title: Supplementation with vitamin C, vitamin E or beta-carotene influences osmotic fragility and oxidative damage of erythrocytes of zinc-deficient rats.
abstract: Dietary zinc deficiency in rats causes increased osmotic fragility of their erythrocytes. In this study, the influence of supplementary antioxidants (vitamin C, vitamin E or beta-carotene) on osmotic fragility, oxidative damage and components of the primary defense system of erythrocytes of zinc-deficient rats was investigated. Indicators of hemolysis in vivo were also examined. Five groups of 12 male rats were force-fed a zinc-adequate diet (control rats), a zinc-deficient diet or a zinc-deficient diet enriched with vitamin C, vitamin E or beta-carotene. Compared with the control rats, the rats fed the zinc-deficient diet without supplementary antioxidants had greater red blood cell osmotic fragility, higher concentrations of thiobarbituric acid-reactive substances and alanine, higher glutathione S-transferase activity, lower concentration of glutathione and activity of glutathione peroxidase as well as lower activity of superoxide dismutase in plasma (P < 0.05). Supplementation with antioxidants generally improved osmotic fragility in zinc-deficient rats without influencing zinc concentration or alkaline phosphatase activity in plasma, indicators of zinc status. At some of the hypotonic saline concentrations tested, vitamin C and beta-carotene significantly affected osmotic fragility. The zinc-deficient rats fed a diet without supplementary antioxidants had significantly higher concentrations of alanine in erythrocytes than the zinc-deficient rats supplemented with vitamin C, vitamin E or beta-carotene and had significantly higher levels of thiobarbituric acid-reactive substances in erythrocytes than the rats supplemented with beta-carotene. There was no indication of hemolysis in vivo in rats fed zinc-deficient diets. The results show that supplementary antioxidants decrease osmotic fragility and oxidative damage of erythrocytes in zinc-deficient rats.
authors.affiliation: Institut für Ernährungsphysiologie der Technischen Universität München-Weihenstephan, 85350 Freising, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Kraus
authors.forename: H P
authors.initials: HP
authors.lastname: Roth
authors.forename: M
authors.initials: M
authors.lastname: Kirchgessner
mesh_terms: D000409:Alanine / Q000032:analysis / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000097:blood; D000596:Amino Acids / Q000032:analysis / Q000378:metabolism; D000818:Animals; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D004912:Erythrocytes / Q000737:chemistry / Q000187:drug effects* / Q000378:metabolism; D005527:Food, Fortified; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D006454:Hemoglobins / Q000032:analysis / Q000378:metabolism; D008297:Male; D009996:Osmotic Fragility / Q000187:drug effects; D016877:Oxidants / Q000032:analysis / Q000378:metabolism; D010084:Oxidation-Reduction; D011188:Potassium / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013438:Sulfhydryl Compounds / Q000032:analysis / Q000378:metabolism; D013482:Superoxide Dismutase / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology*; D015430:Weight Gain / Q000502:physiology; D015032:Zinc / Q000032:analysis / Q000172:deficiency*; D019207:beta Carotene / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D000596:Amino Acids; D006454:Hemoglobins; D016877:Oxidants; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D019207:beta Carotene; D014810:Vitamin E; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000469:Alkaline Phosphatase; D005978:Glutathione; D015032:Zinc; D000409:Alanine; D001205:Ascorbic Acid; D011188:Potassium