A new direction in the study of carbon tetrachloride hepatotoxicity.
An unknown chain of causality links the early events of CCl4 metabolism to emergence of the classical spectrum of pathological changes elicited by this hepatotoxin. Recent developments suggest that an early disturbance in hepatocellular Ca2+ homeostasis may be involved. The possibility that generation of toxic products of lipid peroxidation may act as toxicological "second messengers" linking events near cytochrome P-450 to distant parts of the cell seems unlikely. This mini-review attempts to highlight major recent developments underlying the current situation.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002251:Carbon Tetrachloride / Q000378:metabolism; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology*; D002451:Cell Compartmentation; D056486:Chemical and Drug Induced Liver Injury; D006801:Humans; D050356:Lipid Metabolism; D008054:Lipid Peroxides / Q000096:biosynthesis; D010084:Oxidation-Reduction; D013438:Sulfhydryl Compounds / Q000378:metabolism
D008054:Lipid Peroxides; D013438:Sulfhydryl Compounds; D002251:Carbon Tetrachloride; D002118:Calcium