Polyherbal therapy is said to be a current pharmacological principle having the advantage of producing maximum therapeutic efficacy with minimum side effects. We assessed the antidiabetic efficacy and hence the impact on biochemical indices of toxicity by a combination of extracts from neem and bitterleaf. Thirty rats, 25 diabetic and 5 non-diabetic rats, were used for the study. The diabetic rats were divided equally into five groups and respectively treated: saline (diabetic control), extracts from neem and bitterleaf combined, neem only, bitterleaf only and chlorpropamide for a 24 day period. After oral administration of the first dose of extract (400 mg kg 1 b.w.) and chlorpropamide (4.286 mg kg 1 b.w.), blood glucose was monitored in vivo at various time intervals for 9 h, thereafter daily administration continued for 24 days. Whereas single dose treatment with neem only showed peak reduction (28.56%) an hour after, treatments with combined extracts, bitterleaf and chlorpropamide had their peak reductions all at the 7th hour (24.78, 47.31 and 60.51%, respectively). Percentage reductions in blood glucose relative to their initial values at the end of treatment were 71.05, 44.95, 88.63 and 75.83 for combined extract, neem, bitterleaf and chlorpropamide respectively. The decrease in blood glucose for the groups treated with combined extracts and bitterleaf only compared well (p<0.01) with chlorpropamide and non diabetic control, but not with neem alone. Determination of markers of hepatotoxicity in serum including GPT and GOT activities, total protein, albumin and urea indicated that, of the four treatments, neem provides the best protection against hepatic dysfunction. In the group treated with combined extracts these alternate selective advantages of neem and bitterleaf were expressed as a positive synergy, hence more beneficial than individual treatments.

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BackgroundPlasma alanine transferase(ALT), aspartate transferase(AST), α-glutamyl transferase(GGT), and alkaline phosphatase(ALP) activities are known biomarkers in assessing hepatic functional integrity. A remarkable rise in the activities of these enzymes normally signifies hepatotoxicity of chemical agent(s) in the biological system. Exposure to 17.8 cm3h-1m-3 of PMS blend unleaded gasoline vapors (UGV) for 6 hr/day, 5 days/week for 20 weeks have been reported to cause hepatotoxicity in rats.MethodsIn this study, the comparative hepatoprotective effect of vitamins A (retinol) and E (α-tocopherol) against UGV-induced toxicity was assessed in male and female rats. Retinol and α-tocopherol at prophylactic dosage (400 and 200 IU/kg/day, respectively) were separately administered orally to the test rats concomitant with exposure to UGV in the last two weeks of the experiment.ResultsThe results of this study indicated that exposure to UGV caused significant increase (P < 0.05) in the activities of serum ALT, AST, ALP, GGT and bilirubin in male and female rats. Oral administration of prophylactic doses of retinol and α-tocopherol produced a significant decrease (P < 0.05) in the activities of these parameters in male and female test rats, compared with the non-treated test rats; but insignificant increase(P ≥ 0.05), compared with the control. However, the hepatoprotective effect of α-tocopherol was observed to be more potent than that of retinol.ConclusionsThe result of this study demonstrated that the hepatoprotective potency of α-tocopherol against gasoline vapors toxicity was higher than that of retinol in male and female rats, although the female gender of the animal model responded to treatment with both vitamins better than the males. Hence, the work suggested the beneficial effects of both vitamins against hepatotoxicity in individuals frequently exposed to gasoline vapors.

Summary:The haematological effects following ingestion of shellfish exposed to crude oil polluted water or the pollutant perse were investigated in albino Wistar rats. Feeding of four groups of rats for 28 days duration with two reference casein or shellfish protein control diets (Group A and B), and two test diets (Group C and D) supplemented at varying levels with shellfish which had been previously exposed to crude oil polluted water and the oral gavaging with crude oil at the rate of 3, 6 and 9 ml/kg body weight per day to three groups (groups II, III and IV respectively) of rats for 7 days duration resulted in changes in packed cell volume (PCV), red blood cell (RBC) and white blood cell (WBC) counts, and haemoglobin concentration (Hb) of rats. Group C and D respectively fed 10% and 20% polluted shellfish diets recorded significant (P < 0.05) decreases in PCV and RBC counts while Hb concentration and WBC counts increased. Groups II, III and IV gavaged with varying doses of crude oil recorded significant (P < 0.05 -0.01) dose dependent decrease in PCV and RBC counts when compared to controls (group 1). Hb and WBC counts also increased for these groups but the increase was only significant for WBC counts (P < 0.05) when compared with controls. The results suggest that the ingestion of shellfish exposed to crude oil polluted water or the polluted perse results in haematotoxicity.