Veterinary Surgery & Reproduction
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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 Flavonoid-rich extract of Parquetina nigrescens prevents intestinal ischemia-reperfusion injury in Wistar rats via modulation of inflammatory cytokines and antioxidant defense(Faculty of Veterinary Medicine, University of Ibadan, Nigeria, 2018) Akinrinde, S. A.; Makinde, A. O.; Akinrinmade, J. F.The search for relatively safe and cost-effective strategies at minimizing tissue damage following acute inflammatory bowel conditions still continues. To further explore the mechanisms of protection by Parquetina nigrescens in gut ischemia-reperfusion injury, the present study sought to investigate the effects of the flavonoid-rich extracts of Parquetinanigrescens (FPN) on serum levels of inflammatory cytokines (TNF-alpha and IL-lbeta), the oxidant-antioxidant status, as well as the morphology of the intestinal mucosa in a rat model of ischemia-reperfusion injury. Thirty six male Wistar rats were randomly allocated into 6 groups with the sham-operated group subjected to laparotomy only. In the ischaemia-reperfusion (IR) group, the superior mesenteric artery (SMA) was occluded for 45 minutes, followed by reperfusion for another 45 minutes. Other groups had ischemic pre-conditioning (IP), melatonin (10 mg/kg), FPN1 (250 mg/kg) or FPN2 (500 mg/kg) before IR. Serum cytokine levels were determined, histopathological examination and biochemical analyses of small intestines were carried out. IR produced significant increases (p<0.05) in MDA and TNF-alpha with significant reductions (p<0.05) in GSH, GPx and SOD. FPN2 produced the best am elioration of effects of IR injury on M DA, H20 2, GSH and SOD, as well as the best preservation o f m ucosal integrity at histology. The increased TNF - alpha level was, however, best ameliorated with ischemic preconditioning. Our results provide evidence for the amelioration of IR injury by flavonoids derived from Parquetinanigrescens via anti-inflammatory effects, mainly involving TNF-alpha reduction. This effect was also positively con-elated with reduction in oxidative damage.Item Phytochemical profiling, antioxidant activities and essential oil constituents of Andrographis paniculata(Faculty of Veterinary Medicine, University of Ibadan, Nigeria, 2018) Adesye, B. Q.; Akinrlnde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Afofayan, A. J.; Adedapo, A. A.Oxidative stress is involved in the pathogenesis of various diseases which lead to urgent need to investigate new, safe and effective source of antioxidant agents. This research proposed to investigate in-vitro and phytochemical constituent of the plant Ancirographis paniculatei using phytochemical analysis, GC/MS, DPPH, ABTS, FRAP and NO. Phytochemical analysis of Anclrographis paniculata revealed the presence of tannins, total fiavonoids, total phenol, total flavonols, and total proanthocyanidins. GC/MS analysis of essential oil of AP identified one major compound name benzencpropanoic acid clucked at 3.296 retention time and 0.74 area percentage. The ferric reducing potential of the extracts was concentration dependent and significantly different from that of rutin and vitamin E. The% inhibition of ABTS by the ethanol leaf extract of Anclrographis paniculata was concentration dependent and compared favourably well with the rutin and vitamin E, in DPPH scavenging assays, the IC50 value of the ethanol leaf extract of Andrographis paniculata was < 0.025 mg/ml, while IC50 of rutin and Vitamin E were < 0.025 mg/ml and 0.68mg/ml. Nitric oxide IC50, for extract is 1,05mg/ml, Vitamin E is 1.2 mg/ml, and rutin is < 0.025 mg/ml. The present study showed high level of radical scavenging activity by ethanol leaf .extract of Andrographis paniculata with higher antioxidant activities than Vitamin E but less than that of rutin. This show that Andrographis paniculata has antioxidant properties and the plant epuid be used in the prevention and treatment of diseases associated with oxidative stress.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.