Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice
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 fema...
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2021-01-01
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| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651320314937 |
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doaj-6965dbf5f20d46c1bfea4d01f6a82280 |
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| record_format |
Article |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Huan Liu Huidan Deng Hengmin Cui Zhijie Jian Hongrui Guo Jing Fang Zhicai Zuo Junliang Deng Yinglun Li Xun Wang Ling Zhao |
| spellingShingle |
Huan Liu Huidan Deng Hengmin Cui Zhijie Jian Hongrui Guo Jing Fang Zhicai Zuo Junliang Deng Yinglun Li Xun Wang Ling Zhao Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice Ecotoxicology and Environmental Safety CuSO4 Autophagy MTOR signaling pathway Liver Mouse |
| author_facet |
Huan Liu Huidan Deng Hengmin Cui Zhijie Jian Hongrui Guo Jing Fang Zhicai Zuo Junliang Deng Yinglun Li Xun Wang Ling Zhao |
| author_sort |
Huan Liu |
| title |
Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice |
| title_short |
Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice |
| title_full |
Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice |
| title_fullStr |
Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice |
| title_full_unstemmed |
Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice |
| title_sort |
copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in mice |
| publisher |
Elsevier |
| series |
Ecotoxicology and Environmental Safety |
| issn |
0147-6513 |
| publishDate |
2021-01-01 |
| description |
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. |
| topic |
CuSO4 Autophagy MTOR signaling pathway Liver Mouse |
| url |
http://www.sciencedirect.com/science/article/pii/S0147651320314937 |
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doaj-6965dbf5f20d46c1bfea4d01f6a822802021-04-23T06:14:51ZengElsevierEcotoxicology and Environmental Safety0147-65132021-01-01208111656Copper induces hepatocyte autophagy via the mammalian targets of the rapamycin signaling pathway in miceHuan Liu0Huidan Deng1Hengmin Cui2Zhijie Jian3Hongrui Guo4Jing Fang5Zhicai Zuo6Junliang Deng7Yinglun Li8Xun Wang9Ling Zhao10College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, China; Key Laboratory of Agricultural information engineering of Sichuan Province, Sichuan Agriculture University, Yaan, Sichuan, 625014, China; Corresponding authors at: College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, Sichuan 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, China; Corresponding authors at: College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, Sichuan 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, ChinaCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu 611130, China; Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu 611130, ChinaAlthough 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.http://www.sciencedirect.com/science/article/pii/S0147651320314937CuSO4AutophagyMTOR signaling pathwayLiverMouse |