FACULTY OF VETERINARY MEDICINE
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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 Cobalt chloride-induced hepatic and intestinal damage in rats: protection by ethyl acetate and chloroform fractions of Ocimum gratissimum(Informatics Publishing Limited, 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Nwozuzu, V. C.Cobalt chloride is known to produce symptoms of diarrhea, vomiting and other gastrointestinal disturbances. We investigated the potential roles of the ethyl acetate and chloroform fractions of Ocimum gratissimum (OG), traditionally used to treat diarrhea and other gastrointestinal disorders in protection against cobalt chloride (CoCl2)-induced liver and intestinal damage. Wistar albino rats were given CoCl2 (350 ppm) in drinking water for 7 days, alone or concurrently with either fractions of OG at 100 and 200mg/kg each. Gallic acid (120 mg/kg) was administered to a group of rats as a standard flavonoid. Biochemical indices of oxidative stress, antioxidant enzyme activities, the levels of pro-inflammatory cytokines (Interleukin 1β; IL-1β and Tumor necrosis factor, TNF-α) were evaluated and the histological appearance of the liver and intestinal mucosa was investigated. CoCl2 produced significant elevations (p<0.05) in hydrogen peroxide (H2O2), malondialdehyde (MDA), IL-1β, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP). This was accompanied with significant reductions (p<0.05) in reduced glutathione (GSH), glutathione peroxidase (GPX) and glutathione S-transferase (GST) activities. Liver sections of rats exposed to CoCl2 had poor architecture and areas of necrosis with several dead hepatocytes, while some appeared with hyperchromic nuclei. Intestinal mucosa showed significant loss of absorptive epithelial cells with CoCl2 exposure. Treatment with the fractions from OG produced reduction in H2O2, MDA and IL-1β levels; reduced serum activities of ALT, AST and ALP; restoration of GSH levels and improved activities of GPX and GST. The fractions significantly preserved the hepatic and intestinal architecture.Our results indicate that the fractions of OG exhibited considerable hepatic and intestinal protection by reduction in levels of oxidants and pro-inflammatory cytokines, enhancement of antioxidant enzyme activities and preservation of tissue integrity and might thus be very useful agents in protecting the liver and intestines during concurrent exposure to Cobalt chloride.Item Glycine and L-Arginine supplementation ameliorates gastro-duodenal toxicity in a rat model of NSAID (Diclofenac)-gastroenteropathy via inhibition of oxidative stress(Walter de Gruyter GmbH, 2021) Akinrinde, A. S.; Hameed, H. O.Objectives: This study examined the possible protective roles of exogenous glycine (Gly) and L-Arginine (L-Arg) against Diclofenac (DIC)-induced gastro-duodenal damage in rats. Methods: Rats were divided into Group A (control), Group B (DIC group) and Groups C–F which were pre-treated for five days with Gly1 (250 mg/kg), Gly2 (500 mg/kg), L-Arg1 (200 mg/kg) and L-Arg2 (400 mg/kg), respectively, before co-treatment with DIC for another three days. Hematologi cal, biochemical and histopathological analyses were then carried out. Results: DIC produced significant (p<0.05) reduction in PCV (13.82%), Hb (46.58%), RBC (30.53%), serum total protein (32.72%), albumin (28.44%) and globulin (38.01%) along with significant (p<0.05) elevation of serum MPO activity (83.30%), when compared with control. In addition, DIC increased gastric H2O2 and MDA levels by 33.93 and 48.59%, respectively, while the duodenal levels of the same parameters increased by 19.43 and 85.56%, respectively. Moreover, SOD, GPx and GST activities in the DIC group were significantly (p<0.05) reduced in the stomach (21.12, 24.35 and 51.28%, respectively) and duodenum (30.59, 16.35 and 37.90%, respectively), compared to control. Treatment with Gly and L-Arg resulted in significant amelioration of the DIC-induced alterations although L-Arg produced better amelioration of RBC (29.78%), total protein (10.12%), albumin (9.93%) and MPO (65.01%), compared to the DIC group. The protective effects of both amino acids against oxidative stress parameters and histological lesions were largely similar. Conclusions: The data from this study suggest that Gly or L-Arg prevented DIC-induced gastro-duodenal toxicity and might, therefore be useful in improving the therapeutic index of DIC.Item Exacerbation of diclofenac-induced gastroenterohepatic damage by concomitant exposure to sodium fluoride in rats: protective role of luteolin(Informa UK Limited, 2020) Akinrinde, A. S.; Soetan, K. O.; Tijani, M. O.NSAID-induced gastrointestinal toxicity is associated with non-selective inhibition of cyclooxygenase (COX)-mediated synthesis of prostaglandins. Fluoride salts, known to stimulate COX-2 synthesis, have also been associated with gastrointestinal damage. The effects of fluoride treatment on NSAID toxicity are, however, yet to be clarified. This study examined the effect of sodium fluoride (NaF) on diclofenac (DIC)-induced gastroduodenal and hepatic toxicity in rats. In addition, the potential protective role of Luteolin (Lut), an antioxidant and anti-inflammatory flavonoid, in co-exposure to NaF and DIC was also investigated. Five groups of rats were treated thus: Group A (control): distilled water vehicle for 8 days; Group B: DIC (9 mg/kg) orally, twice daily from days 6 to 8; Group C: NaF (300 ppm) plus DIC for the final 3 days; Groups D and E: Luteolin at 100 mg/kg and 200 mg/kg, respectively, with concurrent NaF and DIC exposures. Rats co-treated with DIC and NaF exhibited the highest severity of dark watery diarrhea and gastroduodenal hemorrhages. NaF aggravated the DIC-induced increases in malondialde hyde (MDA), advanced oxidation protein products (AOPP), protein carbonyls (PC), H2O2, and nitric oxide, while inhibiting glutathione peroxidase (GPx) and glutathione S-transferase (GST) in all the tis sues. In contrast, Luteolin treatment significantly attenuated the gastroduodenal and hepatic damage caused by NaF and DIC co-administration by suppressing oxidative damage and lesions in the tissues. These results show, for the first time, that NaF may enhance diclofenac-induced gastrointestinal toxicity and also suggest that Luteolin may be a promising lead for the treatment of drug-induced gastroenteropathy.Item Luteolin supplementation ameliorates cobalt-induced oxidative stress and inflammation by suppressing NF-кB/Kim-1 signaling in the heart and kidney of rats(Elsevier B.V., 2020) Oyagbemi, A. A.; Akinrinde, A. S.; Adebiyi, O. E.; Jarikre, T. A.; Omobowale, T. O.; Ola-Davies, O. E.; Saba, A. B.; Emikpe, B. O.; Adedapo, A. A.Cobalt-induced cardiomyopathy and renal toxicity have been reported in workers in processing plants, hard metal industries, diamond polishing and manufacture of ceramics. This study was designed to investigate the influence of Luteolin supplementation on cobalt-induced cardiac and renal toxicity in rats. Exposure of rats to cobalt chloride (CoCl2) alone caused significant (p < 0.05) increases in cardiac and renal H2O2, malondialdehyde (MDA) and nitric oxide (NO), along with increased serum myeloperoxidase (MPO) activity. In addition, there were significant (p < 0.05) reductions in cardiac and renal glutathione peroxidase (GPx), glutathione S-transferase (GST) and reduced glutathione (GSH). CoCl2 induced higher immuno-staining of nuclear factor kappa beta (NF-κB) in the heart and kidneys, and the kidney injury molecule (Kim-1) in the kidneys. Treatment with Luteolin or Gallic acid produced significant reversal of the oxidative stress parameters with reductions in NF-κB and Kim-1 expressions, leading to suppression of histopathological lesions observed in the tissues.Item Exacerbation of diclofenac-induced gastroenterohepatic damage by concomitant exposure to sodium fluoride in rats: protective role of luteolin(0148-0545, 2020) Akinrinde, A. S.; Soetan, K. O.; Tijani, M. O.NSAID-induced gastrointestinal toxicity is associated with non-selective inhibition of cyclooxygenase (COX)-mediated synthesis of prostaglandins. Fluoride salts, known to stimulate COX-2 synthesis, have also been associated with gastrointestinal damage. The effects of fluoride treatment on NSAID toxicity are, however, yet to be clarified. This study examined the effect of sodium fluoride (NaF) on diclofenac (DIC)-induced gastroduodenal and hepatic toxicity in rats. In addition, the potential protective role of Luteolin (Lut), an antioxidant and anti-inflammatory flavonoid, in co-exposure to NaF and DIC was also investigated. Five groups of rats were treated thus: Group A (control): distilled water vehicle for 8 days; Group B: DIC (9 mg/kg) orally, twice daily from days 6 to 8; Group C: NaF (300 ppm) plus DIC for the final 3 days; Groups D and E: Luteolin at 100 mg/kg and 200 mg/kg, respectively, with concurrent NaF and DIC exposures. Rats co-treated with DIC and NaF exhibited the highest severity of dark watery diarrhea and gastroduodenal hemorrhages. NaF aggravated the DIC-induced increases in malondialde hyde (MDA), advanced oxidation protein products (AOPP), protein carbonyls (PC), H2O2, and nitric oxide, while inhibiting glutathione peroxidase (GPx) and glutathione S-transferase (GST) in all the tis sues. In contrast, Luteolin treatment significantly attenuated the gastroduodenal and hepatic damage caused by NaF and DIC co-administration by suppressing oxidative damage and lesions in the tissues. These results show, for the first time, that NaF may enhance diclofenac-induced gastrointestinal toxicity and also suggest that Luteolin may be a promising lead for the treatment of drug-induced gastroenteropathy.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 Amelioration of Aflatoxin B1-induced gastrointestinal injuries by Eucalyptus oil in rats(Walter de Gruyter GmbH, 2019) Akinrinde, A. S.; Adebiyi, O. E.; Asekun, A.Background: Eucalyptus oil (EO), derived from Eucalyptus species, possesses vast remedial and healing properties, although its gut health-promoting properties have not been well investigated. In this study, we investigated the chemical composition of a commercial EO formulation and its potential role in protecting against aflatoxinmB1 (AfB1)-induced gastrointestinal damage in rats. Methods: Male Wistar rats were divided into six groups with eight rats each. Control rats were administered with the vehicle (1% Tween 80) for 14 days, while another group was exposed to two oral doses of AFB1 on days 12 and 14. Two other groups were pre-treated with oral doses of EO (50 and 100 mg/kg b.w.) for 14 consecutivedays, along with two oral doses of AfB1 (5 mg/kg b.w.) on days 12 and 14. The remaining two groups weretreated with EO alone at the two doses for 14 days. At the end of the experiment, blood samples, stomachand intestinal tissues were collected for measurement of oxidative stress and antioxidant parameters and lightmicroscopic examination. Results: Gas chromatography-mass spectrometry analysis revealed Eucalyptol (1, 8-cineole) as the main con stituent (67.48%) of the oil. AfB1 administration induced oxidative and inflammatory disturbances, indicated by significantly (p<0.05) increased serum nitric oxide level and myeloperoxidase activity; increased tissue contents of hydrogen peroxide, malondialdehyde and protein carbonyls, accompanied with corresponding histological alterations. AfB1 also induced significant (p<0.05) reductions in glutathione peroxidase and superoxide dismutase (SOD) activities. Treatment with EO produced significant improvements in the biochemical parameters as well as the appearance of the gastric and intestinal mucosa. EO alone, at the two doses tested did not produce any significant changes in the parameters investigated. Conclusion: The findings from this study showed that EO demonstrated protective activity against Aflatoxin induced toxicity in stomach and intestinal tissues and may thus find application in treatment of gastrointestinal disorders.