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Item Gallic acid protects against cyclophosphamide-induced toxicity in testis and epididymis of rats(Blackwell Verlag GmbH, 2015) Oyagbemi, A. A.; Omobowale, T. O.; Saba, A. B.; Adedara, I. A.; Olowu, E. R.; Akinrinde, A. S.; Dada, R. O.The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg 1 for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg 1 on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg 1 ) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg 1 for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione-S-transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA-treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone trea ted rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.Item Evidence of attenuation of intestinal ischemia–reperfusion injury following pre-treatment with methanolic extracts from Chromolena odorata in rats(Natural Health Product Research Society of Canada, 2015) Akinrinmade, J. F.; Akinrinde, S. A.; Odejobi, A.; Oyagbemi, A. A.Background: Chromolena odorata is a tropical species of flowering shrub in the family Asteraceae, leaves of it have been reported to be widely used as herbal remedy for the treatment of various ailments. It is particularly reported to be useful in the healing of wounds. Methods: We investigated the possibility of amelioration of intestinal ischemia–reperfusion (IR) injury in rats trea ted with methanolic extract of C. odorata (MECO). Wistar albino rats were divided randomly into five groups of six animals each as control, IR-treated, IR þ 200 mg/kg MECO, IR þ 400 mg/kg MECO, and IR þ 200 mg/kg vita min C. Pre-treatment with MECO or vitamin C was for 7 days. Results: The contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) were significantly reduced by MECO and vitamin C, while there were significant enhancements of the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), as well as the content of reduced glutathione (GSH) in pre-treated rats compared to IR-treated rats. Glutathione S-transferase (GST) activity was not significantly affected in all the groups. Histopathological examination of small intestinal mucosa revealed significant attenuation of intestinal pathology in animals pre-treated with MECO, while IR injury produced severe villi erosion, necrosis, and inflammatory cell infiltrations. Conclusions: The present study highlights the antioxi dant activities of MECO and its ability to inhibit inflammatory cell infiltration as mechanisms involved in its protection against IR injury in the intestine of rats, an effect that was largely comparable to that of vitamin C.Item Evidence of attenuation of intestinal ischemia–reperfusion injury following pre-treatment with methanolic extracts from Chromolena odorata in rats(Natural Health Product Research Society of Canada, 2015) Akinrinmade, J. F.; Akinrinde, S. A.; Odejobi, A.; Oyagbemi, A. A.Background: Chromolena odorata is a tropical species of flowering shrub in the family Asteraceae, leaves of it have been reported to be widely used as herbal remedy for the treatment of various ailments. It is particularly reported to be useful in the healing of wounds. Methods: We investigated the possibility of amelioration of intestinal ischemia–reperfusion (IR) injury in rats trea ted with methanolic extract of C. odorata (MECO). Wistar albino rats were divided randomly into five groups of six animals each as control, IR-treated, IR þ 200 mg/kg MECO, IR þ 400 mg/kg MECO, and IR þ 200 mg/kg vita min C. Pre-treatment with MECO or vitamin C was for 7 days. Results: The contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) were significantly reduced by MECO and vitamin C, while there were significant enhancements of the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), as well as the content of reduced glutathione (GSH) in pre-treated rats compared to IR-treated rats. Glutathione S-transferase (GST) activity was not significantly affected in all the groups. Histopathological examination of small intestinal mucosa revealed significant attenuation of intestinal pathology in animals pre-treated with MECO, while IR injury produced severe villi erosion, necrosis, and inflammatory cell infiltrations. Conclusions: The present study highlights the antioxi dant activities of MECO and its ability to inhibit inflammatory cell infiltration as mechanisms involved in its protection against IR injury in the intestine of rats, an effect that was largely comparable to that of vitamin C.Item Lack of reversal of oxidative damage in renal tissues of Lead Acetate-Treated rats(Wiley Periodicals, Inc., 2014) Oyagbemi, A. A.; Omobowale, T. O.; Akinrinde, A. S.; Saba, A. B.; Ogunpolu, B. S.; Daramola, O.Removal of lead from the environment of man or otherwise, the movement of man from lead-contaminated areas has been employed as a means of abatement of the toxic effects of lead. Whether toxic effects in already-exposed individuals subside after lead withdrawal remains unanswered. To understand the reversibility of nephrotoxicity induced by lead acetate, male Wistar rats were orally exposed to 0.25, 0.5, and 1.0 mg/mL of lead acetate for 6 weeks. Activities of glutathione-s-transferase, catalase (CAT), superoxide dismutase (SOD) and the concentrations of hydrogen peroxide (H2O2), and malondialdehyde increased significantly (p < 0.05) in a dose dependent manner, whereas reduced glutathione (GSH) level and glutathione peroxidase activity were significantly reduced. The pattern of alterations in most of the oxidative stress and antioxidant parameters remained similar in rats from the withdrawal period, although CAT and SOD activities reduced, in contrast to their elevation during the exposure period. Serum creatinine levels were significantly elevated in both exposure and withdrawal experiments whereas serum blood urea nitrogen levels were not significantly different from the control in both exposure and withdrawal periods. The histological damage observed include multifocal areas of inflammation, disseminated tubular necrosis, and fatty infiltration of the kidney tubules both at exposure and withdrawal periods. The results suggest that lead acetate-induced nephrotoxicity by induction of oxidative stress and disruption of anti-oxidant. The aforementioned alterations were not reversed in the rats left to recover within the time course of study.Item Gastrointestinal protective efficacy of Kolaviron (a bi‑flavonoid from Garcinia kola) following a single administration of sodium arsenite in rats: Biochemical and histopathological studies(Wolters Kluver, 2015) Akinrinde, A. S.; Olowu, E.; Oyagbemi, A. A.; Omobowale, O. T.Background: Arsenic intoxication is known to produce symptoms including diarrhea and vomiting, which are indications of gastrointestinal dysfunction. Objective: We investigated whether Kolaviron (KV) administration protected against sodium arsenite (NaAsO2)-induced damage to gastric and intestinal epithelium in rats. Materials and Methods: Control rats (Group I) were given a daily oral dose of corn oil. Rats in other groups were given a single dose of NaAsO2 (100 mg/kg; intraperitoneal) alone (Group II) or after pretreatment for 7 days with KV at 100 mg/kg (Group III) and 200 mg/kg (Group IV). Rats were sacrificed afterward and portions of the stomach, small intestine and colon were processed for histopathological examination. Hydrogen peroxide, reduced glutathione, malondialdehyde (MDA) concentrations as well as activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione S transferase (GST) and myeloperoxidase (MPO) were measured in the remaining portions of the different gastrointestinal tract (GIT) segments. Results: NaAsO2 caused significant increases (P < 0.05) in MDA levels and MPO activity, with significant reductions (P < 0.05) in GST, GPX, CAT and SOD activities in the stomach and intestines. KV significantly reversed the changes (P < 0.05) in a largely dose-dependent manner. The different segments had marked inflammatory cellular infiltration, with hyperplasia of the crypts, which occurred to much lesser degrees with KV administration. Conclusion: The present findings showed that KV might be a potent product for mitigating NaAsO2 toxicity in the GIT.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.