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Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice.

Abstract：

:Although copper is among the indispensable trace elements in animal physiological processes, it exerts toxicity upon over-exposure. The present study aimed to investigate hepatocyte autophagy induced by CuSO4 and its potential mechanism. A total of 240 ICR mice (four-week-old, 120 males and 120 females) were randomly divided into four groups, in which mice separately received 0, 4, 8, and 16 mg/kg of Cu (Cu2+-CuSO4) for 42 d. The results of increased autophagosomes and autophagy marker LC3B brown cell staining showed that excessive intake of Cu enhanced hepatocyte autophagy. Simultaneously, Cu inhibited the activity of mTOR through suppressing mRNA and protein expressions in mTOR, which in turn up-regulated expression levels of ULK1 and initiated autophagy. Also, over-exposure to Cu increased mRNA and protein expressions of Beclin1, Atg12, Atg5, Atg16L1, Atg7, Atg3, and LC3 and decreased mRNA and protein expressions of p62. These results indicate that excess Cu can enhance hepatocyte autophagy via inhibiting the mTOR signaling pathway and regulating mRNA and protein expressions of factors implicated to autophagy in mice.

journal_name

Ecotoxicol Environ Saf

journal_title

Ecotoxicology and environmental safety

authors

Liu H,Deng H,Cui H,Jian Z,Guo H,Fang J,Zuo Z,Deng J,Li Y,Wang X,Zhao L

doi

10.1016/j.ecoenv.2020.111656

subject

Has Abstract

pub_date

2021-01-15 00:00:00

pages

111656

eissn

0147-6513

issn

1090-2414

pii

S0147-6513(20)31493-7

journal_volume

208

pub_type

杂志文章

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