Selenium supplementation decreases hepatic fibrosis in mice after chronic carbon tetrachloride administration

Ming Ding; James J. Potter; Xiaopu Liu; Michael S. Torbenson; Esteban Mezey

doi:10.1007/s12011-009-8414-x

Selenium supplementation decreases hepatic fibrosis in mice after chronic carbon tetrachloride administration

Ming Ding, James J. Potter, Xiaopu Liu, Michael S. Torbenson, Esteban Mezey

Laboratory Medicine and Pathology

Research output: Contribution to journal › Article › peer-review

20 Scopus citations

Abstract

Oxidative stress stimulates fibrogenesis, and selenium (Se) has antioxidant properties. This study determined whether Se supplementation affects CCl ₄-induced liver injury and fibrosis. Mice were administered CCl ₄ over 4 weeks, while controls received olive oil. Se was provided as sodium selenite in the drinking water. Se increased liver Se-dependent glutathione peroxidase activity and decreased liver malondialdehyde after CCl₄. Se decreased liver inflammation but not necrosis caused by CCl₄. Se increased hepatocyte apoptosis after CCl₄ and the pro-apoptotic BAX and Bcl Xs/l proteins. Stellate cell apoptosis occurred only after CCl₄ in Se-supplemented mice. Se decreased stellate cell number and fibrosis after CCl₄. Liver matrix metalloproteinase-9 increased after CCl₄ with Se supplementation. In conclusion, Se supplementation decreased hepatic fibrosis after CCl₄ in the setting of decreased inflammation but increased apoptosis. The principal mechanisms for the decreased fibrosis are a lower number of collagen-producing stellate cells and increased collagen degradation.

Original language	English (US)
Pages (from-to)	83-97
Number of pages	15
Journal	Biological Trace Element Research
Volume	133
Issue number	1
DOIs	https://doi.org/10.1007/s12011-009-8414-x
State	Published - Jan 2010

Keywords

Apoptosis
Caspases
Collagen
Metalloproteinases
Selenium
Stellate cells

ASJC Scopus subject areas

Biochemistry, medical
Biochemistry
Clinical Biochemistry
Inorganic Chemistry
Endocrinology, Diabetes and Metabolism

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title = "Selenium supplementation decreases hepatic fibrosis in mice after chronic carbon tetrachloride administration",

abstract = "Oxidative stress stimulates fibrogenesis, and selenium (Se) has antioxidant properties. This study determined whether Se supplementation affects CCl 4-induced liver injury and fibrosis. Mice were administered CCl 4 over 4 weeks, while controls received olive oil. Se was provided as sodium selenite in the drinking water. Se increased liver Se-dependent glutathione peroxidase activity and decreased liver malondialdehyde after CCl4. Se decreased liver inflammation but not necrosis caused by CCl4. Se increased hepatocyte apoptosis after CCl4 and the pro-apoptotic BAX and Bcl Xs/l proteins. Stellate cell apoptosis occurred only after CCl4 in Se-supplemented mice. Se decreased stellate cell number and fibrosis after CCl4. Liver matrix metalloproteinase-9 increased after CCl4 with Se supplementation. In conclusion, Se supplementation decreased hepatic fibrosis after CCl4 in the setting of decreased inflammation but increased apoptosis. The principal mechanisms for the decreased fibrosis are a lower number of collagen-producing stellate cells and increased collagen degradation.",

keywords = "Apoptosis, Caspases, Collagen, Metalloproteinases, Selenium, Stellate cells",

author = "Ming Ding and Potter, {James J.} and Xiaopu Liu and Torbenson, {Michael S.} and Esteban Mezey",

note = "Funding Information: Acknowledgments This work was supported by grant AA000626 from the US Public Health Service. M. D. was a postdoctoral fellow on National Research Service Award 2 T32 AA07467 from the National Institute of Alcohol Abuse and Alcoholism (NIH). The authors acknowledge assistance from The Hopkins Digestive Diseases Basic Research Development Center (NIH grant 2464388) in the performance of this study.",

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doi = "10.1007/s12011-009-8414-x",

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journal = "Biological Trace Element Research",

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T1 - Selenium supplementation decreases hepatic fibrosis in mice after chronic carbon tetrachloride administration

AU - Ding, Ming

AU - Potter, James J.

AU - Liu, Xiaopu

AU - Torbenson, Michael S.

AU - Mezey, Esteban

N1 - Funding Information: Acknowledgments This work was supported by grant AA000626 from the US Public Health Service. M. D. was a postdoctoral fellow on National Research Service Award 2 T32 AA07467 from the National Institute of Alcohol Abuse and Alcoholism (NIH). The authors acknowledge assistance from The Hopkins Digestive Diseases Basic Research Development Center (NIH grant 2464388) in the performance of this study.

PY - 2010/1

Y1 - 2010/1

N2 - Oxidative stress stimulates fibrogenesis, and selenium (Se) has antioxidant properties. This study determined whether Se supplementation affects CCl 4-induced liver injury and fibrosis. Mice were administered CCl 4 over 4 weeks, while controls received olive oil. Se was provided as sodium selenite in the drinking water. Se increased liver Se-dependent glutathione peroxidase activity and decreased liver malondialdehyde after CCl4. Se decreased liver inflammation but not necrosis caused by CCl4. Se increased hepatocyte apoptosis after CCl4 and the pro-apoptotic BAX and Bcl Xs/l proteins. Stellate cell apoptosis occurred only after CCl4 in Se-supplemented mice. Se decreased stellate cell number and fibrosis after CCl4. Liver matrix metalloproteinase-9 increased after CCl4 with Se supplementation. In conclusion, Se supplementation decreased hepatic fibrosis after CCl4 in the setting of decreased inflammation but increased apoptosis. The principal mechanisms for the decreased fibrosis are a lower number of collagen-producing stellate cells and increased collagen degradation.

AB - Oxidative stress stimulates fibrogenesis, and selenium (Se) has antioxidant properties. This study determined whether Se supplementation affects CCl 4-induced liver injury and fibrosis. Mice were administered CCl 4 over 4 weeks, while controls received olive oil. Se was provided as sodium selenite in the drinking water. Se increased liver Se-dependent glutathione peroxidase activity and decreased liver malondialdehyde after CCl4. Se decreased liver inflammation but not necrosis caused by CCl4. Se increased hepatocyte apoptosis after CCl4 and the pro-apoptotic BAX and Bcl Xs/l proteins. Stellate cell apoptosis occurred only after CCl4 in Se-supplemented mice. Se decreased stellate cell number and fibrosis after CCl4. Liver matrix metalloproteinase-9 increased after CCl4 with Se supplementation. In conclusion, Se supplementation decreased hepatic fibrosis after CCl4 in the setting of decreased inflammation but increased apoptosis. The principal mechanisms for the decreased fibrosis are a lower number of collagen-producing stellate cells and increased collagen degradation.

KW - Apoptosis

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Selenium supplementation decreases hepatic fibrosis in mice after chronic carbon tetrachloride administration

Abstract

Keywords

ASJC Scopus subject areas

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