Journal
BIOLOGICAL CHEMISTRY
Volume 399, Issue 11, Pages 1237-1248Publisher
WALTER DE GRUYTER GMBH
DOI: 10.1515/hsz-2017-0324
Keywords
environmental liver disease; hepatotoxicity; non-alcoholic fatty liver disease (NAFLD); organo-chlorines; toxicant; toxicant-associated steatohepatitis (TASH)
Categories
Funding
- National Institutes of Health [National Institute of Diabetes and Digestive and Kidney Diseases] [K01 DK096042, R03 DK107912, T32ES011564]
- National Institutes of Health [National Institute of Environmental Health Sciences] [P42 ES023716]
- National Institute of General Medical Sciences of the National Institutes of Health [P20GM113226, P20GM103492]
- National Institute on Alcohol Abuse and Alcoholism of the National Institutes of Health [P50AA024337]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K01DK096042, R03DK107912] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [T32ES011564, P42ES023716] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P20GM103492, P20GM113226] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [P50AA024337] Funding Source: NIH RePORTER
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Occupational and environmental exposures to industrial chemicals are known to cause hepatotoxicity and liver injury, in humans and in animal models. Historically, research has focused on severe acute liver injury (e.g. fulminant liver failure) or endstage diseases (e.g. cirrhosis and HCC). However, it has become recently recognized that toxicants can cause more subtle changes to the liver. For example, toxicant-associated steatohepatitis, characterized by hepatic steatosis, and inflammation, was recently recognized in an occupational cohort exposed to vinyl chloride. At high occupational levels, toxicants are sufficient to cause liver damage and disease even in healthy subjects with no comorbidities for liver injury. However, it is still largely unknown how exposure to toxicants initiate and possibly more importantly exacerbate liver disease, when combined with other factors, such as underlying non-alcoholic fatty liver disease caused by poor diet and/or obesity. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of toxicant-induced liver disease, rational targeted therapy can be developed to better predict risk, as well as to treat or prevent this disease. The purpose of this review is to summarize established and proposed mechanisms of volatile organic compound-induced liver injury and to highlight key signaling events known or hypothesized to mediate these effects.
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