Abstract
ABSTRACTAdministration of DDC (3,5-diethoxycarbonil-1,4-dihydro-2,4,6-trimethylpyridine) (100 mg/kg, i.p.) to male rats produced significant increase in total porphyrins thus giving rise to the biochemical picture of porphyria(s). Porphyrins, accumulated in hepatic porphyria are putative endogenous ligands for peripheral benzodiazepine receptor. A role of peripheral benzodiazepine receptors in cholesterol transport and metabolism is suggested. Hepatic protoporphyria is associated with hepatomegaly, cholestasis and alterations in the microsomal cytochromes. We found that DDC administration in rat induced lipid disturbances and increased significantly total cholesterol in serum and in liver, as well as total phospholipids in liver. 27-Hydroxycholesterol content was significantly increased in serum and liver by DDC, while phenobarbital had no effect. We assume that the observed lipid disturbances are connected to the accumulation of porphyrins. These effects are probably modulated by porphyrin binding to peripheral benzodiazepine receptors.
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