FACULTY OF VETERINARY MEDICINE
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Item Dose‑dependent effects of cobalt chloride supplementation in a rat model of acetic acid‑induced ulcerative colitis(Springer-Verlag London Ltd., 2024) Akinrinde, A. S.; Samuel, E. S.; Adeoye, B. O.Several recent studies have shown that hypoxia preconditioning, often mimicked by sub-toxic levels of cobalt, can protect body tissues against various types of inflammatory and oxidative injuries. The present study was designed to understand the effects of low-to-moderate doses of cobalt chloride (CoCl2) on ulcerative colitis induced by acetic acid in male Wistar rats. Rats were pre-treated with CoCl2 at 10, 30 and 60 mg/kg BW for 7 days prior to, and later along with intra-rectal administration of 4% acetic acid for another 3 days. Rats were euthanized and the colons were examined macroscopically, and histologically, haematological parameters were evaluated in the blood and various oxidative stress parameters and inflammatory cytokines were studied in the colon and blood. Pre-treatment with CoCl2 at 10 mg/kg caused reduction in colonic levels of hydrogen peroxide (H2O2), nitric oxide (NO), advanced oxidation protein products (AOPP) and reduced serum TNF-α, but increased serum IL-10 levels. Conversely, rats treated with higher doses of CoCl2 showed exacerbation of macroscopic scores and histologic damage in the colon, with significantly elevated levels of oxidants and serum TNF-α along with reduced serum IL-10 levels. Values of all the measured haematological parameters (PCV, Hb, RBC, WBC and platelet count) were dose-dependently increased with increasing doses of CoCl2. The results of this study showed that consumption of cobalt at low doses could play a vital role in the control of ulcerative colitis, while higher doses can contribute to exacerbation of intestinal inflammation. Monitoring of cobalt concentrations in food and water consumed by ulcerative colitis patients is imperative to prevent exacerbation of colonic inflammation by cobalt.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 Argania spinosa essential oil ameliorates colonic damage and extraintestinal alterations in a rat model of acetic acid‑induced colitis by suppressing oxidative stress and inflammation(Springer Nature, 2023) Olojo, F. O.; Akinrinde, A. S.; Ogundairo, S. A.; Ubochi, V. C.The present study was designed to elucidate the prophylactic and therapeutic potential of argan oil (AO) (from the kernels of the argan tree, Argania spinosa) against acetic acid (AA)-induced colitis and associated alterations in the liver and kidneys of rats. Colitis was induced by intra-rectal administration of 4% AA solution for 3 consecutive days. Some groups of rats were treated orally with AO (5 mL/kg) for 5 consecutive days before and after AA administration, while other groups were treated with either the vehicle or AO alone. Macroscopic and microscopic lesions in the tissues were assessed, while oxidative stress, antioxidant parameters and myeloperoxidase (MPO) activity were determined by biochemical methods. Haematological and serum chemistry parameters were also evaluated. Administration of AO before or after AA induction produced improvements in body weight gain, faecal consistency, macroscopic and histologic scores of the colonic mucosa compared to rats treated with AA alone. Furthermore, AO treatment caused significant reduction in colonic levels of hydrogen peroxide (H2O2), malondialdehyde (MDA), advanced oxidation protein products (AOPP) and serum MPO activity, while glutathione S-transferase (GST) and superoxide dismutase (SOD) activities were increased in the colon and kidneys, compared to the colitis control. Acetic acid treatment resulted in significant reduction in erythrocyte and leucocyte indices in relation to healthy controls. Taken together, treatment of rats with AO protected colonic tissues from acetic acid-induced inflammation and suggests that the oil may be considered for preventive and therapeutic purposes against inflammatory bowel diseases.Item Zinc and ascorbic acid treatment alleviates systemic inflammation and gastrointestinal and renal oxidative stress induced by sodium azide in rats(Springer Science, 2021) Akinrinde, A. S.; Fapuro, J.; Soetan, K. O.Background: Sodium azide (NaN3) is a chemical of rapidly increasing economic importance but with high toxic attributes. In this study, the effects of zinc (Zn) and ascorbic acid (AsA) supplementation on sodium azide (NaN3) - induced toxicity in the stomach, colon and kidneys were evaluated in Wistar rats. Twenty-eight rats were randomly allocated to four experimental groups as follows: group A (control) given distilled water only; group B (NaN3 only, 20 mg/kg); group C (NaN3 + zinc sulphate, ZnSO4 80 mg/kg); and group D (NaN3 + AsA 200 mg/kg). Results: NaN3 was found to significantly (p < 0.05) induce increases in serum nitric oxide (NO), advanced oxidation protein products (AOPP), myeloperoxidase (MPO) and total protein levels, along with significant (p < 0.05) increase in gastric, colonic and renal malondialdehyde (MDA) and protein carbonyl (PCO) levels. In addition, NaN3 induced significant (p < 0.05) reduction in superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities in the colon and kidneys. Treatment with Zn or AsA caused significant (p < 0.05) reduction in serum levels of oxidative and inflammatory markers, as well as tissue PCO and MDA levels. Moreover, co-treatment with Zn or AsA significantly (p < 0.05) restored colonic and renal levels of antioxidant enzymes, reduced glutathione and protein thiols. Conclusions: This study shows that Zn or AsA supplementation alleviated NaN3 toxicity by suppressing systemic inflammation and preventing oxidative damage in the stomach, colon and kidneys of rats.Item Fluoride‑induced hepatotoxicity is prevented by L‑Arginine supplementation via suppression of oxidative stress and stimulation of nitric oxide production in rats(Springer, 2021) Akinrinde, A. S.; Tijani, M.; Awodele, O. A.; Oyagbemi, A. A.Objective Concerns over fluoride toxicity have increased in recent times due to high exposures from various anthropogenic sources such as industrial sites, fluoride-containing pesticides, drugs, dental products, refridgerants and fire extinguishers. There is, therefore, continued search for agents that could ameliorate the toxicity of this chemical in various body organs. In this study, we sought to investigate the protective effects of L-Arginine (L-Arg), a nitric oxide donor, on liver toxicity induced by sodium fluoride (NaF) in rats. Methods Rats received NaF (300 mg L−1) in drinking water alone or in co-treatment with L-Arg at two different doses, 100 and 200 mg kg−1, by oral gavage, for 7 days. Markers of hepatotoxicity, oxidative stress and antioxidant status were thereafter assessed. Results NaF caused marked increase in serum transaminases: alanine aminotransferase, Aspartate aminotransferase and Alkaline phosphatase, along with atrophy of the centri-lobular hepatic cords and dilatation of the sinusoids. Moreover, NaF stimulated increases in hepatic contents of hydrogen peroxide (H2O2), nitric oxide (NO), protein carbonyls, malondialdehyde and advanced oxidation protein products. NaF also inhibited the activities of antioxidant enzymes, Glutathione peroxidase and Superoxide dismutase. However, L-Arg supplementation caused significant alleviation of NaF hepatotoxicity by reducing lipid and protein oxidation indices, stimulation of antioxidant systems along with increased production of NO. Conclusions L-Arg showed promise as a potential protective agent against NaF-induced hepatotoxicity via restoration of oxidant-antioxidant balance. Further studies are required to understand the involvement of NO signaling in the protective effects of L-Arg against fluoride toxicity.Item Nephroprotective effect of methanol extract of Moringa oleifera leaves on acute kidney injury induced by ischemia-reperfusion in rats(Faculty of Medicine, Makerere University., 2020) Akinrinde, A. S.; Oduwole, O.; Akinrinmade, F. J.; Bolaji-Alab, F. B.Background: Moringa oleifera is known to exhibit protection against oxidative damage due to its rich content of compounds with antioxidant activity. This study investigated the protective effect of the methanol extract of Moringa oleifera (MO) in a rat model of renal ischemia-reperfusion (IR) injury. Methods: Forty two wistar rats were randomly assigned to six groups of seven rats each, as follows: A, control group; B, sham-operated group; C, IR group; D, IR + low dose (200 mg/kg) MO; E, IR + high dose (400 mg/kg) MO and F, IR + Vitamin C (200 mg/kg). Unilateral ischaemia was induced by occluding the left renal artery for 45 minutes followed by rep erfusion up to 24 hours. Results: Moringa oleifera significantly (p<0.05) ameliorated IR-induced increases in malondialdehyde (MDA), protein carbon yls (PC) and advanced oxidation protein products (AOPP), while also decreasing serum BUN and Creatinine levels. Moreover, the low dose of MO caused reductions in renal NO and H2O2 levels, while increasing renal GPx and GST activities. Histopathology revealed marked improvement of tissue alterations induced by IR with both doses of MO. Conclusion: Overall, the methanol extract of M. oleifera effectively attenuated the deleterious effects of renal IR via alleviation of tissue oxidative stress.Item Acute aflatoxin B1-induced gastro-duodenal and hepatic oxidative damage is preceded by time-dependent hyperlactatemia in rats(Springer, 2020) Akinrinde, A. S.; Ogunbunmi, T.; Akinrinmade, F. J.Elevated serum lactate concentration has been used to predict the risk of fatality in various disease states in acutely ill patients or poisoning with different chemicals. However, its utility in predicting disease progression during acute aflatoxicosis has not been investigated. This study was designed to evaluate changes in blood lactate levels following acute exposure to aflatoxin B1 (AFB1) and to determine whether changes in blood lactate levels bear any relationship with biochemical and/or morphological lesions in the stomach, duodenum, and liver. Twenty-one male Wistar rats were randomly divided into three groups (n = 7 rats /group) including Group A (control) receiving vehicle alone and Groups B and C treated with single oral doses of AFB1 at 2.5 and 5 mg/kg, respectively. AFB1 produced significant (p < 0.05) time- and dose-dependent increase in blood lactate concentration as early as 1 h following its administration, with further increases observed at 3 h and 6 h. The hyperlactatemia accompanied tissue oxidative changes including increased H2O2 and MDA, as well as depletion in glutathione, glutathione peroxidase, superoxide dismutase, and total thiols in gastro-duodenal and hepatic tissues. The oxidative changes were reflected in morphological alterations observed at histopathology with more severe lesions observed with the higher dose of AFB1. Serum levels of pro inflammatory cytokines (TNF-α and IL-1β) were, however, differently modified by AFB1 administration. Taken together, the results from this study gives indication that hyperlactatemia may find utility in predicting the severity of tissue damage induced by acute AFB1 exposure.Item Neuroprotection by luteolin and gallic acid against cobalt chloride-induced behavioural, morphological and neurochemical alterations in Wistar rats(Elsevier B.V., 2019) Akinrinde, A. S.; Adebiyi, O. E.Cobalt (Co) intoxication arising from occupational exposures and ion release from metal implants has been associated with neurological alterations such as cognitive decline, incoordination and depression. The present study evaluated the mechanisms of neuro-protection exerted by Luteolin (Lut; 100 mg/kg) and Gallic acid (GA; 120 mg/kg) in Wistar rats exposed to cobalt chloride (CoCl2) at 150 mg/kg for 7 consecutive days. Results indicate that CoCl2 induced neuro-behavioural deficits specifically by decreasing exploratory activities of CoCl2- exposed rats, increased anxiety, as well as significant reduction in hanging latency. Co-treatment with Lut or GA, however, restored these parameters to values near those of normal controls. Moreover, Lut and GA prevented CoCl2-induced increases in hydrogen peroxide (H2O2), malondialdehyde (MDA) and nitric oxide (NO) in the brain, while also restoring the activities of acetylcholinesterase, glutathione S-transferase (GST) and superoxide dismutase (SOD). In addition, Lut and GA produced significant reversal of CoCl2-induced elevation in levels of serum Interleukin 1 beta (IL-1β) and Tumor necrosis factor (TNFα). Meanwhile, immunohistochemistry revealed increased astrocytic expression of glial fibrillary acidic protein (GFAP), with intense calbindin (CB) D-28k staining and pronounced dendrites in the Purkinje cells. In contrast, the CoCl2 group was characterized by decreased number of neurons expressing CB and dendritic loss. Taken together, mechanisms of luteolin and/or gallic acid protection against Co toxicity involved restoration of Ca2+ homeostasis, acetylcholinesterase and antioxidant enzyme activities, as well as inhibition of lipid peroxidation in the brain.Item Alterations in blood pressure, antioxidant status and caspase 8 expression in cobalt chloride-induced cardio-renal dysfunction are reversed by Ocimum gratissimum and gallic acid in Wistar rats(Elsevier GmbH, 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 against cobalt 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). CoCl2 given alone, caused significant increases (p < 0.05) in oxidative stress parameters (hydrogen peroxide, H2O2 and malondialdehyde, MDA) and increased expression of the apoptotic initiator 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 and adaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2 also produced significant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. Oral COG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2 and MDA; with reduced expression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varying degrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures in the rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarction and inflammation and renaltubular necrosis and inflammation were effectively ameliorated by the treatments administered. This study provides evidence for the protective roles of O. gratissimum and gallic acid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptotic caspase 8 in Wistar rats.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.