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The protective effect of α-lipoic acid against bisphenol A-induced neurobehavioral toxicity
Neurochemistry international ( IF 4.2 ) Pub Date : 2018-06-13 , DOI: 10.1016/j.neuint.2018.06.005
Jasim Khan , Shikha Salhotra , Shahzad Ahmad , Shikha Sharma , Sayed Aliul Hasan Abdi , Basu Dev Banerjee , Suhel Parvez , Sarika Gupta , Sheikh Raisuddin

Bisphenol A (BPA), a well-known xenoestrogen, is ubiquitously utilized in manufacturing of polycarbonated plastics. Convincing evidence suggests that BPA induces neurotoxicity and certain behavioral deficits. α-Lipoic acid (ALA) supplementation has shown protective effect against heart and liver diseases, diabetes, and neurological debility associated with aging. We studied the neuromodulatory effect of ALA against neurotoxicity of BPA in vitro in C8-D1A mouse astrocyte cell line and in vivo in C57BL/6J male mice. In vitro ALA (100 μM) protected cells from BPA (30 μM)-induced reactive oxygen species generation and increased activity of glial fibrillary acidic protein. ALA showed reduction in cell death in astrocytes treated with BPA. In vivo ALA (50 mg/kg) increased the neurospecific acetylcholinesterase activity and decreased the monoamine oxidase activity altered by BPA exposure (10 mg/kg, per os x 30 days). In addition to neuroprotective effects, ALA also showed protective effects against BPA-induced oxidative stress. We observed that ALA significantly replenished the declined neurobehavioral and cognitive performances, decreased muscle coordination and alerted short-term recognition memory in mice exposed to BPA. Our results suggest that ALA has a promising role in modulating BPA-induced neurotoxicity in C8-D1A mouse astrocyte cells as well as neurochemical and neurobehavioral deficits in C57BL/6J male mice and its antioxidant and free radical scavenging activities may in part be responsible for such an effect.



中文翻译:

α-硫辛酸对双酚A诱导的神经行为毒性的保护作用

双酚A(BPA)是一种众所周知的异雌激素,广泛用于制造聚碳酸酯塑料。有说服力的证据表明,双酚A会诱发神经毒性和某些行为缺陷。补充α-硫辛酸(ALA)已显示出对心脏和肝脏疾病,糖尿病以及与衰老相关的神经衰弱的保护作用。我们研究了ALA在体外对C8-D1A星形胶质细胞系和在体内对C57BL / 6J雄性小鼠BPA的神经毒性的神经调节作用。体外ALA(100μM)保护细胞免受BPA(30μM)诱导的活性氧种类的产生和胶质原纤维酸性蛋白活性的增加。ALA在用BPA处理的星形胶质细胞中显示出细胞死亡的减少。体内ALA(50 mg / kg)增加了神经特异性乙酰胆碱酯酶的活性,并降低了因BPA暴露而改变的单胺氧化酶活性(10 mg / kg,每os x 30天)。除了神经保护作用外,ALA还显示出对BPA诱导的氧化应激的保护作用。我们观察到,ALA可显着补充暴露于BPA的小鼠的神经行为和认知能力下降,肌肉协调性下降并提醒短期识别记忆。我们的研究结果表明,ALA在调节BPA诱导的C8-D1A星形胶质细胞神经毒性以及C57BL / 6J雄性小鼠的神经化学和神经行为缺陷方面发挥着有希望的作用,其抗氧化剂和自由基清除活性可能是造成这种情况的部分原因效果。

更新日期:2018-06-13
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