Developmental Toxicology Laboratory, Systems Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Post Box No. 80, Lucknow, Uttar Pradesh, 226 001, India.
Academy of Scientific and Innovative Research (AcSIR), CSIR-IITR Campus, Lucknow, Uttar Pradesh, 226 001, India.
Mol Cell Biochem. 2020 Apr;467(1-2):27-43. doi: 10.1007/s11010-020-03694-x. Epub 2020 Feb 14.
Epidemiological evidences have shown an association of exposure to pesticides or heavy metals with increased incidences of Parkinson's disease (PD) in humans. Exposure to pesticides or metals during the decisive period of the brain development increases the susceptibility of dopaminergic neurons upon re-exposure in adult rodents. However, the effect of early life exposure to pesticide on the heavy metal-induced neurodegeneration or heavy metal on pesticide-induced neurodegeneration is not yet explored. The current study explored the effect of developmental exposure to zinc (Zn), a metal or paraquat (PQ), a pesticide on the nigrostriatal dopaminergic neurons of rats challenged to Zn or PQ during adulthood. Exposure of Zn or PQ during adulthood alone exhibited marked reduction in motor activities, striatal dopamine and metabolites, glutathione content and number of dopaminergic neurons. However, the levels of lipid peroxidation, protein carbonyls, superoxide dismutase activity, pro-inflammatory cytokines and 4-hydroxynonenal-protein adducts were increased. While the expression of vesicular monoamine transporter-2 and tyrosine hydroxylase were attenuated, dopamine transporter and microglial marker Iba-1 expression, activated microglia, nuclear factor-kappa B activation, mitochondrial cytochrome c release and caspase-3/9 activation were augmented following Zn or PQ exposure. Albeit postnatal alone exposure did not alter any of the studied parameters, the developmental administration of Zn/PQ in re-challenged adult rats produced more pronounced changes in the aforementioned variables as compared with adulthood Zn or PQ alone intoxicated animals. The results demonstrate that postnatal Zn/PQ intoxication dents the oxidative stress, inflammation, cell death and dopamine metabolism and storage regulating machineries, which speed up the toxicant-induced degeneration during adulthood.
流行病学证据表明,人类接触农药或重金属与帕金森病 (PD) 的发病率增加有关。在大脑发育的关键时期接触农药或金属会增加成年啮齿动物再次接触时多巴胺能神经元的易感性。然而,早期接触农药对重金属诱导的神经退行性变或重金属对农药诱导的神经退行性变的影响尚未得到探索。本研究探讨了发育期暴露于锌 (Zn) 或百草枯 (PQ) 对成年期暴露于 Zn 或 PQ 大鼠黑质纹状体多巴胺能神经元的影响。单独暴露于 Zn 或 PQ 会导致运动活动、纹状体多巴胺和代谢物、谷胱甘肽含量和多巴胺能神经元数量明显减少。然而,脂质过氧化、蛋白质羰基、超氧化物歧化酶活性、促炎细胞因子和 4-羟基壬烯醛-蛋白质加合物的水平增加。虽然囊泡单胺转运体-2 和酪氨酸羟化酶的表达减弱,但多巴胺转运体和小胶质细胞标记物 Iba-1 的表达、激活的小胶质细胞、核因子-κB 激活、线粒体细胞色素 c 释放和 caspase-3/9 激活增加。尽管单独的产后暴露不会改变任何研究参数,但在重新挑战的成年大鼠中发育性给予 Zn/PQ 会导致上述变量发生更明显的变化,而不是单独给予成年 Zn 或 PQ 中毒的动物。结果表明,产后 Zn/PQ 中毒会削弱氧化应激、炎症、细胞死亡和多巴胺代谢和储存调节机制,从而加速成年期毒物诱导的退行性变。