Studies of Ca2+-mediated toxicity in hepatocytes.
Molecular mechanisms involved in the development of toxic cell injury have attracted increased interest in recent years. In particular, the possible existence of a final common pathway in toxic cell killing has been addressed in a number of studies. Recent work from our laboratory suggests that a disruption of intracellular Ca2+ homeostasis may represent a common step in the development of toxic damage to hepatocytes, and that activation of Ca2+-dependent, neutral proteases by a sustained increase in cytosolic free Ca2+ concentration represents one mechanism by which toxic agents can kill hepatocytes.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002451:Cell Compartmentation; D002470:Cell Survival / Q000187:drug effects; D003538:Cystamine / Q000633:toxicity; D006706:Homeostasis; D008099:Liver / Q000166:cytology / Q000502:physiology*; D008862:Microsomes, Liver / Q000378:metabolism; D008930:Mitochondria, Liver / Q000502:physiology; D010447:Peptide Hydrolases / Q000378:metabolism; D010740:Phospholipases / Q000502:physiology; D013438:Sulfhydryl Compounds / Q000502:physiology
D013438:Sulfhydryl Compounds; D010740:Phospholipases; D010447:Peptide Hydrolases; D000252:Calcium-Transporting ATPases; D003538:Cystamine; D002118:Calcium