Evidence for the catabolism of polychlorinated biphenyl-induced cytochrome P-448 by microsomal heme oxygenase, and the inhibition of delta-aminolevulinate dehydratase by polychlorinated biphenyls.

摘要: Polychlorinated biphenyls (PCB) are potent inducers of hepatic microsomal CO-binding hemoprotein P-448 (P1-450) and delta-aminolevulinate synthetase (ALAS) activity. Inorganic cobalt was able to block PCB induction cytochrome modify the effect on ALAS activity in a time-dependent manner. were also found decrease delta-aminolevulinic acid dehydratase (ALAD) liver. Pretreatment rats with (30 min) produced following changes actions heme metabolism liver: (a) augmentation porphyrinogenic PCB, as determined by total porphyrin content activity; (b) inhibition ALAD (c) blockade (cytochrome P-448). did not interfere oxygenase The sequence administration metal important relation contents. When administered 24 h after treatment, magnitude lowered, there great reduction renal response different than that In kidney, blocked depletion cellular cobalt. Furthermore, increased treatment alone or combination It is concluded moiety metabolized system, it suggested for this catabolism take place, must be first converted denatured form hemoprotein, P-420; synthesis kidney liver regulated through mechanisms; ionic controls inhibiting enzyme followed indirect result heme, physiological repressor ALAS, metal-induced oxygenase. Thus may viewed having an overall regulatory role mictochondrial virtue its ability catabolize endogenous heme.