Oxidative stress-mediated apoptosis is involved in bisphenol S-induced reproductive toxicity in male C57BL/6 mice

被引:19
作者
Dai, Wei [1 ]
He, Qing-zhi [2 ]
Zhu, Bi-qi [1 ]
Zeng, Huai-cai [1 ,2 ]
机构
[1] Univ South China, Dept Prevent Med, Hengyang 421001, Peoples R China
[2] Guilin Med Univ, Dept Occupat & Environm Hlth, Guilin, Peoples R China
关键词
apoptosis; bisphenol S; Fas; FasL pathway; oxidative stress; reproductive toxicity; UNITED-STATES; IN-VITRO; ANALOGS; EXPOSURE; EXPRESSION; IMPAIRS; DAMAGE; RATS; FAS; BPA;
D O I
10.1002/jat.4170
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The reproductive toxicity of bisphenol S (BPS) in male mammals and its possible mechanism are not clear. We investigated the effects and possible mechanism of action of BPS on adult male C57BL/6 mice. We found that exposure to 200-mg/kg BPS resulted in a significant decrease in the sperm count in the caput/corpus and cauda epididymis, significantly decreased sperm motility, and significantly increased the sperm deformity. Histological evaluation revealed that BPS exposure caused a decrease of spermatozoa in the lumen of seminiferous tubules and a reduction in the proportion of Stage VII or VIII seminiferous tubules in the BPS-treated groups. Furthermore, ultrastructure analysis revealed BPS-induced mitochondrial damage and apoptosis in spermatogenic cells. Moreover, BPS exposure-induced oxidative stress in testicular tissues. Further, dUTP-biotin nick end labeling (TUNEL) assay showed that BPS induced the apoptosis of spermatogenic cells in a dose-dependent manner. BPS also significantly upregulated cleaved caspase-8, cleaved caspase-9, cleaved caspase-3, Fas, and FasL and significantly downregulated the Bcl-2/Bax ratio. These results suggest that BPS-induced oxidative stress in the testis and spermatogenic cell apoptosis potentially impairs spermatogenesis and sperm function, which may be the mechanism of the reproductive toxicity of BPS. The Fas/FasL and mitochondrial signal pathways may be involved in BPS-induced oxidative stress-related apoptosis. These results suggest that BPS-induced oxidative stress in the testis and spermatogenic cell apoptosis potentially impairs spermatogenesis and sperm function, which may be the mechanism of the reproductive toxicity of BPS. The Fas/FasL and mitochondrial signal pathways may be involved in BPS-induced oxidative stress-related apoptosis.
引用
收藏
页码:1839 / 1851
页数:13
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