GAO Yan-rong, SHI Xue-min, JIA Yu-qiao, WANG Li, TAI Dai-peng, SUN Yao, CHANG Xiang-yu, ZHANG Han, TIAN Jiang, LIU Lu-min, LI Dong-ying. Effects of organic extracts in source water in Baotou section of the Yellow River on germ cell apoptosis and 3-NT/Caspase-3 expressions in testis of male mice[J]. Journal of Environmental and Occupational Medicine, 2019, 36(12): 1137-1142. DOI: 10.13213/j.cnki.jeom.2019.19272
Citation: GAO Yan-rong, SHI Xue-min, JIA Yu-qiao, WANG Li, TAI Dai-peng, SUN Yao, CHANG Xiang-yu, ZHANG Han, TIAN Jiang, LIU Lu-min, LI Dong-ying. Effects of organic extracts in source water in Baotou section of the Yellow River on germ cell apoptosis and 3-NT/Caspase-3 expressions in testis of male mice[J]. Journal of Environmental and Occupational Medicine, 2019, 36(12): 1137-1142. DOI: 10.13213/j.cnki.jeom.2019.19272

Effects of organic extracts in source water in Baotou section of the Yellow River on germ cell apoptosis and 3-NT/Caspase-3 expressions in testis of male mice

  • Background Reproductive health hazards sourced from organic pollutants in river water have become a major concern at present. The pollution of river water in China is mainly caused by organic pollutants.

    Objective This experiment investigates the effects of organic pollutants in source water in Baotou section of the Yellow River on the apoptosis of germ cells and the expressions of 3-nitrotyrosine (3-NT) and cysteinyl aspartate specific proteinase-3 (Caspase-3) in testis of male mice, and preliminarily explores the relevant mechanism of action.

    Methods Sixty SPF ICR male mice were randomly divided into six groups:control group, Yellow River water organic extracts treatment group (YRE-OE group), Yellow River water organic extracts+N-acetylcysteine (NAC) treatment group (YRE-OE+NAC group), tap water organic extracts treatment group (TW-OE group), tap water organic extracts+NAC treatment group (TW-OE+NAC group), and NAC group, with 10 mice in each group. The YRE-OE were administered to all mice by gavage once every other day, and the mice in the YRE-OE+NAC group, TW-OE+NAC group, and NAC group were intraperitoneally injected with 10 g/L NAC in a volume of 0.02 mL/g (in body weight) 1 h before the YRE-OE administration. After four weeks of the exposure, epididymis and testis tissues were isolated to observe germ cell apoptosis under transmission electron microscope; germ cells were counted and sperm malformation was observed; 3-NT expression in testis was detected by ELISA; and Caspase-3 protein expression was detected by Western blotting.

    Results Compared with the control group(4.15±0.06)×107/g, (4.84±0.65)%, the YRE-OE group showed decreased germ cells(2.86±0.06)×107/g and increased sperm malformation rate(19.59±1.49)% (P < 0.05), and the TW-OE group only showed increased sperm malformation rate(7.89±1.16)% (P < 0.05); compared with the YRE-OE group, the YRE-OE+NAC group showed increased germ cells(3.55±0.06)×107/g and decreased sperm malformation rate(11.44±1.22)% (P < 0.05); compared with the TW-OE group, the TWOE+NAC group showed decreased sperm malformation rate(5.62±0.91)% (P < 0.05). Under transmission electron microscope, nuclear fragmentation, reduced cell organelles such as ribosomes and lysosomes, destroyed mitochondrial structure, and abundant apoptosis germ cells were observed in the YRE-OE group; however, such phenomenon was rarely observed in the YRE-OE+NAC group. Compared with the control group, the 3-NT and Caspase-3 expressions were increased in the exposure groups; the YRE-OE+NAC group showed lower 3-NT(8.64±0.40) mg/L and Caspase-3 (0.38±0.02) expressions than the YRE-OE group(12.28±0.78) mg/L, 0.48±0.02, P < 0.05; the TW-OE+NAC group only showed lower 3-NT expression(7.23±0.47) vs. (9.34±0.81) mg/L, P < 0.05 than the TW-OE group.

    Conclusion The organic matters extracted from the Yellow River could cause germ cell apoptosis and increased expressions of 3-NT and Caspase-3 in testis of mice; the germ cell apoptosis mediated by Caspase-3 signaling pathway activated by oxidative stress may be one of the mechanisms of their reproductive toxicity.

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