Lead Induced Disorders in Hematopoietic and DrugMetabolizing Enzyme System and Their Protection by A

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Effect of vitamin C supplementation in restoring lead induced alterations in hematopoietic system and drug metabolizing enzymes were investigated in male rats. Intraperitoneal administration of 20 mg/kg lead produced a significant inhibition of heme synthesis in blood and liver and drug metabolism in liver. Toxic insult by lead also resulted into a marked decline in tissue thiols and vitamin C levels. Oral supplementation of vitamin C (100 mg/kg for 3 days) completely restored blood delta aminolevulinic acid dehydratase, uroporphyrinogen I synthetase and a few drug metabolizing enzymes. Level of vitamin C and sulfhydryl contents too recovered to a great extent. A marked reduction in blood and liver lead concentration occurred on vitamin C supplementation although renal lead contents were marginally reduced in lead exposed animals. The results, thus, indicate a significant protective action of vitamin C against toxic effects of lead on heme synthesis and drug metabolism. Effect of vitamin C supplementation in restoring lead induced alterations in hematopoietic system and drug metabolizing enzymes were investigated in male rats. Intraperitoneal administration of 20 mg / kg lead produced a significant inhibition of heme synthesis in blood and liver and drug metabolism in liver. Toxic insult by lead also resulted in marked decline in tissue thiols and vitamin C levels. Oral supplementation of vitamin C (100 mg / kg for 3 days) completely restored blood delta aminolevulinic acid dehydratase, uroporphyrinogen I synthetase and a few drug metabolizing enzymes. Level of Vitamin C and sulfhydryl contents too recovered to a great extent. A marked reduction in blood and liver lead concentration occurred on vitamin C supplementation due renal lead contents were marginally reduced in lead exposed animals. The results, thus, indicate a significant protective action of vitamin C against toxic effects of lead on heme synthesis and drug metabolism.
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