Tetrachloroethylene is a chlorinated solvent that is primarily used in dry cleaning and degreasing operations. Although the hepatotoxicity caused by tetrachloroethylene has been well documented in literature, it is rarely considered as a cause of acute liver failure. We report a case of a 39-yr-old man who was admitted to our hospital for acute liver failure due to tetrachloroethylene exposure. Histological examination of the liver revealed massive hepatic necrosis, prominently, in zone 3 of the hepatic lobules. The patient underwent supportive treatment along with 3 sessions of plasmapheresis, and consequently, he presented a favorable outcome. Repeat liver biopsy performed 6 months after the patient's discharge showed architectural distortion with postnecrotic cirrhosis. Physicians should be aware of the possibility of acute liver failure induced by tetrachloroethylene. Early plasmapheresis can be effective for individuals with sufficient capacity for hepatocyte regeneration.
Adult ; Carcinogens/*toxicity ; Humans ; Liver Cirrhosis/pathology ; Liver Failure, Acute/chemically induced/*diagnosis/pathology ; Male ; *Occupational Exposure ; Plasmapheresis ; Tetrachloroethylene/*toxicity

OBJECTIVETo explore the different concentrations of trichloroethylene (TCE) or perchloroethylene (PCE) induced cultured normal human epidermal keratinocyte (KC) lipid peroxidation and protective effect of Vitamin E on it.

METHODSKC derived from 3 or more donors were pooled together and cultured with K-SFM. Neutral Red Uptake Assay was used to determine the IC50 of TCE or PCE, and then different concentrations of TCE or PCE were administered for culturing KC; 0.5 mmol/L TCE or 0.2 mmol/L PCE and different concentrations of Vitamin E were used to determine the protective effect of Vitamin E. After 4 hours' culture, kits were used to determine cellular MDA, SOD and ROS level.

RESULTSTreatment of KC with different concentrations of TCE or PCE showed significant dose-related variations in lipid peroxidation, with the higher concentration, higher level of MDA, ROS and lower activity of SOD displayed in this study. Vitamin E 10 - 200 mmol/L dose-dependently attenuated MDA and ROS level, and increased SOD activities.

CONCLUSIONTCE or PCE can induce the lipid peroxidation in cultured KC and Vitamin E protects it from TCE- or PCE-induced peroxidation.

Antioxidants ; pharmacology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Humans ; Keratinocytes ; drug effects ; metabolism ; Lipid Peroxidation ; drug effects ; Malondialdehyde ; metabolism ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism ; Tetrachloroethylene ; toxicity ; Trichloroethylene ; toxicity ; Vitamin E ; pharmacology