ABSTRACT
In the current study, we report perturbations in hepatic, renal and splenic heme synthesis at the level of the rate limiting enzyme, δ-amino levulinic acid synthase (ALA-S) on ethanol administration independently and in conjunction with iron-protoporphyrin (FePP) in male Wistar rats. Excessive ethanol administration (5 ml/kg bw) resulted in a significant induction of hepatic, splenic and renal ALA-S activity. Simultaneous administration of FePP (50 µmol/kg bw) reverted the observed induction response to a sharp decline. The features of the action of ethanol and FePP togetherin vivo, i.e. a substantial inhibition of ALA-S is suggestive of the beneficial effects of this formulation in acute attacks of porphyria.
ABSTRACT
In this communication, we show the modulatory potential of papaverine, an opium alkaloid and a well known vasodilator agent on the ethanol-induced hepatic oxidative stress in male Wistar rats. Ethanol treatment (50% v/v) enhanced lipid peroxidation significantly accompanied by a decline in the activities of glutathione peroxidase (G-Px), glutathione reductase (GR) and depletion in levels of hepatic glutathione (GSH). Ethanol administration increased hepatic glutathione-s-transferases (GST). Enhanced lipid peroxidation induced by ethanol was significantly reduced when papverine was coadministered (P<0.05). In addition, the depleted levels of glutathione and inhibited activities of G-Px and GR recovered significantly (P<0.05) levelling off to control values on co-exposure. Papaverine (200 mg/kg bw) effectively antagonised the ethanol-induced lipid peroxidation and impaired glutathione levels and glutathione dependent enzyme systems. Our results suggest that papaverine is an effective chemopreventive agent in the liver and may suppress the ethanol-induced hepatotoxicity.
