, 1981.
  32. Salonen JT et al. Association between cardiovascular death and myocardial infarction and serum selenium in a matched-pair longitudinal study. Lancet ii:175-9, 1982
  33. Salonen JT, Alfthan G, Huttunen JK, Puska P. Association between serum selenium and the risk of cancer. Am J Epidem 1984; 120: 342-349.
  34. Salonen JT et al. Interactions of serum copper, selenium, and low density lipoprotein cholesterol in atherogenesis. Br Med J 302:756-60, 1991.
  35. Schrauzer GN, Sacher J. Selenium in the maintenance and Therapy of HIV-infected patients. Chem Biol Interact 91:199-205, 1994.
  36. Shamberger RJ, Frost DV. rossible protective effect of selenium against human cancer. Can Med Assoc J 1969; 100: 682.
  37. Shamberger RJ. Biochemistry of selenium. New York: Plenum. 1983.
  38. Sklodowska M, Wasowicz W, Gromnadzinska J, et al. Selenium and vitamin E concentrations in plasma and erythrocytes of angina pectoris patients. Trace Elem Med 8:113-17, 1991.
  39. Stead NW et al. Selenium Se balance in the dependent elderly. Am J Clin Nutr 39:677, 1984.
  40. Stone WL et al. Effects of dietary selenium and vitamin E on plasma lipoprotein cholesterol levels in male rats. Ann Nutr Metab 30:94-103, 1986.
  41. Suadicani P, Hein H, Gyntelberg F. Serum selenium concentration and risk of ischaemic heart disease in an prospective cohort study of 3000 males. Atherosclerosis 96:33-42, 1992.
  42. Sunde RA. Molecular biology of selenoproteins. Ann Rev Nutr 1990; 10: 451-474.
  43. Sword J, Pope A, Hoekstra W. Endotoxin and lipid peroxidation in vitro in selenium- and vitamin E-deficient and -adequate rat tissues. J Nutr 1991; 121: 258-264.
  44. Tarp U et al. Low selenium level in severe rheumatoid arthritis. Scand J Rheumatol 14: 97, 1985.
  45. Tarp U et al. Selenium Treatment in Rheumatoid Arthritis. Scandinavian J of Rheumatol 14: 364-8, 1985.
  46. Vanderpas JB, Contempre B, Duale NL et al. Iodine and selenium deficiency associated with cretinism in northern Zaire. Am J Clin Nutr 1990; 52: 1087-1094.
  47. Van Rij AM et al. Selenium deficiency in total parenteral nutrition. Am J Clin Nutr 32:2076-85, 1979.
  48. Virtamo J et al. Serum selenium and the risk of coronary heart disease and stroke. Am J Epidemiol 122:276-82, 1985.
  49. Winnefeld K, Dawczynski H, Schirrmeister W et al. Selenium in serum and whole blood in patients with surgical interventions. Biological Trace Element Res 1995; 50: 149-155.
  50. Wright JV, Ogle DJ, Hoare L. Improvement of vision in macular degeneration associated with intravenous zinc and selenium therapy: two cases. J Nutr Med 1:133-8, 1990.
  51. Yang GQ Wang SZ, Ahou RH, Sun SZ. Endemic selenium intoxication of humans in China. Am J Clin Nutr 1983- 37: 872-881.
  52. Yu SY et al. Chemoprevention trial of human hepatitis with selenium supplementation in China. Biol Trace Elem Res 21; 1-2:15-22, 1989.
  53. Zazzo JF, Chalas J, Lafont A, et al. Is nonobstructive cardiomyopathy in AIDS a selenium deficiency-related disease? Letter. JPEN J Parenter Enteral Nutr 12; (5):537-8, 1988.
  54. Zielonka E et al. Sulfur and selenium levels in the blood of patients with rheumatoid arthritis and ankylosing spondylitis. Reumatologia 20; 3-4: 217-20, 1982.
  55. Örndahl G et al. Myotonic dystrophy and selenium. Acta Med Scand 211:493-9, 1982.
  56. Örndahl G et al. Selenium therapy of myotonic dystrophy. Acta Med Scand 213;3:237-9, 1983.
  57. Örndahl G et al. Myotonic dystrophy treated with selenium and vitamin E. Acta Med Scand 219:409-44, 1986.

 

Kilder:
Joseph E. Pizzorno Jr., Michael T. Murrey & Melvyn R. Werbach.

Zink, forskningsreferencer

Admin

Januar 1999

1. Aamodt RL, Rumble WF, Johnston GS et al. Absorption of orally administrated 65Zn (zinc) by normal human subjects. Am J Clin Nutr 1981; 34: 2648-2652.
2. Bales CW, Freeland-Graves JH, Askey S et al. Zinc, magnesium, copper, and protein concentrations in human saliva. Age- and sex-related differences. Am J Clin Nutr 1990, 51: 462-469.
3. Balogh Z et al. Plasma Zinc and its relationship to clinical symptoms and drug treatment in rheumatoid arthritis. Ann Rheum Dis 39(4): 329-32, 1980.
4. Berg JM, Shi Y. The galvanization of biology. A growing appreciation for the roles of zinc. Science 1996; 271: 1081-1085.
5. Brody I. Topical treatment of recurrent herpes simplex and post-herpetic erythema multiforme with low concentrations of zinc sulphate solution. Br J Dermatol 104; (2):191-4, 1981.
6. Caselli M, Bicocchi R. Taux serique du zinc chez les malades atteints du syndrome d’immunodeficit acquis. Presse Med 37:1877-8, 1986 (in French).
7. Cunnigham-Rundles S, Cunningham-Rundles WF. Nutrition and immunology. New York: Alan R. Liss. 1988: p 197-214.
8. Cousins RJ, Hempe JM. Zinc. In: Present knowledge in nutrition. 6th edn. Washington, DC: Nutrition Foundation. 1990: p 251-260.
9. Cousins RJ. Zinc. In: Present knowledge in nutrition. 7th edn. Washington, DC: Nutrition Foundation. p 293-306, 1996.
10. Crofton RW et al. Zinc metabolism in celiac disease. Am J Clin Nutr 52; (2):379-82, 1990.
11. DeBartolo HM Jr. Zinc and diet for tinnitus. Am J Otol 10; 3: 256, 1989.
12. De Gordon AM. Effects of adjuvant therapy with zinc in human immunodeficiency infection. Abstract. J Am Coll Nutr 11; (5):601, 1992.
13. De Gordon AM. Evaluation of tissue zinc status through cell-mediated immune response in HIV disease. Abstract. J Am Coll Nutr 11; (5):602, 1992.
14. Eby GA. Use of topical zinc to prevent recurrent herpes simplex infection: Review of literature and suggested protocols. Med Hypotheses 17:157-65, 1985.
15. Eby GA. Linearity in dose-response from zinc lozenges in treatment of common colds. J Pharmacy Technol 11:110-22, 1995.
16. Engel ED et al. Diabetes melitus: Impaired Wound Healing from Zinc Deficiency. J Am Pod Assoc 71: 536-44, 1981.
17. Finnerty EF. Topical zincin the treatment of herpes simplex. Cutis 37; (2):130-1, 1986.
18. Fitzherbert J. Genital herpes and zinc. Med J Aust 1:399, 1979.
19. Gersdorff M et al. The zinc sulfate overload test in patients suffering from tinnitus associated with low serum zinc. Preliminary report. Acta Otorhinolaryngol Belg 41; 3: 498-505, 1987.
20. Gersdorff M et al. A clinical correlation between hypozincemia and tinnitus. Arch Otorhinolaryngol 244; 3:190-3, 1987.
21. Gibson RS, Anderson BM, Scythes CA. Regional differences in hair zinc concentrations. A possible effect of water hardness. Am J Clin Nutr 1983; 37: 37-42.
22. Godfrey JC, Sloane B, Smith D. Zinc gluconate and the common cold: a controlled clinical study. J Int Med Res 20; 3:234-46, 1992.
23. Gordon YJ et al. Irreversible inhibition of herpes simplex virus replication in BSC-1 cells by zinc ions. Antimicrob Agents Chemother 8; (3):377-80, 1975.
24. Grennan DM et al. Serum copper and zinc in rheumatoid arthritis and osteoarthritis. N Z Med J 91; 652: 47-50, 1980.
25. Hambidge KM. Zinc deficiency in young children. Am J Clin Nutr 1997; 65: 160-161.
26. Haring BSA, Van Delft W. Changes in the mineral composition of food as a result of cooking in ‘hard’ and ‘soft’ waters. Arch Environ Health 1981; 36: 33-35.
27. Hegazi SM et al. Effect of Zinc Supplementation on Serum Glucose, Insulin, Glucagon, Glucose-6-Phosphatase and Mineral Levels in Diabetics. J Clin Biochem Nutr 12: 209-15, 1992.
28. Honkanen VEA et al. Plasma zinc and copper concentrations in rheumatoid arthritis: Influence of dietary factors and disease activity. Am J Clin Nutr 54: 1082-6, 1991.
29. Huber AM, Gershoff SN. Effects of zinc deficiency on the oxidation of retinol and ethanol in rats. J Nutr 10:11:1486-90, 1975.
30. King JC, Hambidge KM, Westcott JL et al. Daily variation in plasma zinc concentrations in women fed meals at six-hour intervals. J Nutr 1994; 124: 508-516.
31. King JC. Does poor zinc nutriture retard skeletal growth and mineralization in adolescents? Am J Clin Nutr 1996; 64: 375-376.
32. Kondo T, Toda Y, Matsui H. Effects of exercise and sleep deprivation on serum zinc. J Trace Elem Exp Med 1990; 3: 324-354, 1990.
33. Koyama H, Hosokai H, Tamura S et al. Positive association between serum zinc and apolipoprotein A-II concentrations in middle-aged males who regularly consume alcohol. Am J Clin Nutr 57: 657-661, 1993.
34. Krebs NF, Reidinger CJ, Hartley S et al. Zinc supplementation during lactation. Effects on maternal status and milk zinc concentrations. Am J Clin Nutr 61: 1030-1036, 1995.
35. Krotkiewski M et al. Zinc and muscle strength and endurance. Acta Physiol Scand 116; 3: 309-11, 1982.
36. Mahajan S, Prasad A, Brewer G et al. Effect of changes in dietary zinc intake on taste acuity and dark adaptation in normal human subjects. J Trace Elem Exp Med 5: 33-45, 1992.
37. Mares-Perlman JA et al. Association of zinc and antioxidant nutrients with age-related maculopathy. Arch Ophthalmol 114:991-7, 1996.
38. Masters DG, Keen CL, Lonnerdal B, Hurley LS. Zinc deficiency teratogenicity. The protective role of maternal tissue catabolism. J Nutr 113: 905-912, 1983.
39. Mattingly PC et al. Zinc Sulphate in Rheumatoid Arthritis. Ann Rheuma Dis 41: 456-7, 1982.
40. Meadows NJ, Ruse W, Smith MF et al. Zinc and small babies. Lancet 2: 1135-1137, 1981.
41. Menkes C-J et al. Traitement de la polyarthrite rheumatoide par le sulfate de zinc par os. Presse Med 7: 760, 1978 (French).
42. Mobarhan S et al. Dietary zinc deficiency produces electroretinogram ERG abnormalities without depleting total ocular zinc. Fed Proc 43:685, 1984.
43. Mocchegiani E, Veccia S, Ancarani F, et al. Benefit of Oral Zinc supplementation (as an adjunct to Zidovudine (AZT)) Therapy against Opportunistic Infections in AIDS. Int J Immunopharmacol 17; (9):719-27, 1995.
44. Moser-Veillon PB, Reynolds RD. A longitudinal study of pyridoxine and zinc supplementation of lactating women. Am Clin Nutr 52: 135-141, 1990.
45. Mossad SB, Macknin ML, Medendorp SV et al. Zinc gluconate lozenges for treating the common cold. A randomized, placebo controlled study. Ann Intern Med 125: 81-88, 1996.
46. Mussalo-Rauhamaa H et al. Predictive clinical and laboratory parameters for serum zinc and copper in rheumatoid arthritis. Ann Rheum Dis 47; 10: 816-19, 1988.
47. Naveh Y et al. Zinc metabolism in rheumatoid arthritis: plasma and urinary zinc and relationship to disease activity. J Rheumatol 24; 4: 643-6, 1997.
48. Newsome DA, Swartz M, Leone NC, et al. Oral zinc in macular degeneration. Arch Ophthalmol 106:2:192-8, 1988.
49. Newsome DA et al. Zinc content of human retinal pigment epithelium decreases with age and macular degeneration, but superoxide dismutase activity increases. J Trace Elem Exp Med 8:193-9, 1995.
50. Nishi Y. Anemia and zinc deficiency in the athlete. J Am Col Nutr 15: 323-324, 1996.
51. Pandley SP et al. Zinc in rheumatoid arthritis. Indian J Med Res 81: 618-20, 1985.
52. Peretz A, Nève J, Jeghers O, Pelen F. Zinc distribution in blood components, inflammatory status, and clinical indexes of disease activity during zinc supplementation in inflammatory rheumatic diseases. Am J Clin Nutr 57: 690-4, 1993.
53. Posacki C, et al. Plasma, Copper, Zinc, and Magnesium Levels in Patients with Premenstrual Tension Syndrome, Acta syndrome : Obstet Gynecol Scand 73; 452-5, 1994.
54. Prasad ASP. Clinical biochemical and nutritional spectrum of zinc deficiency in human subjects: An update. Nutr Rev 41: 197-208, 1983.
55. Rangnekar GV, Gamur MS. Serum and urinary zinc levels in urolithiasis. Br J Urology 71:527-9, 1993.
56. Reunanen A, Knekt P, Marniemi J et al Serum calcium, magnesium, copper and zinc and risk of cardiovascular death. Eur J Clin Nutr 50: 431 – 437, .
57. Shambaugh GE Jr. Zinc for tinnitus, imbalance, and hearing loss in the elderly. Am J Otol 7; 6:476-7, 1986.
58. Simmer K, Thompson RP. Maternal zinc and intrauterine growth retardation. Clin Sci 68: 395-399, 1985.
59. Singal PK, Dhillon KS, Beamish RE, et al. Protective action of zinc against catecholamine-induced myocardial changes. Electrocardiographic and ultrastructural studies. Lab Invest 44:426, 1981.
60. Soltan MH, Jenkins DM. Maternal and fetal plasma zinc concentration and fetal abnormality. Br J Obstet Gynaecol 89: 56, 1982.
61. Sandstead HH. WO Atwater memorial lecture. Zinc. Essentially for brain dcvelopment and function. Nutr Rev 1985; 43: 129-137, 1985.
62. Schauss AG, Bryce-Smith D. Nutrients and brain function. Basil: Karger. p 151-162, 1987.
63. Shah DR et al. Effect of oral zinc sulphate on serum lipids and lipoproteins in human subjects. Indian J Physiol Pharmacol 32;1:47-50, 1988.
64. Shambaugh GE Jr – interviewed in Anonymous. Hearing loss may be linked to zinc deficiency. Geriatrics 38; 4:21, 1983.
65. Shambaugh GE Jr. Zinc for tinnitus, imbalance, and hearing loss in the elderly. Am J Otol. 7: 476-477, 1986.
66. Shambaugh GE Jr. Zinc. The neglected nutrient. Am J Otol. 10: 156-160, 1989.
67. Shambaugh GE. Zinc, an essential nutrient for hearing and balance. Int J Biosocial Med Res. 13: 192-199, 1991.
68. Simkin PA. Oral zinc sulphate in rheumatoid arthritis. Lancet ii: 539-42, 1976.
69. Simkin PA. Treatment of Rheumatoid Arthritis with Oral Zinc Sulfate. Agents and Actions; (suppl.) 8: 587-95, 1981.
70. Sturniolo GC, Montino MC, Rossetto L et al. Inhibition of gastric acid secrecion reduces zinc absorption in man. J Am Col Nutr 4: 372-375, 1991.
71. Svenson KL et al. Reduced zinc in peripheral blood cells from patients with inflammatory connective tissue diseases. Inflammation 9; 2: 189-99, 1985.
72. Takihara H, Cosentino MJ, Cockett AT. Effect of low-dose androgen and zinc sulfate on sperm motility and seminal zinc levels in infertile men. Urology 22: 160, 1983.
73. Taper LJ, Oliva JT, Ritchey SJ. Zinc and copper retention during pregnancy. The adequacy of prenatal diets with and without dietary supplementation. Am J Clin Nutr 41: 1184-1192, 1985.
74. Taylor CM, Bacon JR, Aggett PJ et al. Homeostatic regulation of zinc absorption and endogenous losses in zinc-deprived men. Am J Clin Nutr 53: 755-763, 1991.
75. Thomas EA, Bailey LB, Kauwell GA et al. Erythrocyte metallothionein response to dietary zinc in humans. J Nutr 122: 2408-2414, 1992.
76. Tuormaa TE. Adverse effects of zinc deficiency. A review from the literature. J Orthomol Med 10: 149-164, 1995.
77. Ulshafer RJ. Zinc content in melanosomes of degenerating RPE as measured by X-ray maping. Prog Clin Biol Res 314:131-9, 1989.
78. Wagner PA, Bailey LB, Christakis GJ, Dinning JS. Serum zinc concentrations in adolescents as related to sexual maturation. Human Nutr. Clin Nutr 39C: 459, 1985.
79. Zlotkin SH, Casselman CW. Urinary zinc excretion in normal subjects. J Trace Elem Exp Med. 3: 13-21, 1990.

 

Kilder:
Joseph E. Pizzorno Jr., Michael T. Murrey & Melvyn R. Werbach.

Essentielle fedtsyrer, forskningsreferencer

Admin

Januar 1999

1. Adler AJ, Holub BJ: Effect of garlic and fish-oil supplementation on serum lipid and lipoprotein concentrations in hypercholesterolemic men. Am J Clin Nutr 65:445-450, 1997.
2. Albert CM, Hennekens CH, Willett WC, Manson JE, et al.: Fish consumption and risk of sudden cardiac death. JAMA 279:23-28, 1998.
3. Amusquivar E, Ruperez FJ, Barbas C, Herrera E: Low arachidonic acid rather than alpha-tocopherol is responsible for the delayed postnatal development in off… J Nutr 130:11:2855-65, 2000.
4. Annuzzi G, Rivellese A, Capaldo B, Di Marino L, et al.: A controlled study on the effects of n-3 fatty acids on lipid and glucose metabolism in non-insulin-dependent diabet. Atherosclerosis 87:1:65-73, 1991.
5. Appel LJ: The effect of omega-3 polyunsaturated fatty acids on blood pressure. Omega-3 News:1:1-4 , 1994.
6. Ariza-Ariza R, Mestanza-Peralta M, Cardiel MH: Omega-3 fatty acids in rheumatoid arthritis: an overview. Semin Arthritis Rheum 27:6:366-370, 1998.
7. Ascherio A, Rimm EB, Stampfer MJ, Giovannucci EL, et al.: Dietary intake of marine n-3 fatty acids, fish intake, and the risk of coronary disease among men. N Engl J Med 332:15:977-982, 1995.
8. Bagga D, Capone S, Wang HJ, Glaspy JA, et al.: Dietary modulation of omega-3/omega-6 polyunsaturated fatty acid ratios in patients with breast cancer. J Natl Cancer Inst 89:15:1123-31, 1997.
9. Barham JB, Edens MB, Fonteh AN, Johnson MM, et al.: Addition of eicosapentaenoic acid to gamma-linolenic acid-supplemented diets prevents serum arachidonic acid… J Nutr 130:8:1925-1931, 2000.
10. Bartels M, Nagel E, Pichlmayr R What is the role of nutrition in ulcerative colitis? A contribution to the current status of diet therapy in treatm. Langenbecks Archiv fur Chirurgie 380:1:4-11, 1995.
11. Begin ME, Das UN, Ells G, Horrobin DF: Selective killing of human cancer cells by polyunsaturated fatty acids. Prostaglandins Leukotrienes and Medicine 19:177-186, 1985.
12. Begin ME, Das UN: A deficiency in dietary gamma-linolenic and/or eicosapenta- enoic acids may determine individual susceptibility to AIDS. Medical Hypotheses 20 20:1-8, 1986.
13. Belluzzi A, Brignola C, Campieri M, Pera A, et al.: Effect of an enteric-coated fish-oil preparation on relapses in Crohn’s disease. New England Journal of Medicine 334:24:1557-60, 1996.
14. Berth-Jones J, Graham-Brown RA: Placebo-controlled trial of essential fatty acid supplementation in atopic dermatitis published erratum appea. Lancet 341:8860:1557-1560, 1993.
15. Bittiner SB, Tucker WF, Cartwright I, Bleehen SS: A double-blind, randomised, placebo-controlled trial of fish oil in psoriasis. Lancet 1:8582:378-380, 1988.
16. Bjørneboe A, Søyland E, Bjørneboe GE, Rajka G, et al.: Effect of dietary supplementation with eicosapentaenoic acid in the treatment of atopic dermatitis. Br J Dermatol 117:4:463-469, 1987.
17. Bonefeld-Jørgensen EC, Møller SM, Hansen JC: Modulation of atherosclerotic risk factors by seal oil: a preliminary assessment. International. J. of Circumpolar Health 60:25-33, 2001.
18. Brown JE, Wahle KW: Effect of fish-oil and vitamin E supplementation on lipid peroxidation and whole-blood aggregation in man. Clin Chim Acta 193:3:147-56, 1990.
19. Brown M: Do vitamin E and fish oil protect against ischaemic heart disease? Lancet 354:441-442, 1999.
20. Burkow IC, Henderson RJ: Analysis of polymers from autoxidized marine oils by gel permeation HPLC using a light-scattering detector. Lipids 26:3:227-231, 1991.
21. Cathcart ES, Mortensen RF, Leslie CA, Conte JM, et al.: A fish oil diet inhibits amyloid P component (AP) acute phase responses in arthritis susceptible mice. J Immunol 139:1:89-91, 1987.
22. Cathcart ES, Gonnerman WA, Leslie CA, Hayes KC: Dietary n-3 fatty acids and arthritis. J Intern Med Suppl 225:731:217-23, 1989.
23. Cathcart ES, Gonnerman WA: Fish oil fatty acids and experimental arthritis. Rheum Dis Clin North Am 17:2:235-242, 1991.
24. Christensen M S, Mortimer B, Høy C, Redgrave T G: Clearance of Chylomicrons following Fish Oil and seal Oil Feeding Nutr. Res. 15:3:359-368, 1995.
25. Cleland LG, Hill CL, James MJ: Diet and arthritis. Baillieres Clin Rheumatol 9:4:771-85, 1995.
26. Cleland LG, French JK, Betts WH, Murphy GA, et al.: Clinical and biochemical effects of dietary fish oil supplements in rheumatoid arthritis. J Rheumatol 15:10:1471-5, 1988.
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Kilder:
Joseph E. Pizzorno Jr., Michael T. Murrey & Melvyn R. Werbach.

C-vitamin og cancerbehandling 1. del

Claus Hancke

Maj 1997

– Uddrag og kommentarer fra den videnskabelige litteratur

Af Gary Null, PhD, Howard Robins, DPM, Mark Tanenbaum, DPM og redaktør Patrick Jennings.
Townsend Letter for Doctors & Patients – maj 1997

Hvorfor denne kritiske gennemgang af videnskabelig litteratur?

Ordentlig basal ernæring er et vigtigt fundament for sundhed, men der er en voksende erkendelse af at det ikke er nok. Man behøver kun at tage sygdomsstatistikkerne i vores samfund i betragtning – infektionssygdomme er nu den tredjestørste dræber i USA samt den største i hele Verden, og tilfælde af cancer, gigt og psykiske lidelser er ikke formindsket – for at se, at vi er nødsaget til at gå videre end den basale ernæring for at bekæmpe sygdom.

Det er på tide at vi ser mere seriøst på kosttilskud, for bedre at forstå deres rolle i at støtte vores naturlige immunforsvar til at forebygge sygdom og ændre sygdomsforløb.

Folk taler om ortodoks medicin og alternativ medicin, som om der er et stort skel mellem de to, men der er faktisk ikke brug for en sådan adskillelse. Det vigtigste spørgsmål inden for behandling og bevarelsen af ens helbred er egentlig: Hvad virker? og vi skulle have lov til at spørge, mens vi evaluerer tilbuddene fra begge lejre, og til at kombinere det bedste fra dem begge.

Når alt kommer til alt, er det beviset for at noget virker – og ikke prædikatet man giver det – som er den vigtige faktor, der afgør om en bestemt behandling, funktion eller forebyggelsesmetode er af værdi.

Følgende er en oversigt over videnskabelig litteratur vedrørende C-vitaminets indvirkning på cancer. Spørgsmålene bag denne oversigt var motiverede af: ”Hvad virker?” og ”Hvordan skal det bruges?” Som også denne oversigt gør, vil enhver oversigt kun medtage veldesignede forsøg fra peer-reviewede tidsskrifter. De oprindelige tidsskrift-citater er medtaget, ligesom de koncentrerede beskrivelser af de oprindelige forsøgsuddrag er det.

Med andre ord, det følgende er ikke anekdotisk bevisførelse; det er et videnskabeligt bevis. Vi kan bevæge os ud over niveauet, hvor ”quackbusters”, undskyldninger fra specielle interessegrupper og andre tilhængere af jorden-er-flad-bevægelsers intellektuelle udspørgen ønsker at fastholde, at der intet bevis er for næringsstoffers værdi. Helt enkelt fordi det er bevist, og beviset er her.

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Denne oversigtsartikel fremhæver at omkring 90 forsøg vedrørende C-vitamin’s rolle i cancerforebyggelse har været foretaget, og at disse for de flestes vedkommende har fundet statistisk signifikant virkning. Den beskyttende virkning er blevet påvist i forbindelse med cancer i bugspytkirtelen, mundhulen, maven, spiserør, livmoderhals, rektum, bryster og lunger.

– G. Block, et al., Epidemiologic Evidence Regarding Vitamin C and Cancer, American Journal of Clinical Nutrition, 54 (6 Suppl), December 1991, p. 1310S-1314S.

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Daglig indtagelse af 1 gram C-vitamin formindskede mængden af kromosomskade fremkaldt i lymfocytter ved en udsættelse for bleomycin over de sidste 5 timer af en cellekultur. Forfatterne foreslår et lignende forsøg om genetisk ustabilitet kan være en hjælp til at påvise heterozygote med kromosomskade-syndromer og foreslå kost- og livsstilsændringer på grundlag af resultaterne fra denne bleomycin undersøgelse og relaterede fosøg vedrørende genetisk instabilitet.

– H. Pohl and J.A. Reidy, Vitamin C Intake Influences the Bleomycin-induced Chromosome Damage Assay: Implications for Detection of Cancer Susceptibility and Chromosome Breakage Syndromes, Mutat Research, 224(2), October 1989, p. 247-252.

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En trifold antioxidant-vitaminblanding bestående af askorbinsyre, alfa-tokoferol og lecithin sammen med rosmarinekstrakt, med carnosinsyre og carnosol som de to mest aktive ingredienser, viste sig at udvise stærke antimutagene virkninger i Ames tester strain TA102.

Askorbinsyren ansås for at være ansvarlig for denne hæmmende egenskab i vitaminblandingen, mens carnosinsyre blev identificeret som den antimutagene formidler i rosmarinekstrakt. Forfatterne konkluderer at disse antioxidanter måske udviser anticarginogene egenskaber.

– M. Minnunni, et al., Natural Antioxidants as Inhibitors of Oxygen Species Induced Mutagenicity, Mutat Research, 269(2), October 1992, p. 193-200.

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I dette forsøg viste C-vitamin at kunne hæmme nyretumor incidens med omkring 50 % i syriske hamstere, kunne nedsætte koncentrationen af diethylstilbesterol-4′,4″-quinon, den genotoksiske metabolit af diethylstilbestrol in vitro og i hamstere behandlet med stilbene, og nedsætte niveauet i hamstere af DES-DNA -fusioner skabt af quinon-metabolitten.

Forfatterne, som bemærkede at østrogen måske danner tumorer ved deres metaboliske oxidation af tilsvarende quinon-metabolitter, taler for, at C-vitamin kan hæmme dannelsen af tumorer ved at nedsætte koncentrationen af quinon-metabolitter og deres DNA-fusioner.

– J.G. Liehr, Vitamin C Reduces the Incidence and Severity of Renal Tumors Induced by Estradiol or Diethylstilbestrol, American Journal of Clinical Nutrition, 54 (6 Suppl), December 1991, p. 1256S-1260.

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Dette skrift rapporterer om resultaterne af to stort anlagte forsøg med L-askorbinsyre i foder til mus, for at undersøge overlevelsen uden tumorer. Det første viste at forhøjet askorbinsyre i kosten signifikant forsinkede udviklingen af spontan brystkræft, med en gennemsnitlig alder ved den første tumor på 124,9 uger i den højest doserede askorbatgruppe og 82,5 uger i ad libitum-kontrolgruppen. Andelen af mus med tumorer blev også reduceret.

Det andet forsøg opdagede en signifikant forsinkende virkning af askorbat på tumorangreb og nedsættelse af forekomsten af kræft-skader. Omkring 5 gange så mange mus udviklede skader i nul-askorbatgruppen i forhold til askorbatgruppen efter 20 ugers indtagelse.

– L. Pauling, Effect of Ascorbic Acid on Incidence of Spontaneous Mammary Tumors and UV-Light-Induced Skin Tumors in Mice, American Journal of Clinical Nutrition, 54 (6 Suppl), December 1991, p. 1252S-1255S.

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Askorbat stabiliserer den normale tilstand i fugle-seneceller ved at reducere Rous sarcom-virusproduktion og fremme syntesen af differentierede proteiner, som tillader at virus eksisterer i cellen, frem for helt at overtage den.

– R.I. Schwarz, Ascorbate Stabilizes the Differentiated State and Reduces the Ability of Rous Sarcoma Virus to Replicate and to Uniformly Transform Cell Cultures, American Journal of Clinical Nutrition, 54 (6 Suppl), December 1991, p. 1247S-1251S.

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I erindring om at teorier har påvist, at askorbinsyre kan være i stand til at nedsætte risikoen for mavecancer ved at forebygge cancervæksten i mavesyre, har forfatterne målt både askorbinsyre i mavesaft og totalmængden af C-vitamin, og opdaget, at askorbinsyre bliver udskilt i mavesækken, hvorfor mavesaften ofte ligger højere i c-vitamin koncentration end koncentrationen i plasma. Mavesygdomme kan indvirke på denne sekretion, så det medfører lavere mavesaftværdier end plasmaniveauer.

– C.J. Schorah, et al., Gastric Juice Ascorbic Acid: Effects of Disease and Implications for Gastric Carcinogenesis, American Journal of Clinical Nutrition, 58 (1 Suppl), January 1991, p. 287S-293S.

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Dette case-control forsøg evaluerede forbindelsen mellem specifikke substanser i kosten og invasiv kræft i livmoderhalsen hos kvinder i fire latinamerikanske lande. C-vitamin viste sig signifikant at kunne nedsætte risikoen for invasiv kræft i livmoderhalsen, hvilket også viste sig med betakaroten og andre karotenoider.

Disse resultater er i overensstemmelse med andre forsøg, som påpeger, at C-vitamin har en beskyttende rolle i udviklingen af invasiv kræft i livmoderhalsen.

– R. Herrero, et al., A Case-Control Study of Nutrient Status and Invasive Cervical Cancer: I. Dietary Indicators, American Journal of Epidemiology, 134 (11), December 1, 1991.

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2.974 mænd, som deltog i den tredje undersøgelse af det prospektive Basel-forsøg fra 1971-1973, blev undersøgt for plasma-antioxidanterne A-, C- og E-vitamin og karoten. Et gennemsnitlig lavt plasmaniveau af karoten, justeret efter kolesterol og C-vitamin, var forbundet med øget generel cancerdødelighed. Lavere C-vitaminværdier viste en større risiko for mavecancer og gastrointestinal cancer hos ældre mennesker.

I lyset af disse resultater for C-vitamin – og i kombination med resultater fra de andre undersøgte vitaminer – konkluderede forfatterne, at lave antioxidant-niveauer er forbundet med en forhøjet dødelighedsrisiko for adskillige cancertyper.

– H.B. Stahelin, et al. Plasma Antioxidant Vitamins and Subsequent Cancer Mortality in the 12-year Follow-up of the Prospective Basel Study, American Journal of Epidemiology, 133(8), April 15, 1991, p. 766-775.

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Man fandt et omvendt forhold mellem indtagelse af karotenoider, E-vitamin og C-vitamin og hyppigheden af lungecancer hos ikke-rygere i et 20-årigt opfølgningsforsøg bestående af 4.538 finske mænd uden cancer. Forfatterne peger på, at en øget indtagelse af disse næringsstoffer kan vise sig at beskytte mod udvikling af lungecancer hos ikke-rygere.

– P. Knekt, et al. Dietary Antioxidants and the Risk of Lung Cancer, American Journal of Epidemiology, 134(5), September 1, 1991, p. 471-479.

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NAC indgivet i doser fra 0,1 til 10 mmol/L nedsatte antallet af mutagen-inducerede skader pr celle fra 23 – 73 %. På et dosisniveau fra 0,01 til 1 mmol/L nedsatte askorbinsyre kromosomskader med 21 – 58 %.

Disse resultater viser NAC og askorbinsyres beskyttende virkning medieret in vitro imod mutagen-fremkaldt kromosomskade. Forskellen på forekomsten af hoved og halscancer i befolkningsgrupper med forskelligartet kost kan forklares ved relaterede forhold in vivo.

– Z. Trizna, et al. Effects of N-acetyl-L-cysteine and Ascorbic Acid on Mutagen-induced Chromosomal Sensitivity in Patients with Head and Neck Cancers, American Journal of Surgery 162(4), October 1991, p. 294-298.

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158 prøver taget af 139 lungecancerpatienter blev undersøgt for plasmaniveauer og ”buffy-coat” C-vitamin. Kostafhængig hypovitaminosis C viste tendens til at være til stede i størstedelen af prøverne og viste sig at blive forhøjet ved orale tilskud. Prøverne viste, at tumorer havde et større C-vitamin-indhold end normalt lungevæv.

– H.M. Anthony and C.J. Schorah, Severe Hypovitaminosis C in Lung-Cancer Patients: The Utilization of Vitamin C in Surgical Repair and Lymphocyte-Related Host Resistance, British Journal of Cancer, 46(3), Sept. 1982, p. 354-367.

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Betakaroten og askorbinsyre viste sig vedvarende at beskytte imod colorektal cancer i dette case-controlforsøg med 828 patienter med coloncancer og 498 patienter med endetarmscancer i Norditalien.

– M. Ferraroni, et al. Selected Micronutrient Intake and the Risk of Colorectal Cancer. British Journal of Cancer, 70(6), December 1994, p. 1150-1155.

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C-vitamintilskud viste sig at være modsat relateret til blære- og coloncancer hos kvinder i et 8-årigt opfølgningsforsøg begyndt i 1981 med 11.580 beboere uden cancer i et plejehjemsfællesskab.

– A. Shibata, et al. Intake of Vegetables, Fruits, Beta Carotene, Vitamin C and Vitamin Supplements and Cancer Incidence Among the Elderly: A Prospective Study, British Journal of Cancer (1992 Oct) 66(4), Oct. 1992, p. 673-679.

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Dette dobbeltblindede, placebo-kontrollerede forsøg undersøgte forholdet mellem askorbinsyre og store tyktarmssvulster. 3 g. askorbinsyre pr. dag reducerede polypområdet på 9 måneders opfølgning og resulterede i en faldende tendens, både hvad område og antal af rektale polypper angik.

– H.J. Bussey, et al. A Randomized Trial of Ascorbic Acid in Polyposis Coli, Cancer, 50(7), October 1, 1982, p. 1434-1439.

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Human neoplastiske cellelinier MCF-7 (brystcarcinom), KB (oral epidermal carcinom) og AN3-CA (endometrial adenocarcinom) blev undersøgt vedrørende virkninger på in vivo indgivelse af natrium-askorbat (C-vitamin) alene eller i kombination med 2-methyl-1,4-napthoquinon (K3-vitamin).

Når disse blev indgivet hver for sig, viste C-vitamin eller K-vitamin begge væksthæmmende virkning, men kun ved store koncentrationer (henholdsvis 5.10(3) umol/l og 10(5) nmol/l).

Når disse blev givet i kombination med hinanden, viste begge vitaminer en synergistisk hæmning af cellevækst ved 10 til 50 gange lavere koncentrationer. Tilføjelse af katalase til dyrkningsmediet, som indeholdt C-vitamin og K-vitamin, undertrykte totalt denne tumorcellevæksthæmmende virkning.

Forfatterne mener, at dette antyder, at en overproduktion af hydrogenperoxid (brintoverilte) er involveret i mekanismer ansvarlige for C-vitaminets hæmmende virkning af tumorcellevækst.

– V. Noto, et al., Effects of Sodium Ascorbate (Vitamin C) and 2-methyl-1,4-Naphthoquinone (Vitamin K3) Treatment on Human Tumor Cell Growth in Vitro. I. Synergism of Combined Vitamin C and K3 Action, Cancer, 63(5), March 2, 1989, p. 901-906.

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I dette hospitalsbaserede, case-control forsøg over lungecancer, blev en stærk beskyttende effekt mod planocellulær og småcellet carcinom forbundet med C-vitamin-indtagelse fra kosten, baseret på kostspørgeskemaer.

– E.T. Fontham, et al., Dietary Vitamins A and C and Lung Cancer Risk in Louisiana. Cancer, 62(10), November 15, 1988, p. 2267-2273.

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Virkningerne af 6-hydroxydopamin (6-OHDA) og H202 på metaboliske parametre kritiske for celleoverlevelse blev i dette forsøg undersøgt hos celler med et lavt og højt ferritin-indhold med tilstedeværelse og fravær af askorbat. Human neuroblastoma SKN-SH-celler med forskelligt jernindhold blev forbehandlet med 100 uMol FeSO4 og10 uMol desferoxamin i 24-timer.

Den mest udtalte virkning viste sig i de jernrigholdige celler og ved tilstedeværelsen af askorbinsyre. Brug af isoleret CCC PM2 DNA, 6-OHDA og askorbinsyre forårsagede (DNA-) strengbrud, som blev forebygget ved tilstedeværelsen af mannitol eller desferrithiocin. H202-medierede strengbrud sås kun ved tilstedeværelsen af askorbinsyre.

Forfatterne, som fremfører deres data sammen med tidligere forsøgsresultater, indikerer at høje doser af askorbinsyre indtaget kontinuerligt kan være en effektiv ny metode i behandlingen af neuroblastoma.

– G. Bruchelt, et al., Ascorbic Acid Enhances the Effects of 6-Hydroxdopamine and H202 on Iron-Dependent DNA Strand Breaks and Related Processes in the Neuroblastoma Cell Line SK-N-SH, Cancer Research, 51(22), November 15, 1991, p. 6066-6072.

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Dette forsøg, som involverede patienter med akut nonlymfocyt leukæmi, opdagede at antallet af leukæmisk knoglemarvcelle-kolonier dyrket i kultur aftog hos 21 % af kontrol i 7/28 af patienterne ved at tilsætte 0,3 milliM of L-askorbinsyre til kulturmediet. Koncentrationer af L-askorbinsyre så lave som 0,1 milliM var i stand til at undertrykke den leukæmiske celle-koloni i kulturer af både leukæmiske og normale knoglemarvsceller. Dog var 1 milliM af L-askorbinsyre nødvendig til at undertrykke normale myeloid kolonier.

Baseret på deres resultater, the argumenterer forfatterne for at den opnåede suppression var en specifik virkning af L-askorbinsyre og ikke til dets oxidation-nedsættende potentiale eller pH-forandring, siden normale hemopoietiske celler ikke blev undertrykt, medens man opnåede at udvalgte leukæmiske celler in vivo blev påvirket af en koncentration af L-askorbinsyre.

– C.H. Park, Biologial Nature of the Effect of Ascorbic Acids on the Growth of Human Leukemic Cells, Cancer Research, 45(8), August 1985, p. 3969-3973.

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81 patienter med præmaligne mundhuleskader fik 30 mg betacaroten, 1000 mg askorbinsyre og 800 i.e. alfatocoferol dagligt i 9 måneder. 55,6 % oplevede at skaderne var svundet enten fuldstændigt eller delvist.

Baseret på disse resultater anbefaler forfatterne, at man indtager antioxidant-kosttilskud til behandling af præmaligne mundhuleskader.

– G. Kaugars, et al. Serum and Tissue Antioxidant Levels in Supplemented Patients with Premalignant Oral Lesions (Meeting abstract), FASEB Journal, 7(4), 1993, A519.

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Dette forsøg undersøgte niveauer af C-vitamin og askorbinsyre i mavesaften på 77 patienter, som led af fordøjelsesbesvær (dyspepsi). De gastriske koncentrationer af C-vitamin og askorbinsyre var signifikant lavere hos patienter med kronisk mavekatar (gastritis), og man opdagede at patienter med nedsat saltsyreindhold (hypochlorhydia) havde specielt lave niveauer af askorbinsyrekoncentrationer.

– G.M. Sobala, et al., Ascorbic Acid in the Human Stomach, Gastroenterology, 97(2), August 1989, p. 357-368.

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I dette placebo-kontrollerede forsøg blev vitamintilskud undersøgt i relation til disses virkning på celle kinetik ved ikke-afficeret rektal mucosa i patienter med kolorektale adenomer.

A-, C- og E-vitamin blev indgivet til 20 personer (subjekter) 6 måneder efter fuld polypectomi . Resultaterne indikerer at vitamintilskud var effektivt til at reducere abnormaliteter på cellekinetik, som kan indikere en præcancer-tilstand.

– G.M. Paganelli, et al., Effect of Vitamin A, C and E Supplementation on Rectal Cell Proliferation in Patients with Colorectal Adenomas, Journal of the National Cancer Institute, 84(1), January 1, 1992, p. 47-51.

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I dette case-control forsøg af 117 cervikale cancer in situ patienter, fandt man at C-vitamin reducerede cancer-risikoen med 60 %.

– K. E. Brock, et al., Nutrients in Diet and Plasma and Risk of in Situ Cervical Cancer. Journal of the National Cancer Institute, 80(8), June 15, 1988, p. 580-585.

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Dette case-control forsøg af 419 colon- og rektalcancer-patienter viste, at indtag af C-vitamin fra kosten resulterede i nedsat risiko for rektal cancer hos kvinder.

– J.D. Potter and A.J. McMichael, Diet and Cancer of the Colon and Rectum: A Case-Control Study, Journal of the National Cancer Institute, 76(4), April 1986, p. 557-569.

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I forlængelse af, at brugen af askorbat til cancerbehandling begyndte i 1971, involverede dette case-control-forsøg over 300 patienter med cancer, som hver fik 2,5 gram C-vitamin 4 gange dagligt i kombination med standard operativ behandling og strålebehandling (ganske få tilfælde af kemoterapi).

Man opdagede at 266 patienter med uhelbredelig cancer fik signifikant gavn af C-vitaminbehandlingen, som viste sig at have signifikant gavnlige virkninger for dem der led af mave- og coloncancer og en lignende tendens for dem med blærecancer.

Baseret på disse resultater konkluderede forfatterne, at askorbat i høje doser kan forbedre overlevelsen hos visse typer cancer.

– L. Moffat, et al., High Dose Ascorbate Therapy and Cancer, NFCR Cancer Research Association Symposium, (2), 1983, p. 243-256.

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Denne oversigtsartikel om virkningen af A-, C- og E-vitamin samt selen på cancer anfører forskning, der peger på askorbinsyres evne til at forebygge dannelsen af nitrosaminer og andre N-nitroso-forbindelser. Flere forsøg viser også, at tilskud af C-vitamin kan hæmme hud-, nyre-, lunge- og luftrørscancer.

– D.F. Birt, Update on the Effects of Vitamins A, C, and E and Selenium on Carcinogenesis, Proc Soc Exp Biol Med, 183(3), December 1986, p. 311-320.

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Man opdagede at indgivelse af askorbinsyre (0,1 – 20 mkg/ml i første uge) hæmmede røntgen-fremkaldt transformation af C3H1OT1/2 celler på en koncentrations-afhængig måde efter stråling.

Celler udsat for stråling forblev sårbare over for askorbinsyre indtil tidspunktet, hvor morfologisk phenotype kommer til udtryk. På basis af disse fund, postulerer forfatterne, at den neoplastisk transformerede phenotype bliver fremhjulpet ved frie radikaler og peroxyd-radikaler genereret i celler under hele prøveperioden, og de mener, at deres data kan være behjælpelig som en vejledning for kemopreventive indsatser imod strålingsfremkaldt cancer.

– M. Yasukawa, et al., Radiation-induced Neoplastic Transformation of C3HlOT1/2 Cells is Suppressed by Ascorbic Acid, Radiation Research, 120(3), December 1989 p. 456-467.

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I dette forsøg så man, at præbehandling af tumortarget-celler in vitro med en kombination af interferon og askorbat resulterede i en 71 % stigning i væksthæmning af target-celler til sammenligning med interferon alene. Indgivelse af askorbat alene viste minimal virkning på tumortarget-cellevækst i humane monocytter.

– M .J. Skeen, et al., Synergy of Interferon and Ascorbic Acid in Stimulating Human Monocyte Cytostasis Against Tumor Target Cells. Rev Latinoam Oncology Clin, 13(4), 1981, p. 9-14.

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C-vitamin (85 mg/kg) indtagelse har vist sig at resultere i en reduktion af DNA-enkeltstrengbrud foranlediget af ioniseret stråling i humane lymfocytter, indikeret ved en signifikant aftagelse af samlet segmentlængde hos både ubestrålede kontrolpersoner og hos dose-response til ioniseret strålingsskade. Man observerede at virkningen varede op til 6 timer.

– C. F. Arlett, et al., The Modulation of DNA Damage in Human Lymphocytes by Dietary Vitamin C Supplementation, Molecular Mechanisms in Radiation Mutagenesis and Carcinogenesis, April 19-22, 1993, Doorwerth, The Netherlands.

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Patienter med oral leukoplaki blev indgivet 30 mg betacaroten, 1000 mg askorbinsyre og 800 i.e. alfa-tokoferol dagligt i 9 måneder. 55,6 % af de 81 patienter, som fuldførte forsøget, viste enten delvis eller total klinisk helbredelse af deres orale skader.

– G. Kaugars, et al., The Role of Antioxidants in the Treatment of Oral Leukoplakia, CCPC-93: Second International Cancer Chemo Prevention Conf., April 28-30, 1993, Berlin, Germany, p. 65.

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24 lungecancer- og 35 blærecancerpatienter blev behandlet med doser af 5 gram askorbinsyre dagligt. Resultaterne viser, at så høje doser er nyttige til at korrigere for lav koncentration af C-vitamin i blodet og til at forøge forsvarsreaktioner hos patienter, der lider under disse cancertyper.

– A.M. Greco, et al., Study of Blood Vitamin C in Lung and Bladder Cancer Patients Before and After Treatment with Ascorbic Acid: A Preliminary Report, Acta Vitaminol Enzymol, 4(1-2), 1982, p. 155-162.

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Denne oversigtsartikel påpeger, at C-vitamins rolle ved cancerforebyggelse er blevet diskuteret i litteraturen i over 50 år, ligesom den refererer til undersøgelser, som tyder på, at fødevarer rige på C-vitamin forbindes med en lavere risiko for mavecancer og cancer i spiserøret.

Askorbinsyre viste sig at have indvirkning på en række tumorfremkaldende forbindelser, såsom forstadier til N-nitrosoforbindelser, og forebygge tumorer. Dyre- og in vivo-forsøg har også vist at askorbinsyre afbryder tumorpromotion.

Baseret på en oversigt over den eksisterende dokumentation konkluderer forfatterne, at C-vitamin kan hæmme dannelsen af visse cancertyper.

– B.E. Glatthaar, et al., The Role of Ascorbic Acid in Carcinogenesis, Adv Exp Med. Biol, 206, 1986, p. 357-377.

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Indgivelsen af flavoner, quercetin og fisetin, enten alene eller i kombination med askorbinsyre, blev undersøgt for (disses) virkning på pladeepitelcarcinom (HTB 43) in vitro. Fisetin og quercetin (2 mkg/ml) svækkede signifikant cellevæksten kombineret med askorbinsyre (2 mkg/ml) på 72 timer. Askorbinsyre givet alene havde ingen virkning, heller ikke når den blev givet sammen med flavoner.

– C. Kandaswami, et al. Ascorbic Acid-enhanced Antiproliferative Effect of Flavonoids on Squamous Cell Carcinoma in Vitro, Anticancer Drugs, 4(1), February 1993, p. 91-96.

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Denne oversigtsartikel over forholdet mellem C- og E-vitamin og cancer omtaler forsøg som antyder, at indtagelse af fødevarer der indeholder C-vitamin forbindes med en nedsat risiko for mavecancer og cancer i spiserøret.

Tilskud med C-vitamin har vist sig at kunne hæmme nerve-, lunge-, nyre- og hudcancer. Forsøg har også vist, at C-vitamin er i stand til at hæmme tumorcellevækst og carcinogenfremkaldt DNA-skade. In vitro og dyreforsøg har vist, at C-vitamin hæmmer udviklingen af carcinogene nitrosaminer.

– L.H. Chen, et al. Vitamin C, Vitamin E and Cancer, Anticancer Research, 8(4), July-August 1988, p. 739-748.

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Tidligere forskning har påvist C-vitamin som cytotoksisk over for neuroblastomceller in vitro og in vivo. I dette forsøg viste askorbinsyre sig at være mere cytotoksisk end Dehydro-askorbinsyre i neuroblastome SK-NSH-celler.

Man opdagede også, at optagelsen af [14C] askorbinsyre og [14C] Dehydro-askorbinsyre blev svækket af gluthathion og diethiothreitol. [14C] Dehydro-askorbinsyre var delvist nedsat reduceret til [14C] askorbinsyre, når denne først var i cellen.

Forfatterne argumenterer for at deres resultater tilføjer støtte til tidligere tiltro til, at askorbinsyre opfører sig som en pro-oxidant indeni neuroblastomceller og de anbefaler brugen af askorbinsyre ved behandling af neuroblastomer.

– S.L. Baader, et al., Uptake and Cytotoxicity of Ascorbic Acid and Dehydroascorbic Acid in Neuroblastoma (SK-N-SH) and Neuroectodermal (SK-N-LO) Cells, Anticancer, 14(1A), January-February 1994 p. 221-227.

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L-askorbat og dets oxidative produkt dehydro-askorbat har vist sig at være dræbende eller cytotoksisk over for hurtigtvoksende maligne celler, samtidig med at det er mindre giftigt over for ikke-maligne celler.

Det samme sås med D-askorbat og D-isoaskorbat. Supplerende forsøg har vist, at askorbatets indvirkning på cellevækst var et resultat af dets direkte dødbringende effekt, fremfor dets cytostatiske natur.

– P.Y. Leung, et al. Cytotoxic Effect of Ascorbate and its Derivatives on Cultured Malignant and Nonmalignant Cell Lines, Anticancer Research, 13(2), March-April 1993, p. 475-480.

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Under hensyntagen til den strålebeskyttende virkning af C-vitamin på patienter med nakke- og halscancer bør bemærkes, anbefaler denne afhandling oral indgivelse af askorbinsyre til de nævnte cancerpatienter.

– R. Garcia-Alejo Hernandez, et al., Radioprotective Effect of Ascorbic Acid on Oral Structures in Patients with Cancer of the Head and Neck, Av Odontoestomatol, 5(7), September 1989, p. 469-472.

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I dette forsøg så man, at doser af 2 mM askorbinsyre havde en stærk cytotoksisk virkning på neuroblastom-, osteosarcom-, rhabdomyosarcom- og retinoblastom-celler dyrket in vitro. Askorbinsyre indgivet i små doser som 0,2 mM vedbliver at være cytotoksisk over for neuroblastom-, osteosarcom- og retinoblastom-celler, men stimulerer væksten af rhabdomyosarcom-celler.

– M. A. Medina, et al. Ascorbic Acid is Cytotoxic for Pediatric Tumor Cells Cultured in Vitro, Biochem Mol Biol Int, 34(5), November 1994, p. 871-874.

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I dette case-controlforsøg af 723 mavecancerpatienter, opdagede man, at der var et signifikant forebyggende effekt mellem askorbinsyre og risikoen for at udvikle sygdommen.

– C. La Vecchia, et al. Selected Micronutrient Intake and the Risk of Gastric Cancer. Cancer Epidemiol Biomarkers Prevention, 3(5), July-August 1994, p. 393-398.

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I dette case-control-forsøg over biopsi-bekræftede cervikal intraepithelial neoplasia (CIN)-patienter, så man at lav C-vitamin fra kosten gav øget cervikal intraepithelial neoplasia.

– J. VanEenwyk, et al. Folate, Vitamin C, and Cervical Intraepithelial Neoplasia. Cancer Epidemiol Biomarkers Prevention, 1(2), January-February 1992, p. 119-124.

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Dette forsøg undersøgte virkninger af nitrogenoxid og askorbat på humane hjernetumorceller i kontroller. Resultaterne viste, at kombinationen af nitroprussid og askorbat kunne være en effektiv tilgang til behandlingen af hjernetumorer.

– Y.S. Lee and R.D. Wurster. Potentiation of Anti-Proliferative Effect of Nitroprusside by Ascorbate in Human Brain Tumor Cells, Cancer Letters, 78(1-3), April 1, 1994, p. 19-23.

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Dette forsøg opdagede, at de cytotoksiske virkninger af askorbinsyre på to følsomme lymfocyt-tumorer og cellelinier var afhængig af dosering og tid. Forfatterne foreslår, at tilstedeværelsen af lymfocytlinier med forskellig følsomhed over for askorbinsyre måske bør overvejes i en brugbar model i undersøgelsen af C-vitamins indvirkning på cancerceller.

– T.L. Kao, et al. Inhibitory Effects of Ascorbic Acid on Growth of Leukemic and Lymphoma Cell Lines, Cancer Letters, 70(1-2), June 15, 1993, p. 101-106.

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I dette forsøg så man, at C-vitamin havde to forskellige virkninger på mutational specificitet af 6 antineoplastiske medikamenter. Forfatterne anfører, at sådanne resultater er signifikante med hensyn til den kliniske forebyggelse af tumorer,

– Z.Z. Zhao and M.T. Huang. A Study of Vitamin Inhibition on the Mutagenicity of the Antineoplastic Drugs, Chung Hua Yu Fang I Nsuch Tsa Chih, 26(5), September 1992, p. 291-293.

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I forlængelse af at DES eller østradiol-behandlede syriske han-hamstre, der er blevet givet tilskud med C-vitamin har vist sig at hæmme nyre-carciogenese, blev virkningerne af indgivet C-vitamin på en række biokemiske markører i forhold til nyre-carciogenese undersøgt. Resultaterne tyder på, at C-vitamin hæmmer østrogen-fremkaldt carciogenese ved at formindske koncentrationer af østrogen-quinonmetabolitter og deres DNA-addukter.

– J.G. Liehr, et al. Mechanism of Inhibition of Estrogen-Induced Renal Carcinogenesis in Male Syrian Hamsters by Vitamin C, Carcinogenesis, 10(11), November 1989, p. 1983-1988.

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43 patienter blev behandlet med orale tilskud af C-vitamin. Behandling med C-vitamin hos patienter med en normal maveslimhinde resulterede i en forhøjelse af intragastriske askorbatniveauer i alle tilfælde. C-vitamintilskud formindskede DNA-skade i maveslimhinden hos 28 ud af 43 patienter, hvilket antyder, at C-vitamin muligvis spiller en beskyttende rolle imod angreb af mavecancer.

– G.W. Dyke, et al., Effect of Vitamin C Supplementation on Gastric Mucosal DNA Damage, Carcinogenesis, 15(2), p. 291-295.