{"title":"基于砷暴露的神经毒性的能量动力学变化:全面回顾。","authors":"Anuj Choudhary, Ruchi Pandey, Debiprasad Padhy, Dipak Rathod, Krishna Murti, Vivek Dave, Sameer Dhingra, Mahesh Rachamalla, Nitesh Kumar","doi":"10.2174/0109298673315956240829094938","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The by-product of naturally occurring rock, soil with different agricultural and industrial processes contaminated groundwater with a toxic metalloid- Arsenic (As3+), which results in different toxicities within the human body and in developing fetus.</p><p><strong>Aim: </strong>The present study emphasizes evaluating the presence of oxidative stress and excessive generation of reactive oxygen species (ROS) resulting in mitochondrial dysfunction and caspase activation followed by apoptosis due to arsenic-induced neurotoxicity along with epigenetic modifications at different molecular targets.</p><p><strong>Methods: </strong>Published articles available on PubMed and Scopus were studied and summarized.</p><p><strong>Results: </strong>The precise mechanism causing arsenic-induced neurotoxicity at a critical stage of brain development is still unknown, while increased oxidative stress led to mitochondrial dysfunctions which are known to play a prominent role in this. AMPK acts as a metabolic checkpoint and restores ATP levels through a different anabolic pathway in energy starvation. At the same time, arsenic-induced AMPK activation leads to autophagy and neuronal cell death.</p><p><strong>Conclusion: </strong>This review summarized the molecular mechanisms involved in arsenic-induced neurotoxicity, which can help develop suitable future ameliorative and therapeutic strategies.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.5000,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Changes in Energy Dynamics in Arsenic Exposure Based Neurotoxicity: A Comprehensive Review.\",\"authors\":\"Anuj Choudhary, Ruchi Pandey, Debiprasad Padhy, Dipak Rathod, Krishna Murti, Vivek Dave, Sameer Dhingra, Mahesh Rachamalla, Nitesh Kumar\",\"doi\":\"10.2174/0109298673315956240829094938\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The by-product of naturally occurring rock, soil with different agricultural and industrial processes contaminated groundwater with a toxic metalloid- Arsenic (As3+), which results in different toxicities within the human body and in developing fetus.</p><p><strong>Aim: </strong>The present study emphasizes evaluating the presence of oxidative stress and excessive generation of reactive oxygen species (ROS) resulting in mitochondrial dysfunction and caspase activation followed by apoptosis due to arsenic-induced neurotoxicity along with epigenetic modifications at different molecular targets.</p><p><strong>Methods: </strong>Published articles available on PubMed and Scopus were studied and summarized.</p><p><strong>Results: </strong>The precise mechanism causing arsenic-induced neurotoxicity at a critical stage of brain development is still unknown, while increased oxidative stress led to mitochondrial dysfunctions which are known to play a prominent role in this. AMPK acts as a metabolic checkpoint and restores ATP levels through a different anabolic pathway in energy starvation. At the same time, arsenic-induced AMPK activation leads to autophagy and neuronal cell death.</p><p><strong>Conclusion: </strong>This review summarized the molecular mechanisms involved in arsenic-induced neurotoxicity, which can help develop suitable future ameliorative and therapeutic strategies.</p>\",\"PeriodicalId\":10984,\"journal\":{\"name\":\"Current medicinal chemistry\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.5000,\"publicationDate\":\"2024-09-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current medicinal chemistry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2174/0109298673315956240829094938\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current medicinal chemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/0109298673315956240829094938","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
背景:目的:本研究强调评估氧化应激的存在和活性氧(ROS)的过度生成导致线粒体功能障碍和caspase激活,随后砷诱导的神经毒性导致细胞凋亡,以及不同分子靶点的表观遗传修饰:方法:研究并总结了发表在PubMed和Scopus上的文章:结果:在大脑发育的关键阶段,砷诱导神经毒性的确切机制尚不清楚,而氧化应激增加导致线粒体功能障碍,众所周知,线粒体功能障碍在其中发挥着重要作用。AMPK 作为代谢检查点,在能量饥饿时通过不同的合成代谢途径恢复 ATP 水平。同时,砷诱导的 AMPK 激活会导致自噬和神经细胞死亡:本综述总结了砷诱导神经毒性的分子机制,有助于未来制定合适的改善和治疗策略。
Changes in Energy Dynamics in Arsenic Exposure Based Neurotoxicity: A Comprehensive Review.
Background: The by-product of naturally occurring rock, soil with different agricultural and industrial processes contaminated groundwater with a toxic metalloid- Arsenic (As3+), which results in different toxicities within the human body and in developing fetus.
Aim: The present study emphasizes evaluating the presence of oxidative stress and excessive generation of reactive oxygen species (ROS) resulting in mitochondrial dysfunction and caspase activation followed by apoptosis due to arsenic-induced neurotoxicity along with epigenetic modifications at different molecular targets.
Methods: Published articles available on PubMed and Scopus were studied and summarized.
Results: The precise mechanism causing arsenic-induced neurotoxicity at a critical stage of brain development is still unknown, while increased oxidative stress led to mitochondrial dysfunctions which are known to play a prominent role in this. AMPK acts as a metabolic checkpoint and restores ATP levels through a different anabolic pathway in energy starvation. At the same time, arsenic-induced AMPK activation leads to autophagy and neuronal cell death.
Conclusion: This review summarized the molecular mechanisms involved in arsenic-induced neurotoxicity, which can help develop suitable future ameliorative and therapeutic strategies.
期刊介绍:
Aims & Scope
Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews and guest edited thematic issues written by leaders in the field covering a range of the current topics in medicinal chemistry. The journal also publishes reviews on recent patents. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.