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Toxic mechanisms of microcystins in mammals.
Toxicology Research ( IF 2.1 ) Pub Date : 2017-04-24 , DOI: 10.1039/c7tx00043j
Nicole L McLellan 1 , Richard A Manderville 2
Affiliation  

Microcystins, such as microcystin-leucine arginine (MC-LR), are some of the most toxic and prevalent cyanotoxins produced by cyanobacteria in freshwater and saltwater algal blooms worldwide. Acute and chronic exposures to microcystins are primarily known to cause hepatotoxicity; cellular damage and genotoxicity within mammalian livers. However, in vivo studies indicate that similar damage may occur in other mammalian organs and tissues, such as the kidney, heart, reproductive systems, and lungs - particularly following chronic low-dose exposures. Mechanisms of toxicity of mycrocystins are reviewed herein; including cellular uptake, interaction with protein phosphatases PP1 and PP2A, cytoskeletal effects, formation of oxidative stress and induction of apoptosis. In general, the mode of action of toxicity by MCs in mammalian organs are similar to those that have been observed in liver tissues. A comprehensive understanding of the toxic mechanisms of microcystins in mammalian tissues and organs will assist in the development of risk assessment approaches to public health protection strategies and the development of robust drinking water policies.

中文翻译:

微囊藻毒素在哺乳动物中的毒性机制。

微囊藻毒素,例如微囊藻毒素-亮氨酸精氨酸(MC-LR),是蓝藻在全球淡水和盐水藻华中产生的最具毒性和最普遍的氰毒素。众所周知,急性和慢性暴露于微囊藻毒素会引起肝毒性。哺乳动物肝脏中的细胞损伤和遗传毒性。但是,体内研究表明,在其他哺乳动物的器官和组织中,例如肾脏,心脏,生殖系统和肺部,也可能发生类似的损害-特别是在长期低剂量暴露后。在此综述了霉菌毒素的毒性机理。包括细胞摄取,与蛋白磷酸酶PP1和PP2A的相互作用,细胞骨架作用,氧化应激的形成和凋亡的诱导。一般来说,MC在哺乳动物器官中的毒性作用方式与在肝组织中观察到的相似。对微囊藻毒素在哺乳动物组织和器官中的毒性机制的全面理解将有助于制定公共卫生保护策略的风险评估方法,并制定强有力的饮用水政策。
更新日期:2017-04-24
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