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双酚 A 暴露会导致果蝇患帕金森样疾病。

Bisphenol A exposure is involved in the development of Parkinson like disease in Drosophila melanogaster.

机构信息

Laboratory of Pharmacological and Toxicological Evaluations Applied to Bioactive Molecules, Federal University of Pampa, Itaqui Campus, RS, Brazil.

Laboratory of Pharmacological and Toxicological Evaluations Applied to Bioactive Molecules, Federal University of Pampa, Itaqui Campus, RS, Brazil; Department of Nutrition, Federal University of Pampa, Itaqui Campus, RS, Brazil.

出版信息

Food Chem Toxicol. 2020 Mar;137:111128. doi: 10.1016/j.fct.2020.111128. Epub 2020 Jan 14.

Abstract

The pathogenesis of Parkinson's disease has not been fully clarified yet but its cause is known to be multifactorial. One of these factors is oxidative stress induced by exposure to environmental toxifiers. We studied the effect of Bisphenol A (BPA) at concentrations of 0.5 mM and 1 mM, the concentration of 1 mM corresponding to Lowest Observed Adverse Effect Level (LOAEL) for humans in adult Drosophila melanogaster. The BPA induced oxidative stress was established by increased levels of malondialdehyde, reactive species, and decreased activity of the antioxidant enzymes superoxide dismutase and catalase, and detoxificant enzyme glutathione-S-transferase. Associated with oxidative stress, there was a reduction of acetylcholinesterase activity and a reduction of dopamine levels, which are related to the decreased locomotion activity as observed in negative geotaxis, open field and equilibrium behaviors in group exposed to 1 mM of BPA. Oxidative stress also impaired mitochondrial and cellular metabolic activity in the head causing an increase in the mortality of flies exposed to both BPA concentrations. Therefore, BPA induced Parkinsonian-like changes in flies and it is possible that the oxidative stress is closely related to this effect, providing new insights for future studies.

摘要

帕金森病的发病机制尚未完全阐明,但已知其病因是多因素的。其中一个因素是暴露于环境毒物引起的氧化应激。我们研究了双酚 A(BPA)在 0.5 mM 和 1 mM 浓度下的作用,1 mM 的浓度对应于成年黑腹果蝇中人类的最低观察不良效应水平(LOAEL)。BPA 通过增加丙二醛、活性物质的水平和降低抗氧化酶超氧化物歧化酶和过氧化氢酶以及解毒酶谷胱甘肽-S-转移酶的活性来诱导氧化应激。与氧化应激相关的是乙酰胆碱酯酶活性的降低和多巴胺水平的降低,这与在接触 1 mM BPA 的组中观察到的负趋地性、开阔场和平衡行为中的运动活性降低有关。氧化应激还损害了头部的线粒体和细胞代谢活性,导致接触两种 BPA 浓度的苍蝇死亡率增加。因此,BPA 诱导果蝇出现帕金森样变化,氧化应激可能与这种效应密切相关,为未来的研究提供了新的见解。

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