Zinc deficiency causes oxidative damage to proteins, lipids and DNA in rat testes.
Zinc deficiency causes oxidative damage to proteins, lipids and DNA in rat testes.
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DOI：
10.1093/jn/125.4.823
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发表时间：
1995-04
期刊：
影响因子：
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通讯作者：
Patricia I Oteiza;K. Olin;C. Fraga;C. Keen;C. Keen
中科院分区：
文献类型：
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作者：
Patricia I Oteiza;K. Olin;C. Fraga;C. Keen;C. Keen
为探讨缺锌对睾丸蛋白质、脂质和DNA氧化损伤的影响，给刚断乳的雄性大鼠自由采食低锌（0.5 μ g Zn/g）和高锌（25 μ g Zn/g）饲料14 d。第三组是限制摄入足够的锌饮食的量消耗的低锌饮食喂养组。与自由进食对照组相比，低锌饮食组大鼠睾丸谷氨酰胺合成酶活性较低，铁离子刺激的2-硫代巴比妥酸反应物质（TBARS）产生量较低，蛋白质羰基浓度较高（P < 0.05），8-氧代-2 '-脱氧鸟苷水平较高（P = 0.06）。限食对照组睾丸中的谷氨酰胺合成酶活性介于自由采食对照组和缺锌动物的值之间。与自由采食对照组相比，限制性对照组的蛋白质羰基含量较高，而刺激的TBARS产量较低（P < 0.05）。限制性对照组睾丸DNA中8-氧-2 '-脱氧鸟苷含量低于缺锌组（P < 0.05）。缺锌组和限锌组大鼠睾丸铁含量均高于自由采食组（P < 0.05）。观察到的氧化损伤可能是由于继发于组织铁积累和/或锌依赖性抗氧化过程减少的活性氧产生增加而发生的。
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.