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Biochemical and Molecular Bases of Lead-Induced Toxicity in Mammalian Systems and Possible Mitigations
Chemical Research in Toxicology ( IF 3.7 ) Pub Date : 2018-09-04 00:00:00 , DOI: 10.1021/acs.chemrestox.8b00193 Nitika Singh 1 , Abhishek Kumar 1 , Vivek Kumar Gupta 1 , Bechan Sharma 1
Chemical Research in Toxicology ( IF 3.7 ) Pub Date : 2018-09-04 00:00:00 , DOI: 10.1021/acs.chemrestox.8b00193 Nitika Singh 1 , Abhishek Kumar 1 , Vivek Kumar Gupta 1 , Bechan Sharma 1
Affiliation
The effects of lead exposure on mammals are reported to be devastating. Lead is present in all the abiotic environmental components such as brass, dust, plumbing fixtures, soil, water, and lead mixed imported products. Its continuous use for several industrial and domestic purposes has caused a rise in its levels, thereby posing serious threats to human health. The mechanisms involved in lead-induced toxicity primarily include free-radical-mediated generation of oxidative stress which directly imbalances the prooxidants and the antioxidants in body. The toxicity of lead involves damage primarily to major biomolecules (lipid, protein, and nucleic acids) and liver (hepatotoxicity), nervous system (neurotoxicity), kidney (nephrotoxicity) and DNA (genotoxicity), present in animals and humans. The activation of c-Jun NH2-terminal kinase, phosphoinositide 3-kinase, or Akt and p38 mitogen activated protein kinase signaling pathways are important for lead cytotoxicity. Lead increased apoptosis through signaling cascade and associated factors and significantly impairs cell differentiation and maturation. In addition, lead has great impact on metabolic pathways such as heme synthesis, thereby leading to the onset of anemia in lead exposed people. This review encompasses an updated account of varied aspects of lead-induced oxidative stress and the biomolecular consequences such as perturbations in physiological processes, apoptosis, carcinogenesis, hormonal imbalance, loss of vision, and reduced fertility and their possible remediation through synthetic (chelators) and natural compounds (plant-based principles). This paper is primarily concerned with the biomedical implications of lead-induced generation of free radical and the toxicity management in the mammalian system.
中文翻译:
哺乳动物系统中铅诱导的毒性的生化和分子基础以及可能的缓解方法
据报道,铅对哺乳动物的影响是毁灭性的。铅存在于所有非生物环境成分中,例如黄铜,灰尘,卫生设备,土壤,水和铅混合进口产品中。连续将其用于多种工业和家庭用途已导致其含量上升,从而对人类健康构成了严重威胁。铅引起的毒性的机制主要包括自由基介导的氧化应激的产生,其直接失衡体内的前氧化剂和抗氧化剂。铅的毒性主要涉及对动物和人类体内存在的主要生物分子(脂质,蛋白质和核酸)和肝脏(肝毒性),神经系统(神经毒性),肾脏(肾毒性)和DNA(遗传毒性)的损害。c-Jun NH2末端激酶的激活,磷酸肌醇3激酶,或Akt和p38丝裂原活化的蛋白激酶信号通路对铅细胞毒性很重要。铅通过信号级联反应和相关因子增加细胞凋亡,并显着损害细胞分化和成熟。此外,铅对诸如血红素合成等代谢途径有很大影响,从而导致铅暴露人群贫血的发生。这篇综述涵盖了铅诱导的氧化应激和生物分子后果(例如生理过程中的摄动,细胞凋亡,癌变,荷尔蒙失衡,视力丧失,生育力下降以及它们可能通过合成(螯合剂)修复)的各个方面的最新情况天然化合物(基于植物的原理)。
更新日期:2018-09-04
中文翻译:
哺乳动物系统中铅诱导的毒性的生化和分子基础以及可能的缓解方法
据报道,铅对哺乳动物的影响是毁灭性的。铅存在于所有非生物环境成分中,例如黄铜,灰尘,卫生设备,土壤,水和铅混合进口产品中。连续将其用于多种工业和家庭用途已导致其含量上升,从而对人类健康构成了严重威胁。铅引起的毒性的机制主要包括自由基介导的氧化应激的产生,其直接失衡体内的前氧化剂和抗氧化剂。铅的毒性主要涉及对动物和人类体内存在的主要生物分子(脂质,蛋白质和核酸)和肝脏(肝毒性),神经系统(神经毒性),肾脏(肾毒性)和DNA(遗传毒性)的损害。c-Jun NH2末端激酶的激活,磷酸肌醇3激酶,或Akt和p38丝裂原活化的蛋白激酶信号通路对铅细胞毒性很重要。铅通过信号级联反应和相关因子增加细胞凋亡,并显着损害细胞分化和成熟。此外,铅对诸如血红素合成等代谢途径有很大影响,从而导致铅暴露人群贫血的发生。这篇综述涵盖了铅诱导的氧化应激和生物分子后果(例如生理过程中的摄动,细胞凋亡,癌变,荷尔蒙失衡,视力丧失,生育力下降以及它们可能通过合成(螯合剂)修复)的各个方面的最新情况天然化合物(基于植物的原理)。