刘歆蕾, 毕晓洁, 钱雯, 许永劼, 李兴, 潘卫. 敌百虫经口染毒对妊娠大鼠及其子代脑和生殖腺的影响[J]. 环境与职业医学, 2020, 37(10): 1005-1010. DOI: 10.13213/j.cnki.jeom.2020.20066
引用本文: 刘歆蕾, 毕晓洁, 钱雯, 许永劼, 李兴, 潘卫. 敌百虫经口染毒对妊娠大鼠及其子代脑和生殖腺的影响[J]. 环境与职业医学, 2020, 37(10): 1005-1010. DOI: 10.13213/j.cnki.jeom.2020.20066
LIU Xinlei, BI Xiao-jie, QIAN Wen, XU Yong-jie, LI Xing, PAN Wei. Effects of oral trichlorfon on brains and gonads of pregnant rats and their progeny[J]. Journal of Environmental and Occupational Medicine, 2020, 37(10): 1005-1010. DOI: 10.13213/j.cnki.jeom.2020.20066
Citation: LIU Xinlei, BI Xiao-jie, QIAN Wen, XU Yong-jie, LI Xing, PAN Wei. Effects of oral trichlorfon on brains and gonads of pregnant rats and their progeny[J]. Journal of Environmental and Occupational Medicine, 2020, 37(10): 1005-1010. DOI: 10.13213/j.cnki.jeom.2020.20066

敌百虫经口染毒对妊娠大鼠及其子代脑和生殖腺的影响

Effects of oral trichlorfon on brains and gonads of pregnant rats and their progeny

  • 摘要: 背景

    敌百虫作为一种应用广泛的有机磷农药,其神经毒性及生殖毒性与氧化应激的关系尚未完全阐明。

    目的

    研究敌百虫染毒后妊娠母鼠及其子鼠脑组织和生殖腺的病理改变,并探讨敌百虫是否通过氧化应激导致神经毒性和生殖毒性。

    方法

    随机选取48只受孕的雌性SD大鼠分为对照组和2、10、50 mg·kg-1敌百虫染毒组,每组12只,于发情前期开始持续经口染毒至分娩。分娩后,分离各母鼠及其子鼠的脑及生殖腺(卵巢/睾丸),并抽取母鼠全血。通过HE染色观察脑及生殖腺的病理变化;ELISA法检测组织中的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)含量;气相色谱法检测产后母鼠全血中敌百虫代谢产物磷酸二甲酯(DMP)的浓度。分析母鼠DMP与子代各组织中氧化指标的相关性。

    结果

    在产后母鼠的大脑中,10、50 mg·kg-1敌百虫染毒组SOD活性高于对照组分别为(15.72±2.31)、(15.50±2.29)、(13.00±1.72)U·mg-1,以蛋白计,余同(P < 0.05),两组母鼠出现轻度脑水肿。在子鼠的大脑中,50 mg·kg-1敌百虫染毒组MDA含量高于对照组分别为(1.42±0.49)、(1.02±0.18)nmoL·g-1,以蛋白计,余同(P < 0.05),50 mg·kg-1染毒组子鼠出现脑水肿。在产后母鼠的卵巢中,50 mg·kg-1敌百虫染毒组形成更多闭锁卵泡,且其MDA含量高于对照组(1.37±0.30)、(1.03±0.18)nmoL·g-1P < 0.05)。在子鼠的生殖腺中,相较于对照组,50 mg·kg-1敌百虫染毒组的雌、雄子鼠均出现MDA含量增加以及SOD和GSH-Px活性降低(P < 0.05),且雌性子鼠卵巢结构被破坏,卵泡形成异常,雄性子鼠睾丸间质充血,生精细胞不规则且数量减少。此外,50 mg·kg-1敌百虫染毒组产后母鼠全血中DMP质量浓度高于10 mg·kg-1染毒组分别为(984.52±207.94)、(271.83±80.97)mg·L-1P < 0.01);随着母鼠全血DMP质量浓度升高,子鼠睾丸的SOD活性下降,且二者呈线性负相关(r=-0.638,P < 0.05)。

    结论

    妊娠母鼠经一定剂量敌百虫的暴露后,母鼠及其子代均产生神经毒性和生殖毒性,氧化应激可能是其中的机制之一。

     

    Abstract: Background

    Trichlorfon is a widely used organophosphorus pesticide, but the relationship between its neurotoxicity and reproductive toxicity and oxidative stress has not been fully elucidated.

    Objective

    This experiment observes the pathological changes of brain tissues and gonads of pregnant rats and their offspring after prenatal trichlorfon exposure, and explores whether trichlorfon causes neurotoxicity and reproductive toxicity through oxidative stress.

    Methods

    Forty-eight pregnant SD rats were randomly divided into a control group and 2, 10, and 50 mg·kg-1 trichlorfon exposure groups, with 12 rats in each group, and continuously received designed oral administration from proestrus to parturition. After delivery, the brains and gonads (ovaries/testicles) of the dams and their offspring were isolated, and the whole blood samples of the dams were collected. The pathological changes of the brains and gonads were observed by HE staining; the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) were detected by ELISA; the concentration of trichlorfon metabolite dimethyl phosphate (DMP) in the blood of mother rats were measured by gas chromatography. The correlations between maternal DMP and offspring's oxidative stress indicators were evaluated.

    Results

    In the brains of postpartum mother rats, the SOD activities of the 10 and the 50 mg·kg-1 trichlorfon exposure groups were higher than that of the control grouprespectively (15.72±2.31), (15.50±2.29), and (13.00±1.72) U·mg-1, calculated by protein, thereafter (P < 0.05), and mild cerebral edema accompanied. In the brains of neonatal rats, the MDA content of the 50 mg·kg-1 trichlorfon exposure group was higher than that of the control grouprespectively (1.42±0.49) and (1.02±0.18) nmol·g-1, calculated by protein, thereafter (P < 0.05), and cerebral edema also occurred. In the ovaries of postpartum mother rats, the 50 mg·kg-1 trichlorfon exposure group formed more atresia follicles, and their average MDA content was higher than the control group's(1.37±0.30) and (1.03±0.18) nmol·g-1 respectively (P < 0.05). In the gonads of neonatal rats, both sexes of the 50 mg·kg-1 trichlorfon exposure group had increased MDA content and decreased SOD and GSH-Px activities compared with the control group (P < 0.05), and the histopathological changes were damaged ovarian structure and follicle formation in the female offspring rats, and testicular congestion and irregular and reduced spermatogenic cells in the male offspring rats. In addition, the blood DMP concentrations of postpartum mother rats of the 50 mg·kg-1 trichlorfon exposure group was higher than that of the 10 mg·kg-1 trichlorfon exposure group(984.52±207.94) and (271.83±80.97) mg·L-1 respectively (P < 0.01); as the maternal blood DMP concentration increased, the offspring's testicular SOD activity decreased, and the two showed a linear negative correlation (r=-0.638, P < 0.05).

    Conclusion

    After prenatal exposure to trichlorfon at designed doses, both pregnant rats and their progeny produce neurotoxicity and reproductive toxicity, and oxidative stress may be one of their mechanisms.

     

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