ISOLATION, PURIFICATION AND POSSIBLE PROTECTIVE EFFECT OF SESAMIN AGAINST HEAVY METAL-MEDIATED REDOX IMBALANCE IN RAT

Abstract

The present study sought to isolate, purify and evaluate the possible protective effect of sesamin against some heavy metal-mediated redox imbalance in rat cerebral, hepatic and renal tissues in vitro and in vivo. These heavy metals are lead, cadmium and iron. The effects of sesamin on lipid peroxidation were investigated in vitro in the presence of lead, cadmium and iron. In the in vivo study, experimental rats received sesamin (10 mg/kg/day) orally. After 30 minutes different sets of rats were administered lead acetate (15 mg/kg body weight/day intraperitoneally) for 7 days, ferrous sulphate (30 mg/kg body weight/day intraperitoneally) for 10 days and cadmium chloride (5 mg/kg body weight/day orally) for 28 days. The ability of sesamin to inhibit cerebral, hepatic and renal lipid peroxidation was examined in vitro and in vivo by measuring the level of formation of thiobarbituric acid reactive species. The effect of sesamin on the activities of the purine-dependent signalling enzymes, NTPDase and 5’- nucleotidase was also examined by measuring the nucleotide hydrolysing ability of these enzymes respectively. The results showed that sesamin inhibited cerebral, hepatic and renal lipid peroxidation (induced by Pb, Cd and Fe) in vitro in a concentration-dependent manner by preventing the formation of thiobarbituric acid reactive substances. In contrast, the in vivo result revealed that Pb, Cd and Fe induced cerebral, hepatic and renal lipid peroxidation as typified by an increased amount of malondialdehyde (MDA) production in these tissues. The cerebral, hepatic and renal glutathione level as well as radical scavenging ability of the tested tissues was significantly reduced in Pb-, Cd- and Fe-treated experimental animals whereas sesamin restored their alterations to control level. Moreso, the cerebral, hepatic and renal activities of NTPDase, 5’-nucleotidase, δ-aminolevulinic acid dehydratase (ALAD) and Na + /K + -ATPase were significantly reduced in Pb-, Cd- and Fe-treated experimental animals and sesamin was able to restore the activities of these enzymes to control level. Furthermore, an elevated level of serum hepatic markers such as serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT) was also observed in Pb-, Cd- and Fe-treated experimental animals while sesamin reduced the activities of the ALT and AST enzymes in the serum. The results from the present investigation suggest that lead, cadmium and iron evoked an enhanced ROS in the cerebral, hepatic and renal tissues through different mechanisms of generating free radicals that ultimately led to a disturbed redox system and altered activities of some purine-dependent signalling enzymes which could be considered as a contributing factor to their toxicity. It could be concluded that treatment with sesamin was effective in protecting against cerebral, hepatic and renal damage mediated by Pb, Cd and Fe.