title: Rifampicin, halothane and glucose as mediators of lysosomal enzyme release and tissue damage.
abstract: It is suggested that the important drugs rifampicin and halothane and the raised glucose levels in diabetes mellitus exert injurous effects on cells through a lysosomal mechanism. Further evidence is given of by time rifampicin induction of beta-glucuronidase and beta-N acetylglucosaminidase and its possible relation to hepatitis and pancreatitis. On the basis of preliminary data halothane may cause hepatitis connected to lysosomal enzyme release in the presence of other aggravating factors common to the perioperative period. The onset of diabetic vascular complications may be related to the similar raised levels of lysosomal enzymes found in insulin, drug and diet controlled disease. Release of these enzymes into plasma may be a marker of important changes in the lysosome, whether due to enzyme induction or damage, and could be a primary mechanism of many disease processes including some thought to be mainly autoimmune in character. Routine estimation in the clinical laboratory along with existing cytoplasmic and microsomally derived enzymes in the chemical screen would be a useful way of surveying lysosomal changes in the wide spectrum of disease in a general hospital.
authors.forename: W
authors.initials: W
authors.lastname: Perry
mesh_terms: D000118:Acetylglucosaminidase / Q000378:metabolism; D001327:Autoimmune Diseases / Q000201:enzymology; D003925:Diabetic Angiopathies / Q000201:enzymology; D005947:Glucose / Q000378:metabolism*; D005966:Glucuronidase / Q000378:metabolism; D006221:Halothane / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D008247:Lysosomes / Q000187:drug effects / Q000201:enzymology*; D012293:Rifampin / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D005966:Glucuronidase; D000118:Acetylglucosaminidase; D005947:Glucose; D006221:Halothane; D012293:Rifampin