Browsing by Author "Omobowale, T. O."

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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.
Alterations in blood pressure, antioxidant status and caspase 8expression in cobalt chloride-induced cardio-renal dysfunction arereversed by Ocimum gratissimum and gallic acid in Wistar rats
(Elsevier B.V., 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 againstcobalt 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). CoCl2given alone, caused significant increases (p < 0.05) in oxidative stress parameters(hydrogen peroxide, H2O2and malondialdehyde, MDA) and increased expression of the apoptotic initia-tor 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 andadaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2also produced signifi-cant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. OralCOG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2and MDA; with reducedexpression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varyingdegrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures inthe rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarctionand inflammation and renal tubular necrosis and inflammation were effectively ameliorated by the treat-ments administered. This study provides evidence for the protective roles of O. gratissimum and gallicacid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptoticcaspase 8 in Wistar rats.
Ameliorative effect of gallic acid in doxorubicin-induced hepatotoxicity in wistar rats through antioxidant defense system
(Taylor & Francis, 2017-07) Omobowale, T. O.; Oyagbemi, A. A.; Ajufo, U. E.; Adejumobi, A. O.; Ola-Davies, O. E.; Adedapo, A. A.; Yakubu, M. A.
Hepatotoxicity has been found to be one of the main side effects associated with doxorubicin (Dox) administration in cancer therapy. The aim of the present study was to examine the ameliorative effect of gallic acid (GA) in Dox-induced hepatotoxicity. Sixty male Wistar rats of 10 rats per group were used in this study and were randomly divided into 6 experimental groups (A–F). Rats in Group A served as the control group and received distilled water orally for 7 days; Group B was given Dox at 15 mg/kg bodyweight intraperitoneally (IP) on Day 8. Group Cwas given GA at 60 mg/kg body weight orally for 7 days + Dox at 15 mg/kg IP on Day 8. Group D was given GA at 120 mg/kg body weight orally for 7 days +Dox at 15 mg/kg IP on day 8. Rats in Groups E and F were administered GA alone at 60 and 120 mg/kg bodyweight orally for 7 days, respectively. Dox administration led to a significant reduction in hepatic reduced glutathione and nonprotein thiol (NPT) together with significant increase in hepatic malondialdehyde, hydrogen peroxide generation, superoxide dismutase, and catalase activity; hepatic glutathione peroxidase and glutathione-S-transferase activity were significantly inhibited in Dox-treated rats. The serum alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin concentrations were significantly elevated following Dox administration. Pretreatment with GA ameliorated Dox-induced hepatotoxicity and oxidative stress. The results suggest that GA may offer protection against hepatic damage in Dox cancer chemotherapy.
Ameliorative effect of gallic acid on doxorubicin-induced cardiac dysfunction in rats
(De Gruyter, 2017) Omobowale, T. O.; Oyagbemi, A. A.; Folasire, A. F.; Ajibade, T. O.; Asentiga, E. R.; Adejumobi, O. A.; Ola-Davies, O. E.; Oyetola, O.; James, G.; Adedapo, A. A.; Yakubu, M. A.
Background: The use of doxorubicin (DOX) as an antineoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Methods: Sixty male rats (Wistar strain) were used in this study. They were divided into six groups (A–F) each containing 10 animals. Group A was the control. Rats in Groups B, C, and D were treated with DOX at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in Groups C and D had been treated orally with GA for 7 days at the dosage of 60 and 120 mg/kg, respectively. Animals from Groups E and F received only 60 and 120 mg/kg GA, respectively, which were administered orally for 7 days. Results: The exposure of rats to DOX led to a significant (p 0.05) decrease in the cardiac antioxidant defence system and elevation of creatine kinase myocardial band and lactate dehydrogenase. The electrocardiography results showed a significant decrease in heart rate, QRS, and QT-segment prolongation. GA alone improved the antioxidant defence system. Conclusions: The GA pretreatment significantly alleviated GA-associated ECG abnormalities, restored the antioxidant status and prevented cardiac damage.
Cobalt chloride exposure dose dependently induced hepatotoxicity through enhancement of cyclooxygenase-2 (COX-2)/B- cell associated protein X (BAX) signaling and genotoxicity in wistar rats
(Wiley, 2017-02) Awoyemi, O. V.; Okotie, U. J.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ola-Davies, O. E.; Ogunpolu, B. S.
Cobalt chloride (CoCl2) is one of the many environmental contaminants, used in numerous industrial sectors. It is a pollutant with deadly toxicological consequences both in developing and developed countries. We investigated toxicological impact of CoCl2 on hepatic antioxidant status, apoptosis, and genotoxicity. Forty Wistar rats were divided into four groups, 10 rats per group: Group 1 served as control and received clean tap water orally; Group 2 received CoCl2 solution (150 mg/L); Group 3 received CoCl2 solution (300 mg/L); and Group 4 received CoCl2 (600 mg/L) in drinking water for 7 days, respectively. Exposure of rats to CoCl2 led to a significant decline in hepatic antioxidant enzymes together with significant increase in markers of oxidative stress. Immunohistochemistry revealed dose-dependent increase in cyclooxygenase-2 and BAX expressions together with increased frequency of Micronucleated Polychromatic Erythrocytes. Combining all, CoCl2 administration led to hepatic damage through induction of oxidative stress, inflammation, and apoptosis.
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.
Cobalt Chloride-induced Hepatic and Intestinal damage in rats: Protection by ethyl acetate and chloroform fractions of Ocimum gratissimum2016
(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 CoCl2had 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.
Cobalt chloride-induced oxidant-antioxidant imbalance in rat erythrocytes: The modulatory role of Kolaviron
(Faculty of Veterinary Medicine, University of Ibadan, Nigeria., 2018) Akinrinde, A. S.; Idowu, O. O.; Oyagbemi, A. A.; Omobowale, T. O.
Cobalt stimulates erythrocyte production via mechanisms that mimic physiological adaptations to hypoxic conditions. However, little is known about alterations in the balance of erythrocyte antioxidant defense system produced by cobalt. We investigated the effect of Kolaviron (KV) on cobalt chloride (CoCl2)-induced disturbances in erythrocyte antioxidant status and hematological parameters and compared the effects with those of Gallic acid (GA). Groups of rats were orally treated with either KV1 (100 mg/kg), KV2 (200 mg/kg) or GA (120 mg/kg), along with CoCl2 (350 ppm) in drinking water for 14 days. CoCl, produced significant (p<0.05) increases in packed cell volume, hemoglobin and red blood cell count, but no alterations in erythrocyte morphology, in the same way as rats treated with KV or GA. Significant (p<0.05) elevation in malondialdehyde (MDA) content and reductions in total thiols and reduced glutathione (GSH) in the CoCl2 group were indications of oxidative stress. KV produced significant (p<0.05) reduction in MDA, while restoring the levels of GSH and total thiols with elevations in" glutathione S-transferase and superoxide dismutase. Our results indicate that CoCl2-induced erythropoiesis was accompanied by altered antioxidant status of the erythrocytes. Kolaviron, however, ameliorated the disturbancesin erythrocyte antioxidant defense system.
Concentration-dependent inhibition of acetylcholinesterase by organophosphate poisoning in dogs: a biochemical and electrocardiographic study
(Society of Toxicology, India, 2016) Ola-Davies, O. E.; Oyagbemi, A. A.; Omobowale, T. O.
Organophosphate poisoning (OP) is one of the most common poisonings in developing countries. In this study, twenty-four dogs in four groups of six each were used. Control group bathed with water only, group B with 16% Coumaphos (recommended), groups C and D with times 10 and 20 of 16% Coumaphos, respectively. Blood was collected from cephalic vein for biochemical assays. Electrocardiographic parameters were assessed from a Lead-II electrocardiogram. There was a significant increase (p<0.05) in total cholesterol in group B and D compared to the control. LDL-cholesterol decreased significantly (p<0.05) in all groups compared to the control. The activity of superoxide dismutase (SOD) reduced (p<0.05) significantly across all the groups and even after 36 hours of exposure. However, the activity of the glutathione peroxidase (GPx) was not affected following exposure to OP. The serum reduced glutathione (GSH) fell in a concentration dependent manner in all animals exposed to OP. Coumaphos exposure led to a significant (p<0.05) increase in serum MDA in a concentration dependent manner after 36 hours post exposure. The serum nitric oxide (NO) and MPO content increased (p<0.05) significantly following exposure to different concentrations of Coumaphos. The activity of Acetyl cholinesterase (AchE) fell significantly from the normal concentration of the OP down to the highest concentration. The activity of serum creatine phosphokinase (CK) increased (p<0.05) significantly in groups C and D compared to the control and recommended concentration. Electrocardiographic abnormalities recorded included low-voltage R-waves, first degree heart block, significant increased (p<0.05) heart rate (HR) and shortened QT interval compared to the control and recommended concentrations. Taking together, coumaphos poisoning caused an inhibition of AchE and significant potentially fatal arrrhythmais via induction of oxidative stress.
Dirofilaria immitis infection in a three year old doberman: A case report
(The University of Veterinary Medicine and Pharmacy in Kosice, 2011) Ajadi, R. A.; Omobowale, T. O.; Igado, O. O.; Adejinmi, J.O.; Adedokuii, O.A.; Nottidge, H. O.
A three-year- old male Doberman that was presented at the Veterinary Teaching Hospital of the University of Ibadan, Nigeria with the complaint of anorexia, bloody diarrhea and weight loss was diagnosed with a chronic form of heartworm disease based on the findings at the physical examination which included a complete blood count, liver function tests and thoracic radiography. The physical examination revealed that the dog’s mucous membranes were pale and there was a copious bilateral macopurulent ocular discharge present. There was subcutaneous oedema on the ventral thoracic region, while auscultation revealed tachypnea and an irregular heart rhythm. The results of the hematology and liver enzyme tests revealed moderate anaemia, which was normochromic and normocytic. There was mild neutrophilia, eosinopaenia and monocytopaenia. Both the alkaline phosphatase (ALP) and aspartate transaminase (AST) were markedly elevated. Also, the serum albumin concentrations and the albumin/globulin ratio were both markedly lowered. The direct blood smear revealed that the dog was negative for both Babesia canis and Erlichia canis, but positive for microfilaria. The microfilaria was 309 ±30µ in length and the anterior and posterior widths were 12±2.4µ and 9±1.6µ, respectively. The lateral thoracic radiograph showed that the heart was normal in size, while the pulmonary vasculatures were visible and within normal range. The health of the dog improved following treatment with levamisole and gentaprim. This case confirms the efficacy of levamisole in combination with gentaprim in the management of canine heart worm disease.
Dirofilaria immitis infection in a three year old doberman: A case report
(The University of Veterinary Medicine and Pharmacy in Kosice, 2011) Ajadi, R. A.; Omobowale, T. O.; Igado, O. O.; Adejinmi, J. O.; Adedokun, O. A.; Nottidge, H. O
A three-year- old male Doberman that was presented at the Veterinary Teaching Hospital of the University of Ibadan, Nigeria with the complaint of anorexia, bloody diarrhea and weight loss was diagnosed with a chronic form of heartworm disease based on the findings at the physical examination which included a complete blood count, liver function tests and thoracic radiography. The physical examination revealed that the dog’s mucous membranes were pale and there was a copious bilateral mucopurulent ocular discharge present. There was subcutaneous oedema on the ventral thoracic region, while auscultation revealed tachypnea and an irregular heart rhythm. The results of the hematology and liver enzyme tests revealed moderate anaemia, which was normochromic and normocytic. There was mild neutrophilia, eosinopaenia and monocytopaenia. Both the alkaline phosphatase (ALP) and aspartate transaminase (AST) were markedly elevated. Also, the serum albumin concentrations and the albumin/globulin ratio were both markedly lowered. The direct blood smear revealed that the dog was negative for both Babesia canis and Erlichia canis, but positive for microfilaria. The microfilaria was 309 ±30p in length and the anterior and posterior widths were 12±2.4p and 9±1.6ji, respectively. The lateral thoracic radiograph showed that the heart was normal in size, while the pulmonary vasculatures were visible and within normal range. The health of the dog improved following treatment with levamisole and gentaprim. This case confirms the efficacy of levamisole in combination with gentaprim in the management of canine heart worm disease.
Effect of exposure and withdrawal on lead-induced toxicity and oxidative stress in cardiac tissues of rats
(Society of Toxicology, India, 2016) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Ola-Davies, O. E.; Saba, A. B.; Olukayode, O. J.; Adeolu, 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.
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.
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, S. A.; 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 H2 O2 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.
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.
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.
Failure of recovery from lead induced hepatoxicity and disruption of erythrocyte antioxidant defence system in Wistar ratsTemidayo
(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 toxicologicalconsequences both in the developing and developed countries. The liver and erythrocyteantioxidant status and markers of oxidative were assessed. Exposure of rats to PbA ledto significant decline (p < 0.05) in hepatic and erythrocyte glutathione peroxidase (GPx),glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reducedglutathione (GSH) content. Similarly, malondialdehyde (MDA) and H2O2concentrations weresignificantly (p < 0.05) elevated. Histopathology and immunohistology of liver of rats exposedto 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 afterwithdrawal of the exposed PbA for the period of the study. In conclusion, experimentalanimals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyteantioxidant defence system via free radical generation and oxidative stress.
Gallic acid ameliorates Cyclophosphamide-Induced neurotoxicity in Wistar rats Through Free radical scavenging activity and improvement in antioxidant defense system
(Taylor & Francis, 2016) Oyagbemi, A. A.; Omobowale, T. O.; Saba, A. B.; Olowu, E. R.; Dada, R. O.; Akinrinde, A. S.
Cyclophosphamide (CPA) is a widely used anticancer chemotherapeutic agent and its toxicity has been associated with its toxic metabolites phosphormide mustard. Therefore, the ameliorative effect of Gallic acid against neurotoxicity was examined in this study. Sixty rats were grouped into 10 rats per group. Group 1 received saline orally.Group 2 received CPA at 100 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4were treated with Gallic acid (GA) at 60 and 120 mg/kg body weight only for 10 days and also received a single dose of CPA (100 mg/kg) intraperitoneally on day 1, respectively. Rats in groups 5 and 6 receivedGAat 60 and 120 mg/kg body weight only for 10 days. Groups 3, 4, 5, and 6 received GA orally. The cerebellar and cerebral malondialdehyde (MDA) contents and hydrogen peroxide generation were significantly (p < .05) elevated. The cerebellar and cerebral catalase (CAT), superoxide dismutase and glutathione-S-transferase (GST) activities were significantly (p < .05) reduced in CPA treated group. The activity of glutathione peroxidase (GPx) was significantly increased in rats that were treatment with CPA. Also, nitrite content was significantly elevated in the brain of rats that received the toxic dose of CPA. All these findings suggest that treatment with GA (60 and 120 mg/kg) ameliorated the neurotoxicity induced by CPA via reduction of oxidative stress and increase in antioxidant defense system. Combining all, chemotherapeutic agents with structure/function similar to GA could be of potential benefit to the pharmaceutical industries as an adjuvant in chemotherapy with little or no side effects.
Gallic acid ameliorates Cyclophosphamide-Induced neurotoxicity in Wistar rats through free radical scavenging activity and improvement in antioxidant defense system
(Taylor & Francis Group, LLC, 2016) Oyagbemi, A. A.; Omobowale, T. O.; Saba, A. B.; Olowu, E. R.; Dada, R. O.; Akinrinde, A. S.
Cyclophosphamide (CPA) is a widely used anticancer chemotherapeutic agent and its toxicity has been associated with its toxic metabolites phosphormide mustard. Therefore, the ameliorative effect of Gallic acid against neurotoxicity was examined in this study. Sixty rats were grouped into 10 rats per group. Group 1 received saline orally. Group 2 received CPA at 100 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4 were treated with Gallic acid (GA) at 60 and 120 mg/kg body weight only for 10 days and also received a single dose of CPA (100 mg/kg) intraperitoneally on day 1, respectively. Rats in groups 5 and 6 received GA at 60 and 120 mg/kg body weight only for 10 days. Groups 3, 4, 5, and 6 received GA orally. The cerebellar and cerebral malondialdehyde (MDA) contents and hydrogen peroxide generation were significantly (p < .05) elevated. The cerebellar and cerebral catalase (CAT), superoxide dismutase and glutathione-S-transferase (GST) activities were significantly (p < .05) reduced in CPA treated group. The activity of glutathione peroxidase (GPx) was significantly increased in rats that were treatment with CPA. Also, nitrite content was significantly elevated in the brain of rats that received the toxic dose of CPA. All these findings suggest that treatment with GA (60 and 120 mg/kg) ameliorated the neurotoxicity induced by CPA via reduction of oxidative stress and increase in antioxidant defense system. Combining all, chemotherapeutic agents with structure/function similar to GA could be of potential benefit to the pharmaceutical industries as an adjuvant in chemotherapy with little or no side effects.
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 treated rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.