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Heavy metal associated health hazards: An interplay of oxidative stress and signal transduction
Chemosphere ( IF 8.8 ) Pub Date : 2020-09-16 , DOI: 10.1016/j.chemosphere.2020.128350
Jagdish Gopal Paithankar , Sanjay Saini , Shiwangi Dwivedi , Anurag Sharma , Debapratim Kar Chowdhuri

Heavy metal-induced cellular and organismal toxicity have become a major health concern in biomedical science. Indiscriminate use of heavy metals in different sectors, such as, industrial-, agricultural-, healthcare-, cosmetics-, and domestic-sectors has contaminated environment matrices and poses a severe health concern. Xenobiotics mediated effect is a ubiquitous cellular response. Oxidative stress is one such prime cellular response, which is the result of an imbalance in the redox system. Further, oxidative stress is associated with macromolecular damages and activation of several cell survival and cell death pathways. Epidemiological as well as laboratory data suggest that oxidative stress-induced cellular response following heavy metal exposure is linked with an increased risk of neoplasm, neurological disorders, diabetes, infertility, developmental disorders, renal failure, and cardiovascular disease. During the recent past, a relation among heavy metal exposure, oxidative stress, and signaling pathways have been explored to understand the heavy metal-induced toxicity. Heavy metal-induced oxidative stress and its connection with different signaling pathways are complicated; therefore, the systemic summary is essential. Herein, an effort has been made to decipher the interplay among heavy metals/metalloids (Arsenic, Chromium, Cadmium, and Lead) exposures, oxidative stress, and signal transduction, which are essential to mount the cellular and organismal response. The signaling pathways involved in this interplay include NF-κB, NRF2, JAK-STAT, JNK, FOXO, and HIF.



中文翻译:

重金属相关的健康危害:氧化应激和信号转导的相互作用

重金属引起的细胞和生物毒性已经成为生物医学中的主要健康问题。在工业,农业,医疗保健,化妆品和家庭部门等不同部门中滥用重金属已经污染了环境基质,并引起了严重的健康问题。异源生物介导的作用是普遍存在的细胞反应。氧化应激就是这种主要的细胞反应之一,这是氧化还原系统失衡的结果。此外,氧化应激与大分子损伤以及几种细胞存活和细胞死亡途径的活化有关。流行病学和实验室数据表明,重金属暴露后氧化应激诱导的细胞反应与肿瘤,神经系统疾病,糖尿病,不育症,发育障碍,肾衰竭和心血管疾病。在最近的过去,已经探索了重金属暴露,氧化应激和信号传导途径之间的关系,以了解重金属诱导的毒性。重金属诱导的氧化应激及其与不同信号途径的联系是复杂的。因此,系统总结是必不可少的。在本文中,已经做出了努力来破解重金属/准金属(砷,铬,镉和铅)暴露,氧化应激和信号转导之间的相互作用,这对于提高细胞和生物反应至关重要。这种相互作用涉及的信号传导途径包括NF-κB,NRF2,JAK-STAT,JNK,FOXO和HIF。已经探索了重金属暴露,氧化应激和信号传导途径之间的关系,以了解重金属诱导的毒性。重金属诱导的氧化应激及其与不同信号途径的联系是复杂的。因此,系统总结是必不可少的。在本文中,已经做出了努力来破解重金属/准金属(砷,铬,镉和铅)暴露,氧化应激和信号转导之间的相互作用,这对于提高细胞和生物反应至关重要。这种相互作用涉及的信号传导途径包括NF-κB,NRF2,JAK-STAT,JNK,FOXO和HIF。已经探索了重金属暴露,氧化应激和信号传导途径之间的关系,以了解重金属诱导的毒性。重金属诱导的氧化应激及其与不同信号途径的联系是复杂的。因此,系统总结是必不可少的。在本文中,已经做出了努力来破解重金属/准金属(砷,铬,镉和铅)暴露,氧化应激和信号转导之间的相互作用,这对于提高细胞和生物反应至关重要。这种相互作用涉及的信号传导途径包括NF-κB,NRF2,JAK-STAT,JNK,FOXO和HIF。重金属诱导的氧化应激及其与不同信号途径的联系是复杂的。因此,系统总结是必不可少的。在本文中,已经做出了努力来破解重金属/准金属(砷,铬,镉和铅)暴露,氧化应激和信号转导之间的相互作用,这对于提高细胞和生物反应至关重要。这种相互作用涉及的信号传导途径包括NF-κB,NRF2,JAK-STAT,JNK,FOXO和HIF。重金属诱导的氧化应激及其与不同信号途径的联系是复杂的。因此,系统总结是必不可少的。在本文中,已经做出了努力来破解重金属/准金属(砷,铬,镉和铅)暴露,氧化应激和信号转导之间的相互作用,这对于提高细胞和生物反应至关重要。这种相互作用涉及的信号传导途径包括NF-κB,NRF2,JAK-STAT,JNK,FOXO和HIF。

更新日期:2020-09-16
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