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固体废弃物浸出液引起的线粒体功能障碍为浸出液诱导细胞死亡和病理生理紊乱的机制提供了新的见解。

Mitochondrial dysfunctions elicited by solid waste leachates provide insights into mechanisms of leachates induced cell death and pathophysiological disorders.

机构信息

Cell Biology and Genetics Unit, Department of Zoology, University of Ibadan, Ibadan, Nigeria; Department of Toxicology, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Technical University of Dortmund, 44139, Dortmund, Germany.

Health and Toxicity Cell (HTC), CSIR-National Environmental Engineering Research Institute (NEERI), Nagpur, 440020, India; Academy of Scientific, Innovative Research (AcSIR), Ghaziabad, U.P, India.

出版信息

Chemosphere. 2022 Nov;307(Pt 4):136085. doi: 10.1016/j.chemosphere.2022.136085. Epub 2022 Aug 22.

DOI:10.1016/j.chemosphere.2022.136085
PMID:36007733
Abstract

Emissions (mainly leachates and landfill gases) from solid waste facilities are laden with mixtures of dangerous xenobiotics implicated with significant increase in various pathophysiological disorders including cancer, and eventual mortality of exposed wildlife and humans. However, the molecular mechanisms of solid waste leachates induce pathophysiological disorders and cell death are still largely unknown. Although, evolving evidence implicated generation of reactive oxygen species and oxidative stress as the possible mechanism. Recent scientific reports are linking reactive oxygen species and mitochondrial dysfunctions as the player mechanism in pathophysiological disorder and apoptosis induced by xenobiotics in solid waste leachates. This systematic review presents an explicit discussion of recent scientific findings on the structural and functional alterations in mitochondria induced by solid waste leachates as the molecular mechanisms plausibly responsible for the pathophysiological disorders, cancer and cell death reported in landfill toxicology and epidemiological studies. This review aims to increase scientific understanding on solid waste leachate induced mitochondria dysfunctions as the key player in molecular mechanisms of solid waste induced toxicity. The findings in this review were mainly from using primary cells, cell lines, Drosophila and fish. Whether the findings will similarly be observed in mammalian test systems in vivo and particularly in exposed humans, remained to be investigated. Improvement in technological advancements, enforcement of legislation and regulations, and creation of sophisticated health surveillance against exposure to solid waste leachates, will expectedly mitigate human exposure to solid waste emissions and contamination of the environment.

摘要

固体废物设施排放的废气(主要是渗滤液和垃圾填埋气)中含有多种危险的异生物质,这些异生物质与多种病理生理紊乱(包括癌症)的显著增加有关,并最终导致暴露于其中的野生动物和人类死亡。然而,固体废物渗滤液诱导病理生理紊乱和细胞死亡的分子机制在很大程度上仍然未知。尽管有越来越多的证据表明活性氧和氧化应激的产生是可能的机制。最近的科学研究报告将活性氧和线粒体功能障碍联系起来,作为固体废物渗滤液中的异生物质诱导病理生理紊乱和细胞凋亡的可能机制。本系统评价明确讨论了最近关于固体废物渗滤液引起的线粒体结构和功能改变的科学发现,这些改变可能是导致垃圾填埋场毒理学和流行病学研究中报告的病理生理紊乱、癌症和细胞死亡的分子机制。本综述旨在提高人们对固体废物渗滤液诱导的线粒体功能障碍作为固体废物诱导毒性的分子机制中关键因素的科学认识。本综述中的发现主要来自于使用原代细胞、细胞系、果蝇和鱼类。这些发现是否也会在体内的哺乳动物测试系统中,特别是在暴露于固体废物渗滤液的人群中观察到,仍有待研究。技术进步的提高、立法和法规的执行以及针对固体废物渗滤液暴露的复杂健康监测的建立,有望减轻人类接触固体废物排放物和环境污染的程度。

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