Godwin O. Emerole
University of Ibadan
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Featured researches published by Godwin O. Emerole.
Clinical and Experimental Pharmacology and Physiology | 2005
Oluwatosin A. Adaramoye; Vo Nwaneri; Kc Anyanwu; Ebenezer O. Farombi; Godwin O. Emerole
1. The hypolipidaemic effect of kolaviron, a mixture of Garcinia biflavonoid 1 (GB1), Garcinia biflavonoid 2 (GB2) and kolaflavanone, used in the treatment of various ailments in southern Nigeria, was investigated in rats. The ability of Questran (Bristol‐Myers Squibb, Hounslow, UK), a hypolipidaemic therapeutic drug, to attenuate hypercholesterolaemia in rats was also examined.
Pharmaceutical Biology | 2002
E. Olatunde Farombi; Olayide O. Akanni; Godwin O. Emerole
The antioxidant and scavenging properties of kolaviron, a flavonoid extract of Garcinia kola seeds, were evaluated in a series of in vitro assays involving free radicals and reactive oxygen species. Kolaviron exhibited markedly reducing power and antioxidant activity by inhibiting the peroxidation of linoleic acid. Kolaviron exhibited 57% scavenging effect on superoxide at a concentration of 1 mg/ml and 85% scavenging effect on hydrogen peroxide at a concentration of 1.5 mg/ml. Similarly, kolaviron, at a concentration of 2 mg/ml, elicited an 89% scavenging effect on a,a-diphenyl-ß-picrylhydrazyl radical, indicating that the extract has effective activities as a hydrogen donor and as a primary antioxidant to react with lipid radicals. Kolaviron reacted with hydroxyl radical (·OH) by inhibiting deoxyribose oxidation induced by a Fenton-type reaction system (Fe 3+ + EDTA/H 2 O 2 /ascorbic acid). The second-order rate constant for the reaction with ·OH was approximately 1.1 × 10 10 M -1 sec -1. Kolaviron was effective at preventing microsomal lipid peroxidation induced by iron/ascorbate in a concentration dependent manner. The overall antioxidant activity of kolaviron on lipid peroxidation might be attributed to its properties of scavenging free radicals and active oxygen species and may relate directly to prevention of propagation of in vivo lipid peroxidation.
Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology | 2000
E. Olatunde Farombi; Babatunde I Olowu; Godwin O. Emerole
Changes in microsomal drug oxidizing enzymes, microsomal lipids, hepatic glutathione (GSH), glutathione S-trans-ferase (GST) and malondialdehyde (MDA) formation following administration of rats with therapeutic doses of three structurally related antimalarial drugs, amodiaquine (AQ), mefloquine (MQ) and halofantrine (HF) were investigated. There was a significant decrease in the activities of aniline hydroxylase, p-nitroanisole O-demethylase and pentoxyresorufin O-dealkylase in AQ, MQ and HF treated rats. AQ elicited the greatest effect with 50, 37 and 67% reductions in the activities of aniline hydroxylase, p-nitroanisole O-demethylase and pentoxyresorufin O-dealkylase, respectively. All the drugs prolonged hexobarbital-sleeping time to varying extents. The three drugs increased significantly the cholesterol per phospholipid ratio. AQ, MQ and HF decreased significantly the GSH level, GST activity and increased the formation of MDA. The results indicate that the alterations in hepatic microsomal components and lipid peroxidation caused by the antimalarials are related to the structural differences in the compounds.
Andrologia | 2009
G.N. Egbunike; Godwin O. Emerole; T.A. Aire; Fidelis I. Ikegwuonu
Rats chronically treated with sublethal doses of anatoxin B1 suffered severe testicular degeneration and impaired spermatocytogenesis with a concomitant drop in the rate and efficiency of spermatozoal production. Although the major part of sperm maturation was disturbed, there was no noticeable reduction in the viability of spermatozoa in storage, hence a fairly high degree of fertilisation occurred. That the treatment made the uterine environment less compatible with normal foetal development was demonstrated by the smaller litter size and higher embryo mortality.
Drug and Chemical Toxicology | 2003
E. Olatunde Farombi; Yvonne Y. Shyntum; Godwin O. Emerole
Abstract Background. It is known that malaria infection is accompanied by increased production of reactive oxygen species (ROS) and that malaria parasites are sensitive to oxidative damage. This has been proved by the efficacy of some antimalarial drugs that are known to act via generation of ROS when administered clinically or experimentally. Objective. There is lack of information on the effect of chloroquine on the antioxidant defense systems of normal and malaria infected humans. Since chloroquine has remained the mainstay of therapeutic regimen in malaria endemic zones, the present investigation was therefore undertaken to study the status of blood antioxidant defense mechanism, and oxidative stress following chloroquine treatment in normal and plasmodium infected humans. Methods. Ten healthy persons (5 males and 5 females) with the same age range (18–35 years) were taken as control group. Ten other individuals were treated with 25 mg/kg body with chloroquine over three days. Ten patients with malaria, not under antimalarial therapy were taken as another group, while another set of 10 patients with malaria were treated with 25 mg/kg body weight over three days. Results. The activity of superoxide dismutase was increased by 23% in individuals treated with chloroquine compared to controls while the activity of the enzyme decreased by 26% in malaria patients and by 43% in malaria patients treated with chloroquine. In all the treatment groups, the activities of catalase and glutathione peroxidase were lowered (P<0.001). Similarly the levels of vitamins A, C, and β-carotene were decreased in the treatment groups while plasma ceruloplasmin was increased in the groups. Glutathione and cholesterol levels were decreased while malondialdehyde level was increased significantly. Conclusion. Chloroquine treatment mediated oxidative stress in the host and this effect was exacerbated in Plasmodium falciparum infected patients administered with the drug.
Biochemical Pharmacology | 1983
Godwin O. Emerole; M.Ira Thabrew
Alterations in microsomal drug metabolizing enzymes and phospholipids following prolonged exposure to chloroquine have been investigated. The levels of microsomal aminopyrine-N-demethylase, aniline hydroxylase and both microsomal and cytosolic glutathione-S-transferase are reduced in treated rats. Microsomal epoxide hydrolase is unaffected by the treatment. An increase in the cholesterol-phospholipid ratio and a decrease in the phosphocholine-sphingomyelin ratio occur. There is a general reduction in the total microsomal phospholipid level though the percentage content of sphingomyelin is higher in all cases. The reduction in microsomal phospholipid level is probably due to a reduced incorporation of acetate into microsomal phospholipids as shown in this study using radioactive sodium acetate.
Fundamental & Clinical Pharmacology | 2006
Martins Ekor; Ebenezer O. Farombi; Godwin O. Emerole
Gentamicin (GM) is one of the most important of the aminoglycoside antibiotics used widely for the treatment of serious and life‐threatening infections and whose clinical use is limited by its nephrotoxicity. As the pathogenesis of GM‐induced renal dysfunction and injury involves reactive oxygen species, the polyphenolic constituents of soybean with antioxidant property may protect against GM‐induced renal toxicity. We therefore tested this hypothesis using phenolic extract of soybean (PESB) on GM‐induced nephrotoxicity rat model. Administration of GM (80 mg/kg, s.c.) for 12 days to rats induced marked renal failure, characterized by a significantly increased plasma creatinine, urea and Na+ ions levels, with K+ depletion. This was also associated with decreases in the activity of the renal antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione‐S‐transferase (GST)] measured and depletion of both blood and renal reduced glutathione (GSH) levels. The activities of membrane‐bound glucose‐6‐phosphatase (G6Pase) and 51‐nucleotidase (51‐NTD) enzymes as well as γ‐glutamyltransferase (γ‐GT) and aspartate aminotransferase (AST) (enzymes that are located in the proximal tubule) were decreased. Renal histology examination further confirmed the damage to the kidney as it reveals severe necrosis of the proximal renal tubules with deposition of colloid casts. These alterations were ameliorated in rats pretreated with PESB. The decrease in the activities of SOD, CAT, GST as well as GSH depletion observed in GM‐treated rats was prevented in the rats pretreated with PESB. The activities of γ‐GT, AST and G6Pase were also increased in the kidney. These protective effects were dose dependent except for G6Pase activity and GSH levels that were preserved only at 500 mg/kg dose of PESB, and 5′‐NTD activity that was dose dependently decreased. Furthermore, the extent of tubular damage induced by GM was reduced in rats that also received PESB. The lower dose (500 mg/kg) of the extract, however, appeared to provide better histological protection. These results suggest that the PESB has protective effects on GM‐mediated nephropathy and this may be related to the action of the antioxidant polyphenolic content of the soybean.
Clinica Chimica Acta | 1999
E. Olatunde Farombi; Oluyemi Akinloye; Clement O. Akinmoladun; Godwin O. Emerole
Five days intraperitoneal administration of rats with chlordiazepoxide (0.4 mg/kg), griseofulvin (7 mg/kg), rifampicin (8. 6 mg/kg), phenytoin (4.3 mg/kg) and phenobarbitone (1.4 mg/kg; an established inducer of microsomal enzymes) caused a significant increase in serum triacylglycerol (P<0.001) and the activities of aniline hydroxylase, aminopyrine N-demethylase and p-nitroanisole O-demethylase (P<0.001). Aniline hydroxylase, aminopyrine N-demethylase and p-nitroanisole O-demethylase activities were increased 1.48-, 1.15- and 1.47-fold, respectively, in chlordiazepoxide-treated rats, 1.65-, 1.20- and 1.38-fold in griseofulvin-treated rats, 1.74-, 1.36- and 1.44-fold in rifampicin-treated rats, 1.56-, 1.29- and 1.62-fold in phenytoin-treated rats and 2.26-, 1.72- and 1.93-fold in phenobarbitone-treated rats. Chlordiazepoxide, griseofulvin, rifampicin, phenytoin and phenobarbitone increased the activity of cytosolic phosphatidate phosphohydrolase by 52, 58, 67, 73 and 82%, respectively, while the drugs elicited 50, 60, 60, 73 and 87% increases in the activity of the microsomal phosphatidate phosphohydrolase. Similarly, chlordiazepoxide, griseofulvin, rifampicin, phenytoin and phenobarbitone elicited 2.4-, 2.39-, 2.34-, 1.69- and 3.75-fold increases in serum triacylglycerol concentrations. The correlations between serum triacylglycerol concentrations and the activities of aniline hydroxylase, aminopyrine N-demethylase and p-nitroanisole O-demethylase were significant in all treatment groups (r=0.83, r=0.92 and r=0.87, respectively, n=30, P<0.001). Our results suggest that induction of hepatic enzymes by the administered drugs may lead to hypertriglyceridaemia as an adverse effect, possibly by inducing the activity of regulatory enzymes in the biosynthesis of triglyceride.
Toxicology | 1981
Godwin O. Emerole; M.Ira Thabrew; V. O. Anosa; Dominic A. Okorie
Imperatorin, oxypeucedanine and chalepin are furanocoumarins isolated from Clausena anisata a medicinal plant common in West Africa. Only chalepin is found to have anticoagulant activity when administered to rats at a single dose. Aniline hydroxylase activity was appreciably depressed by each of the substances. Ethylmorphine demethylase, hepatic DNA, reduced glutathione and glucose-6-phosphatase were unaffected by these compounds when administered at a dose of 50 mg/kg for 3 days prior to sacrifice. Under similar conditions only chalepin treatment resulted in alpha-1-globulin increase and a decrease in beta-globulin content of the serum. Intraperitoneal treatment with chalepin (100 mg/kg) for 2 days resulted in the death of 4 rats out of 10 within a 48 h of treatment. Livers of dead rats showed generalized necrosis of hepatocytes. No deaths were recorded for imperatorin and oxypeucedanine. Rats surviving after 8 weeks showed no changes in hepatic enzyme activity, reduced glutathione and DNA concentrations. However, chalepin and imperatorin induced alterations in the serum protein pattern within this period. Liver lesions were observed in chalepin treated animals and were characterized by very mild necrosis of hepatocytes. No lesions were observed in the livers of rats treated with imperatorin and oxypeucedanine.
Food and Chemical Toxicology | 1997
Ebenezer O. Farombi; J.O. Nwankwo; Godwin O. Emerole
The possible modulatory effect of browned yam flour, a local dietary staple in south western Nigeria, on the toxicity of 7,12-dimethylbenzanthracene (DMBA), 3-methylcholanthrene (3-MC), carbon tetrachloride (CCl4) and bromobenzene (BrB) in rats was investigated. Feeding rats with 25% browned yam flour 2 wk before treatment with 65 mg/kg DMBA (single dose) and 5 mg/kg 3-MC and continued for 3 wk significantly decreased the reduction in final body weight or weight gain and organ weights caused by the two compounds. Similarly, the diet decreased the reduction in body weight or weight gain and the increase in relative liver weight mediated by oral treatment with 0.5 ml CCl4/kg and 2.5 mmol BrB/kg body weight. Incorporation of 25% browned yam flour into rat diet significantly reduced the DMBA-mediated decrease in haemoglobin content, packed cell volume, red blood cell count and white blood cell count by 7, 5, 20 and 10%, respectively; while the diet reduced the 3-MC-mediated decrease in these parameters by 15, 28, 9 and 17%, respectively. The same diet elicited 23, 45, 13 and 33% decreases in CCl4 mediated reduction in these parameters and 23, 18, 16 and 29% in the case of BrB. Browned yam flour diet caused 10, 14 (P < 0.001) and 4% (P < 0.05) reductions in the DMBA-mediated increase in serum aspartate aminotransferase, alanine aminotransferase and serum alkaline phosphatase, respectively; and 32, 31 (P < 0.05) and 13% (P < 0.001) in the case of the 3-MC-mediated increase. Also, the diet reduced CCl4-mediated increase in the activities of these by 40, 34 and 31%, respectively and by 23, 30 and 29% following BrB treatment. These results suggest that browned yam flour diet could possibly be a modulator of chemically induced toxicity.