Zinc deficiency causes oxidative damage to proteins, lipids and DNA in rat testes

• Published in: The Journal of nutrition Vol. 125; no. 4; p. 823
• Main Authors: Oteiza, P I, Olin, K L, Fraga, C G, Keen, C L
• Format: Journal Article
• Language: English
• Published: United States 01-04-1995
• Subjects: Animals; DNA - analysis; DNA - metabolism; Glutamate-Ammonia Ligase - metabolism; Iron - analysis; Iron - metabolism; Lipid Metabolism; Lipid Peroxidation; Lipids - analysis; Male; Oxidation-Reduction; Proteins - analysis; Proteins - metabolism; Rats; Rats, Sprague-Dawley; Testis - chemistry; Testis - enzymology; Testis - metabolism; Thiobarbituric Acid Reactive Substances - metabolism; Zinc - deficiency; Zinc - physiology
• ISSN: 0022-3166

To investigate the effects of zinc deficiency on oxidative damage to testes proteins, lipids and DNA, weanling male rats were allowed free access to low (0.5 microgram Zn/g) or adequate (25 micrograms Zn/g) zinc diets for 14 d. A third group was restricted intake of the adequate Zn diet to the amount consumed by the low Zn diet-fed group. Compared with ad libitum-fed controls, testes from rats fed the low zinc diet had lower glutamine synthetase activity, lower Fe(2+)-stimulated 2-thiobarbituric acid-reactive substances (TBARS) production, higher protein carbonyl concentrations (P < 0.05), and higher 8-oxo-2'-deoxyguanosine levels (P = 0.06). Glutamine synthetase activity in testes of the food-restricted controls was between the values for the ad libitum controls and zinc-deficient animals. Protein carbonyls were higher in the restricted controls compared with the ad libitum controls, whereas stimulated TBARS production was lower (P < 0.05). Levels of 8-oxo-2'-deoxyguanosine were lower in testes DNA of the restricted controls than in the zinc-deficient group (P < 0.05). Testes iron concentrations were higher in the zinc-deficient and restricted control rats than in ad libitum controls (P < 0.05). The oxidative damage observed may have occurred as a consequence of increased reactive oxygen species generation secondary to tissue iron accumulation and/or reductions in zinc-dependent antioxidant processes.