Cadmium-induced testicular damage is associated with mineral imbalance, increased antioxidant enzymes activity and protein oxidation in rats
Cadmium-induced testicular damage is associated with mineral imbalance, increased antioxidant enzymes activity and protein oxidation in rats
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DOI：
10.1016/j.ifs.2017.03.007
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发表时间：
2017-04-15
期刊：
影响因子：
6.1
通讯作者：
Pinto da Matta, Sergio Luis
中科院分区：
文献类型：
--
作者：
Cupertino, Marli do Carmo;Novaes, Romulo Dias;Pinto da Matta, Sergio Luis
目的：目前，与镉诱导的睾丸毒性相关的病理表现谱知之甚少。因此，我们研究了镉（Cd）暴露对睾丸矿物质生物利用度、抗氧化酶活性、睾丸结构和生殖细胞超微结构的影响。方法：将30只大鼠随机分为5组：生理盐水、0.9%NaCl、Cd 1-Cd 4、0.67、0.74、0.86和1.1 mg Cd/kg。镉暴露后7天，动物被安乐死，睾丸被收集用于生化分析，以及光，扫描和透射电镜。关键发现：镉暴露诱导剂量依赖性睾丸毒性。肾小管和肾小管间室的镉和钙（Ca）的存款，显着的结构和超微结构的病理性重塑，并减少铁，硒，镁，铜，锌和总蛋白的分布的目标。尽管上调抗氧化酶的活性（即过氧化氢酶[CAT]和超氧化物歧化酶[SOD]），形态和分子睾丸损伤，如蛋白质氧化没有得到预防，特别是与高剂量的镉。由于非变性组织区域也存在钙沉积，钙失衡不仅是镉诱导的睾丸毒性和生殖细胞死亡的结果，而且也是原因。总之，我们的研究结果表明，镉暴露诱导剂量依赖性睾丸营养不良性钙化，这与抗氧化酶活性增加和蛋白质氧化，矿物质失衡，生殖细胞钙化和死亡有关。虽然增加的CAT和SOD活性代表了对镉诱导的毒性的反调节反应，但这种反应不足以防止睾丸病理性重塑。(C)2017爱思唯尔公司All rights reserved.
Aims: Currently, the spectrum of pathological manifestations associated with cadmium-induced testicular toxicity is poorly understood. Thus, we investigated the impact of cadmium (Cd) exposure on testicular mineral bioavailability, activity of antioxidant enzymes, testicular structure and germ cells ultrastructureAMain methods: Cadmium chloride was administered in a single dose to thirty rats equally randomized into five groups: Saline, 0.9% NaCl; Cd1 - Cd4, 0.67, 0.74, 0.86 and 1.1 mg Cd/kg. Seven days after Cd exposure, animals were euthanized and testes were collected for biochemical analysis, as well as light, scanning and transmission electron microscopy.Key findings: Cadmium exposure induced dose-dependent testicular toxicity. Tubular and intertubular compartments were targets of Cd and calcium (Ca) deposits, marked structural and ultrastructural pathologic remodeling, and a reduced distribution of iron, selenium, magnesium, copper, zinc and total protein. Despite upregulation in antioxidant enzyme activities (i.e. catalase [CAT] and superoxide dismutase [SOD]), morphologic and molecular testis damage such as protein oxidation was not prevented, especially with higher doses of Cd. As non-degenerated tissue areas also presented Ca deposits, Ca imbalance was not only a consequence but also a cause of Cd-induced testis toxicity and germ cell deathSignificance: Taken together, our findings indicated that Cd exposition induced dose-dependent testicular dystrophic calcification, which was associated with increased antioxidant enzymes activity and protein oxidation, mineral imbalance, germ cell calcification and death in rats. Although increased CAT and SOD activity represents a counter-regulatory reaction to cadmium-induced toxicity, this reaction is insufficient to prevent testicular pathological remodeling. (C) 2017 Elsevier Inc. All rights reserved.