FACULTY OF VETERINARY MEDICINE
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Item In utero exposure to bisphenol A alters prostatic responses in adult male rats: Protective effects of melatonin(PCJHBA, 2020) Olukole S. G.; Aina, O. O.; Lanipekun, D. O.; Olaogun, S. C.; Ola-Davies, O. E.; Adeleke, R. A.; Ogundipe, G. A. T.; Oke, B. O.Exposure to bisphenol A (BPA), an endocrine disrupting chemical (EDC), has been shown to result in a number of reproductive dysfunction. Melatonin (MLT) is a potent antioxidant known to protect against EDC-induced toxicity. We aimed at investigating the protective effects of MLT on prostate gland dysfunction in the F1 adult male Wistar rats exposed to BPA in utero. Rats, confirmed pregnant were divided into five groups (n=5): Control: 0.2 ml canola oil; BPA 25 μg/kg/day; BPA 250 μg/kg/day; BPA 25 μg/kg/day + MLT 1 mg/kg/day and BPA 250 μg/kg/day + MLT 1 mg/kg/day. Blood sample was collected for serum hormonal and biochemical assays. Histopathology of the prostate gland was carried using standard methods. Prostatic index was significantly increased in BPA-treated rats compared to control (p˂0.05). BPA induced prostatic oxidative stress and caused significant decreases in the levels of serum T and LH but resulted in significant increases in the levels of PSA, PAC and TAC. Prostatic lesions observed in the BPA groups rats included hyperplasia (functional, reactive and atypical). These were attenuated in the rats co-treated with MLT. BPA induced marked prostatic alterations, while melatonin co-administration protected against these alterations.Item Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor(Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.Item Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor(Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.Item Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor(Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.Item Taurine and protocatechuic acid attenuate Vincristine sulphate‑induced bone marrow, liver and intestinal injuries via anti‑oxidative, anti‑inflammatory and anti‑apoptotic activities(Springer Nature, 2024) Akinrinde, A. S.; Ajao, J. J.; Oyagbemi, A. A.; Ola-Davies, O. E.Chemotherapy with Vincristine (Vcr) is often compromised by undesirable gastrointestinal, myeloid and hepatic effects. In this study, we evaluated and compared the efficacy of taurine (Tau) and/or protocatechuic acid (Pca) in alleviating Vcr-induced hepatotoxicity, enterotoxicity and myelotoxicity in rats. In two cycles of five daily injections each, rats were exposed to Vcr (0.1 mg/kg, i.p.) alone or in combination with orally administered Tau (50 mg/kg) and/or Pca (50 mg/kg). Blood was collected for haematology and measurement of liver enzymes and inflammatory cytokines. Genotoxicity assay was performed on bone marrow, while the liver and intestines were subjected to biochemical assays, histopathology and immunohisto-chemical staining. Administration of Vcr triggered bone marrow suppression (anaemia, leucopenia, thrombocytopenia and increased frequency of micronucleated polychromatic erythrocytes, MnPCEs), increased serum transaminases (ALT, AST) and alkaline phosphatase (ALP) and altered hepatic and intestinal morphology. However, supplementation with Tau and/ or Pca alleviated most of the toxic effects of Vcr by reducing tissue levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) and advanced oxidation protein products (AOPP), but stimulating glutathione S-transferase (GST) and glutathione per oxidase (GPx) activities. In addition, Tau and/or Pca enhanced anti-inflammatory (reduced serum TNFα) and anti-apoptotic mechanisms (reduced cytochrome c/Bax expression and increased Bcl-2 expression) in the ileum and liver. Overall, Tau or Pca protected the liver, ileum and bone marrow against Vcr-induced toxicities via antioxidant, anti-inflammatory and anti-apoptotic mechanisms. The data supports their individual use, rather than their combination, as adjuvant therapy in patients undergoing chemotherapeutic intervention.Item Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor(Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.Item Supplementation with sesame oil suppresses genotoxicity, hepatotoxicity and enterotoxicity induced by sodium arsenite in rats(BioMed Central, 2023) Akinrinde, A. S.; Oyewole, S. O.; Ola-Davies, O. E.Background Sesame oil, an edible essential oil, is known to be rich in unsaturated fatty acids, vitamins and lignans with several reported health-promoting benefts. Acute arsenic poisoning produces toxic hepatitis, bone marrow depression and adverse gastrointestinal responses. In this study, we investigated the protective efect of sesame seed oil (SSO) against genotoxicity, hepatotoxicity and colonic toxicity induced by sodium arsenite (SA) in Wistar rats. Methods Twenty-eight male Wistar albino rats were randomly allocated into four groups: control, SA only (2.5 mg/ kg), SA + SSO (4 ml/kg) and SSO alone for eight consecutive days. Liver function and morphology, bone marrow micronuclei induction, colonic histopathology, mucus production and immune expression of Bcl-2, carcinoembryonic antigen (CEA), MUC1 and cytokeratins AE1/AE3 were evaluated. Results SA provoked increased serum activities of liver enzymes, including alanine aminotransferase (ALT) and aspar tate aminotransferase (AST), and caused severely altered morphology of hepatic and colonic tissues with increased frequency of micronucleated polychromatic erythrocytes (MnPCEs/1000PCE) in the bone marrow. In addition, SA triggered increased expression of colonic CEA and MUC1 but weak Bcl-2 immunoexpression. However, cotreatment with SSO demonstrated protective activities against SA-induced damage, as indicated by signifcantly reduced serum ALT and AST, fewer micronucleated bone marrow erythrocytes and well-preserved hepatic and colonic morphologies compared to the SA-treated rats. Furthermore, SSO protected the colonic mucosa by boosting mucus production, elevating anti-apoptotic Bcl-2 expression and reducing CEA expression. GC–MS analysis of SSO revealed that it was predominated by linoleic acid, an omega-3 fatty acid, and tocopherols. Conclusions Our data indicated that SSO protected the liver, colon and bone marrow potentially via anti-infam matory and anti-apoptotic activities. The data suggest that sesame oil has potential therapeutic applications against chemical toxicities induced by arsenic.Item Luteolin normalizes Blood Pressure via its antioxidant activity and down-regulation of Renal Angiotensin II receptor and Mineralocorticoid receptor expressions in rats co-exposed to Diclofenac and Sodium Fluoride(Physiological Society of Nigeria, 2022) Ajibade, T. O.; Akinrinde, A. S.; Adetona, M. O.; Adedapo, A. D. A.; Oyagbemi, A. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Oguntibeju, O. O.; Yakubu, M. A.This study was designed to investigate the modulatory role of Luteolin (Lut), a flavonoid phytochemical, on haemodynamic parameters and the potential mechanisms involving renal Angiotensin II (AT2R) and Mineralocorticoid (MCR) receptors in renal toxicity induced by co-exposure to Diclofenac (Dcf) and sodium fluoride (NaF) in rats. Male Wistar rats were administered with either vehicle (control), Dcf only (9 mg/kg orally) or concurrently with NaF (300 ppm in drinking water). Other groups were treated with LutA (100 mg/kg) or LutB (200 mg/kg) along with Dcf and NaF exposures. All treatments lasted 8 days, following which blood pressure indices were measured using tail-cuff plethysmography. Renal expressions of AT2R and MCR were studied with immunohistochemistry, while biomarkers of oxidative and antioxidant status were also measured in the kidneys. Systolic, diastolic and mean arterial pressures were significantly (p<0.05) reduced in Dcf-treated rats, compared to control values. However, co-treatment with NaF or Lut restored these parameters. While the expression of AT2R and MCR was high in the Dcf and Dcf+NaF groups, treatment with Lut caused obvious reduction in the renal expression of these receptors. Increased lipid peroxidation (Malondialdehyde) and protein oxidation (protein carbonyls)with a lowering of reduced glutathione levels contributed to the renal toxicity of Dcf, and these were significantly ameliorated in Lut-treated rats. In conclusion, the preservation of haemodynamic indices by Luteolin in the experimental rats was probably mediated by mechanisms involving down-regulation of renal expressions of AT2R and MCR, reduction of oxidative stress and an improvement of renal antioxidant status.Item Effect of exposure and withdrawal on lead-induced toxicity and oxidative stress in cardiac tissues of rats(Informatics Publishing Limited, 2016) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Ola-Davies, O. E.; Saba, A. B.; Olopade, J. O.; Adedapo, 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 Effect of exposure and withdrawal on lead-induced toxicity and oxidative stress in cardiac tissues of rats(Informatics Publishing Limited, 2016) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Ola-Davies, O. E.; Saba, A. B.; Olopade, J. O.; Adedapo, 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.