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Articles by J.A. Badmus
Total Records ( 2 ) for J.A. Badmus
  O.T. Adedosu , J.A. Badmus , O.K. Afolabi and O.F. Yakubu
  Natural plant products are considered as possible protective agents against arsenite induced toxicity. Effects of methanolic leaf extract of Ocimum gratissimum were investigated in sodium arsenite exposed rats. Animals were randomly divided into four groups of five per group. Group A (control), Group B (sodium arsenite alone), Group C (extract and sodium arsenite) and Group D (extract only). Rats were orally pretreated with 100 mg kg-1 b.wt. extract for 14 days while 2.5 mg kg-1 b.wt. arsenite was administered intraperitoneally on the 14th day and animals were sacrificed after 24 h. Plasma Alanine Amino Transferase (ALT), Alkaline Phosphatase (ALP) and Gamma Glutamyl Transferase (GGT) were evaluated. Hepatic lipid peroxidation as Malondialdehyde (MDA) and reduced Glutathione (GSH) levels were also assessed. Introduction of sodium arsenite in rats triggered significant increases in plasma ALT, ALP and GGT (p<0.05) levels. Significant increase (p<0.05) in hepatic MDA concentration and depletion in GSH level were obtained. The methanolic leaf extract with arsenite modulated the activities of ALT, ALP and GGT to their normal levels. The extract reversed sodium arsenite-induced decrease in hepatic GSH to their normal levels while significant effect on hepatic MDA level was not observed. Group treated with the extract alone showed no adverse effects on the parameters. The properties exhibited by the extract may be due to the presence of certain bioactive compounds in it. The results obtained from this study underpin the importance of further research to obtain bioactive substance from the leaf of Ocimum gratissimum.
  S.F. Ige , R.E. Akhigbe , A.A. Adewale , J.A. Badmus , S.B. Olaleye , F.O. Ajao , W.A. Saka and O.Q. Owolabi
  This study aims at investigating the effect of pre-treatment, co-treatment and post-treatment with Allium cepa extract, AcE, on cadmium-induced renal toxicity and confirming possible mechanisms by which Allium cepa extract reduce/restore cadmium induces nephrotoxicity. Thirty male Sprague Dawley rats were used. They were divided into 5 groups (n = 6). Group 1 was used as control. Group 2 was intraperitoneally administered 1.5 mL kg-1 BW of 0.3 mg L-1 of cadmium sulphate for 3 days. Group 3 was pretreated with 1.0 mL kg-1 BW of AcE for 8 weeks followed by intraperitoneal administration of 1.5 mL kg-1 b.wt. of 0.3 mg L-1 of cadmium sulphate. Group 4 was co-treated with 1.5 mL kg-1 BW of 0.3 mg L-1 of cadmium sulphate for 3 days and 1.0 mL kg-1 BW of AcE for 8 weeks simultaneously. Group 5 was post-treated with 1.0 mL kg-1 BW of cadmium sulphate for 8 weeks following a 3 day course of 1.5 mL kg-1 BW of 0.3 mg L-1 of cadmium sulphate intraperitoneal administration. All groups were allowed free access to standard rat chow and water throughout the period of experiment. After the experiment period, rats were sacrificed by cervical dislocation and blood sample were obtained via cardiac puncture. The kidneys were also excised. Changes in body and kidney weights were determined. Renal weight index, 24 h urine volume, renal clearance and lipid peroxidation status were also determined. There was no significant change in body and kidney weight and renal weight index in all groups. Renal clearance and 24 h urine volume were significantly reduced in group 2 rats when compared to all groups. Renal clearance was also reduced in group 3 and 5, though this decrease was only significant when compared with the control group. Plasma and tissue SOD activities were significantly increased in group 2. Plasma and tissue MDA levels were significantly increased in group 2, 3 and 5. This study shows that cadmium induces nephrotoxicity by impairing renal functions and stimulating lipid peroxidation. Pre-treatment and post-treatment of AcE in cadmium-treated rats produced mild protective potentials. However, co-treatment with AcE during cadmium administration showed significant antioxidative potentials in preventing cadmium-induced nephrotoxicity.
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