STZ-induced diabetes in mice and heme pathway enzymes. Effect of allylisopropylacetamide and α-tocopherol

Abstract

A frequent coexistence of diabetes and porphyria disease has been reported. Under normal conditions, porphyrin biosynthesis is well regulated to only form the amount of heme required for the synthesis of the various hemoproteins. The activity of some heme enzymes and rhodanese in streptozotocin (STZ) induced diabetic mice and in allylisopropylacetamide (AIA) induced experimental acute porphyria mice has been examined. The role of α-tocopherol (α-T), reported to prevent protein glycation in vitro, has also been investigated. AIA induced hepatic δ-aminolevulinic acid synthetase (ALA-S) activity in control animals but was ineffective in the diabetic group. α-Tocopherol did not modify ALA-S activity in either group. δ-Aminolevulinic acid dehydratase (ALA-D) and deaminase activities were significantly diminished both in liver and blood of diabetic animals. α-Tocopherol prevented inhibition of ALA-D, deaminase and blood rhodanese activities in diabetic animals but α-tocopherol by itself did not affect the basal levels of the enzymes studied. The potential use of a-tocopherol to prevent late complications of diabetes, including the onset of a porphyria like syndrome is considered.