Evidence against a role for disturbed hepatocellular calcium homeostasis in the fatty liver of carbon tetrachloride hepatotoxicity.
A consensus does not exist regarding the nature of mechanisms linking the initial events of CCl4 metabolism to emergence of the classical indices of CCl4 liver cell injury. The possibility that a CCl4-dependent disturbance of intrahepatocellular calcium homeostasis might be a linking mechanism was investigated with isolated hepatocytes in suspension. CCl4-dependent inhibition of very low density lipoprotein secretion was studied. On the basis of kinetic data, dose-response data, and failure of elevated cytosolic calcium levels to inhibit lipid secretion, it was concluded that disturbed intracellular calcium homeostasis probably is not important in CCl4-dependent inhibition of secretion of very low density lipoproteins.
D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002250:Carbon Radioisotopes; D002251:Carbon Tetrachloride / Q000378:metabolism / Q000633:toxicity*; D004072:Digitonin / Q000494:pharmacology; D005234:Fatty Liver / Q000139:chemically induced / Q000378:metabolism*; D006706:Homeostasis / Q000187:drug effects; D066298:In Vitro Techniques; D008079:Lipoproteins, VLDL / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D002250:Carbon Radioisotopes; D008079:Lipoproteins, VLDL; D000001:Calcimycin; D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D004072:Digitonin; D002118:Calcium