FACULTY OF VETERINARY MEDICINE
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Item Failure of recovery from lead induced hepatotoxicity and disruption of erythrocyte antioxidant defense system in Wistar rats(Elsevier B. V., 2014) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Saba, A. B.; Daramola, O. T.; Ogunpolu, B. S.; Olopade, J. O.Lead acetate (PbA) is one of the major environmental contaminants with grave toxicological consequences both in the developing and developed countries. The liver and erythrocyte antioxidant status and markers of oxidative were assessed. Exposure of rats to PbA led to significant decline (p < 0.05) in hepatic and erythrocyte glutathione peroxidase (GPx), glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) content. Similarly, malondialdehyde (MDA) and H2O2 concentrations were significantly (p < 0.05) elevated. Histopathology and immunohistology of liver of rats exposed to PbA showed focal areas of necrosis and COX-2 expression after 6 weeks of PbA withdrawal. Taken together, hepatic and erythrocytes antioxidant defence system failed to recover after withdrawal of the exposed PbA for the period of the study. In conclusion, experimental animals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyte antioxidant defence system via free radical generation and oxidative stress.Item Alterations in blood pressure, antioxidant status and caspase 8expression in cobalt chloride-induced cardio-renal dysfunction arereversed by Ocimum gratissimum and gallic acid in Wistar rats(Elsevier B.V., 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ajibade, T. O.The protective abilities of the chloroform extract of Ocimum gratissimum (COG) and gallic acid againstcobalt chloride (CoCl2) − induced cardiac and renal toxicity were evaluated. Rats were exposed to CoCl2(350 ppm) for 7 days, either alone, or in combination with COG (100 and 200 mg/kg) or gallic acid(120 mg/kg). CoCl2given alone, caused significant increases (p < 0.05) in oxidative stress parameters(hydrogen peroxide, H2O2and malondialdehyde, MDA) and increased expression of the apoptotic initia-tor caspase 8 in the heart and kidneys. There was significant reduction (p < 0.05) in reduced glutathione(GSH) in cardiac and renal tissues; reduction in superoxide dismutase (SOD) activity in the kidneys andadaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2also produced signifi-cant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. OralCOG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2and MDA; with reducedexpression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varyingdegrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures inthe rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarctionand inflammation and renal tubular necrosis and inflammation were effectively ameliorated by the treat-ments administered. This study provides evidence for the protective roles of O. gratissimum and gallicacid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptoticcaspase 8 in Wistar rats.Item Failure of recovery from lead induced hepatoxicity and disruption of erythrocyte antioxidant defence system in Wistar ratsTemidayo(Elsevier B.V., 2014) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Saba, A. B.; Daramola, O. T.; Ogunpolu, B. S.; Olopade, J. O.Lead acetate (PbA) is one of the major environmental contaminants with grave toxicologicalconsequences both in the developing and developed countries. The liver and erythrocyteantioxidant status and markers of oxidative were assessed. Exposure of rats to PbA ledto significant decline (p < 0.05) in hepatic and erythrocyte glutathione peroxidase (GPx),glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reducedglutathione (GSH) content. Similarly, malondialdehyde (MDA) and H2O2concentrations weresignificantly (p < 0.05) elevated. Histopathology and immunohistology of liver of rats exposedto PbA showed focal areas of necrosis and COX-2 expression after 6 weeks of PbA withdrawal.Taken together, hepatic and erythrocytes antioxidant defence system failed to recover afterwithdrawal of the exposed PbA for the period of the study. In conclusion, experimentalanimals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyteantioxidant defence system via free radical generation and oxidative stress.Item Ameliorative effect of gallic acid in doxorubicin-induced hepatotoxicity in wistar rats through antioxidant defense system(Taylor & Francis, 2017-07) Omobowale, T. O.; Oyagbemi, A. A.; Ajufo, U. E.; Adejumobi, A. O.; Ola-Davies, O. E.; Adedapo, A. A.; Yakubu, M. A.Hepatotoxicity has been found to be one of the main side effects associated with doxorubicin (Dox) administration in cancer therapy. The aim of the present study was to examine the ameliorative effect of gallic acid (GA) in Dox-induced hepatotoxicity. Sixty male Wistar rats of 10 rats per group were used in this study and were randomly divided into 6 experimental groups (A–F). Rats in Group A served as the control group and received distilled water orally for 7 days; Group B was given Dox at 15 mg/kg bodyweight intraperitoneally (IP) on Day 8. Group Cwas given GA at 60 mg/kg body weight orally for 7 days + Dox at 15 mg/kg IP on Day 8. Group D was given GA at 120 mg/kg body weight orally for 7 days +Dox at 15 mg/kg IP on day 8. Rats in Groups E and F were administered GA alone at 60 and 120 mg/kg bodyweight orally for 7 days, respectively. Dox administration led to a significant reduction in hepatic reduced glutathione and nonprotein thiol (NPT) together with significant increase in hepatic malondialdehyde, hydrogen peroxide generation, superoxide dismutase, and catalase activity; hepatic glutathione peroxidase and glutathione-S-transferase activity were significantly inhibited in Dox-treated rats. The serum alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin concentrations were significantly elevated following Dox administration. Pretreatment with GA ameliorated Dox-induced hepatotoxicity and oxidative stress. The results suggest that GA may offer protection against hepatic damage in Dox cancer chemotherapy.Item Effect of exposure and withdrawal on lead-induced toxicity and oxidative stress in cardiac tissues of rats(Society of Toxicology, India, 2016) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Ola-Davies, O. E.; Saba, A. B.; Olukayode, O. J.; Adeolu, A. A.Lead poisoning continues to pose a serious health challenge and more significantly so in developing countries with ineffective waste disposal systems. Recent efforts at solving lead poisoning issues have seen entire towns being resettled from lead-contaminated areas. This study was designed to investigate whether withdrawal of lead exposure results in a resolution of toxic effects of lead in cardiac tissues. Adult male Wistar rats were exposed orally to lead acetate (PbA) at doses of 0.25, 0.5, and 1.0 mg/ml for 6-week duration, after which one-half was sacrificed and the remaining left for a further 6 weeks without lead treatment. Exposure of rats to PbA produced significant decline (P < 0.05) in the activities of antioxidant parameters, including superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT), and reduced glutathione (GSH), whereas malondialdehyde (MDA) concentration was significantly elevated. Animals from the withdrawal period exhibited a similar pattern of alterations, with a significant (P < 0.05) reduction in GSH, GPx, and SOD and a significant elevation in MDA and H2O2 concentrations. However, GST activity was elevated, whereas CAT activity remained unaltered in the withdrawal period. The results of this study showed that cardiotoxicity indicated by induction of oxidative stress and reduction in antioxidant parameters failed to resolve upon withdrawal of lead exposure in male rats during the period of study.Item Concentration-dependent inhibition of acetylcholinesterase by organophosphate poisoning in dogs: a biochemical and electrocardiographic study(Society of Toxicology, India, 2016) Ola-Davies, O. E.; Oyagbemi, A. A.; Omobowale, T. O.Organophosphate poisoning (OP) is one of the most common poisonings in developing countries. In this study, twenty-four dogs in four groups of six each were used. Control group bathed with water only, group B with 16% Coumaphos (recommended), groups C and D with times 10 and 20 of 16% Coumaphos, respectively. Blood was collected from cephalic vein for biochemical assays. Electrocardiographic parameters were assessed from a Lead-II electrocardiogram. There was a significant increase (p<0.05) in total cholesterol in group B and D compared to the control. LDL-cholesterol decreased significantly (p<0.05) in all groups compared to the control. The activity of superoxide dismutase (SOD) reduced (p<0.05) significantly across all the groups and even after 36 hours of exposure. However, the activity of the glutathione peroxidase (GPx) was not affected following exposure to OP. The serum reduced glutathione (GSH) fell in a concentration dependent manner in all animals exposed to OP. Coumaphos exposure led to a significant (p<0.05) increase in serum MDA in a concentration dependent manner after 36 hours post exposure. The serum nitric oxide (NO) and MPO content increased (p<0.05) significantly following exposure to different concentrations of Coumaphos. The activity of Acetyl cholinesterase (AchE) fell significantly from the normal concentration of the OP down to the highest concentration. The activity of serum creatine phosphokinase (CK) increased (p<0.05) significantly in groups C and D compared to the control and recommended concentration. Electrocardiographic abnormalities recorded included low-voltage R-waves, first degree heart block, significant increased (p<0.05) heart rate (HR) and shortened QT interval compared to the control and recommended concentrations. Taking together, coumaphos poisoning caused an inhibition of AchE and significant potentially fatal arrrhythmais via induction of oxidative stress.