[Behaviour of the hepatic glutathione (GSH) in the rat in continuous administration of hexachlorobenzene (HCB) (author's transl)].
Adult male Wistar rats were fed with a diet containing 0.05% hexachlorobenzene (HCB) over a period of at least 90 days. At intervals group of 4 animals each were killed and the GSH- and cytochrom P-450-content, the 7-ethoxycoumarin-deethylation activity were measured in the liver. At the same time the urinary porphyrin excretion was determined. After ten days a massive induction of the microsomal mixed function monooxygenase system could be demonstrated, whereas the porphyria (e.g. an increased excretion of urinary porphyrins) became manifest after 56 days HCB-exposure. At the same time (56th day of experiment) the GSH content in the liver rapidly decreased. It is assumed that at the beginning of th HCB-feeding the microsomal mixed function monooxygenase are induced and the uroporphyrinogen decarboxylase is inhibited. This inhibition causes an accumulation of highly carboxylated porphyrins in the liver. Later on (around the 56th day of HCB exposure) a hepatic GSH decrease leads to an increase of heavy metal ions and to a disturbance of the heme biosynthesis that means the manifestation of the HCB-porphyria.
D000818:Animals; D002722:Chlorobenzenes / Q000494:pharmacology*; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D004032:Diet; D005978:Glutathione / Q000378:metabolism*; D006581:Hexachlorobenzene / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D006899:Mixed Function Oxygenases / Q000378:metabolism; D011166:Porphyrins / Q000652:urine; D051381:Rats; D013997:Time Factors; D014575:Uroporphyrinogen Decarboxylase / Q000037:antagonists & inhibitors
D002722:Chlorobenzenes; D011166:Porphyrins; D006581:Hexachlorobenzene; D003577:Cytochrome P-450 Enzyme System; D006899:Mixed Function Oxygenases; D014575:Uroporphyrinogen Decarboxylase; D005978:Glutathione
Verhalten des hepatischen Glutathion (GSH) bei der Ratte unter kontinuierlicher Hexachlorobenzol(HCB)-Gabe.