An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo

Abstract Backgroud Drinking water contamination with hexavalent chromium [Cr (VI)] has become one of the most serious public health problems, thus the investigation of Cr (VI)-induced hepatotoxicity has attracted much attention in recent years. Methods In the present study, by determining the indice...

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Main Authors: Xiali Zhong, Ming Zeng, Huanfeng Bian, Caigao Zhong, Fang Xiao
Format: Article
Language:English
Published: BMC 2017-06-01
Series:Journal of Occupational Medicine and Toxicology
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12995-017-0161-x
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author Xiali Zhong
Ming Zeng
Huanfeng Bian
Caigao Zhong
Fang Xiao
author_facet Xiali Zhong
Ming Zeng
Huanfeng Bian
Caigao Zhong
Fang Xiao
author_sort Xiali Zhong
collection DOAJ
description Abstract Backgroud Drinking water contamination with hexavalent chromium [Cr (VI)] has become one of the most serious public health problems, thus the investigation of Cr (VI)-induced hepatotoxicity has attracted much attention in recent years. Methods In the present study, by determining the indices of hepatotoxicity induced by Cr (VI), the source of accumulated reactive oxygen species (ROS), and the protective effect of the antioxidant Vitamin C (Vit C), we explored the mechanisms involved in Cr (VI)-induced hepatotoxicity in vitro and in vivo. Results We found Cr (VI) caused hepatotoxicity characterized by the alterations of several enzymatic and cytokine markers including aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukine-1β (IL-1β), and tumor necrosis factor-α (TNF-α), etc. ROS production after Cr (VI) exposure was origins from the inhibition of electron transfer chain (ETC) and antioxidant system. Vit C inhibited ROS accumulation thus protected against Cr (VI)-induced hepatotoxicity in L-02 hepatocytes and in the rat model. Conclusions We concluded that ROS played a role in Cr (VI)-induced hepatotoxicity and Vit C exhibited protective effect. Our current data provides important clues for studying the mechanisms involved in Cr (VI)-induced liver injury, and may be of great help to develop therapeutic strategies for prevention and treatment of liver diseases involving ROS accumulation for occupational exposure population.
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spelling doaj.art-e5efb581cd894e8aa342e56d4a2f60412022-12-22T03:19:31ZengBMCJournal of Occupational Medicine and Toxicology1745-66732017-06-0112111210.1186/s12995-017-0161-xAn evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivoXiali Zhong0Ming Zeng1Huanfeng Bian2Caigao Zhong3Fang Xiao4Department of Health Toxicology, Xiangya School of Public Health, Central South UniversityDepartment of Health Toxicology, Xiangya School of Public Health, Central South UniversityShajing Institution of Health Supervision of Baoan DistrictDepartment of Health Toxicology, Xiangya School of Public Health, Central South UniversityDepartment of Health Toxicology, Xiangya School of Public Health, Central South UniversityAbstract Backgroud Drinking water contamination with hexavalent chromium [Cr (VI)] has become one of the most serious public health problems, thus the investigation of Cr (VI)-induced hepatotoxicity has attracted much attention in recent years. Methods In the present study, by determining the indices of hepatotoxicity induced by Cr (VI), the source of accumulated reactive oxygen species (ROS), and the protective effect of the antioxidant Vitamin C (Vit C), we explored the mechanisms involved in Cr (VI)-induced hepatotoxicity in vitro and in vivo. Results We found Cr (VI) caused hepatotoxicity characterized by the alterations of several enzymatic and cytokine markers including aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukine-1β (IL-1β), and tumor necrosis factor-α (TNF-α), etc. ROS production after Cr (VI) exposure was origins from the inhibition of electron transfer chain (ETC) and antioxidant system. Vit C inhibited ROS accumulation thus protected against Cr (VI)-induced hepatotoxicity in L-02 hepatocytes and in the rat model. Conclusions We concluded that ROS played a role in Cr (VI)-induced hepatotoxicity and Vit C exhibited protective effect. Our current data provides important clues for studying the mechanisms involved in Cr (VI)-induced liver injury, and may be of great help to develop therapeutic strategies for prevention and treatment of liver diseases involving ROS accumulation for occupational exposure population.http://link.springer.com/article/10.1186/s12995-017-0161-xHexavalent chromium [Cr (VI)]Reactive oxygen species (ROS)HepatotoxicityVitamin C (Vit C)Mitochondrial respiratory chain complex I (MRCC I)
spellingShingle Xiali Zhong
Ming Zeng
Huanfeng Bian
Caigao Zhong
Fang Xiao
An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo
Journal of Occupational Medicine and Toxicology
Hexavalent chromium [Cr (VI)]
Reactive oxygen species (ROS)
Hepatotoxicity
Vitamin C (Vit C)
Mitochondrial respiratory chain complex I (MRCC I)
title An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo
title_full An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo
title_fullStr An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo
title_full_unstemmed An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo
title_short An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo
title_sort evaluation of the protective role of vitamin c in reactive oxygen species induced hepatotoxicity due to hexavalent chromium in vitro and in vivo
topic Hexavalent chromium [Cr (VI)]
Reactive oxygen species (ROS)
Hepatotoxicity
Vitamin C (Vit C)
Mitochondrial respiratory chain complex I (MRCC I)
url http://link.springer.com/article/10.1186/s12995-017-0161-x
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