Biochemistry
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Item Kolaviron protects against ethylene glycol monoethyl ether-induced toxicity in boar spermatozoa(Blackwell Verlag GmbH, 2014) Adedara, I. A.; Farombi, E. O.This study investigated the ameliorative effects of kolaviron (a biflavonoid from the seed of Garcinia kola) and vitamin C on ethylene glycol monoethyl ether (EGEE)-induced oxidative damage in boar spermatozoa in vitro. EGEE (1.0 mM) was incubated with boar spermatozoa for 3 h with or without either kolaviron (50 and 100 lM) or vitamin C (1.0 mM). Spermatozoa parameters were determined hourly during the incubation period, whereas aminotransferases and alkaline phosphatase activities and oxidative stress indices were assessed after the incubation period. Results showed a time-dependent decline in spermatozoa motility and viability with significant elevation in total abnormalities in EGEE-treated spermatozoa. Exposure to EGEE resulted in significant increase in aminotransferases, alkaline phosphatase and superoxide dismutase (SOD) activities, whereas it markedly decreased glutathione (GSH) level, catalase (CAT) and glutathione S-transferase (GST) activities with concomitant increase in hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels. Pre-treatment of spermatozoa with kolaviron or vitamin C significantly decreased H2O2 and MDA levels, improved spermatozoa characteristics and ameliorated oxidative damage in EGEE-treated spermatozoa. Taken together, EGEE exhibited its spermatotoxicity via induction of oxidative stress. The protective effects by kolaviron and vitamin C against EGEE-induced oxidative damage may be due to their intrinsic antioxidative potentials.Item Kolaviron and vitamin E ameliorate hematotoxicity and oxidative stress in brains of prepubertal rats treated with an anticonvulsant phenytoin(Informa Healthcare USA, 2014) Owoeye, O.; Adedara, I. A.; Bakare, O. S.; Adeyemo, O. A.; Egun, C.; Farombi, E. O.Phenytoin (PHT), an anticonvulsant agent, widely used for the treatment of epilepsy has been reported to exhibit toxic side effects. The present study investigated the protective effects of kolaviron and vitamin E on hematotoxicity and neurotoxicity induced by phenytoin, in prepubertal male rats. The animals were treated with PHT (75 mg/kg) separately or in combination with either kolaviron (200 mg/kg) or vitamin E (500 mg/kg) for 14 days. Phenytoin treatment significantly decreased the hemoglobin, white blood cells, lymphocytes and mean corpuscular volume levels without affecting red blood cell, packed cell volume, neutrophils, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration when compared with the control rats. There was a significant increase in lipid peroxidation and hydrogen peroxide levels with marked depletion in antioxidant status in brains of PHT-treated rats when compared with the control. Although PHT treatment had no effect on the granular layer, widest diameter of Purkinje cells and Purkinje layer of the cerebellum, it significantly reduced its molecular layer and the density of Purkinje cell. Administration of PHT significantly reduced the densities of the granule cells of the dentate gyrus and the pyramidal neurons of the cornu ammonis of hippocampus proper. Co-treatment with kolaviron and vitamin E effectively reversed the PHT-mediated alterations in the hematology, brain antioxidant status and histomorphometry when compared to PHT only. Taken together, the present data indicate the abilities of kolaviron and vitamin E to ameliorate phenytoin-induced hematotoxicity and oxidative stress in brains of rats.Item Kolaviron prevents ethylene glycol monoethyl ether-induced testicular apoptosis via down-regulation of stress proteins, Fas/Fas-L and caspases expressions in rats(Informa Healthcare USA, Inc., 2013) Adedara, I. A.; Mathur, P. P.; Farombi, E. O.This study investigated the protective role of kolaviron, a natural antioxidant biflavonoid isolated from the seed of Garcinia kola, in ethylene glycol monoethyl ether (EGEE)-induced testicular dysfunction in male rats. Adult male Wistar rats were exposed to EGEE (200 mg/kg) separately or in combination with either kolaviron (100 or 200 mg/kg) or vitamin E (50 mg/kg) for 14 days. Immunoblot analysis revealed that EGEE exposure alone significantly increased stress-inducible proteins levels. The increased protein expression of active caspases, Fas and Fas-L, was accompanied by nuclear factor kappa B downregulation and elevation of cytosolic cytochrome c level in EGEE-treated rats. In addition, the observation from immunofluorescence staining was consistent with the increased TUNEL-positive nuclei in the testes of EGEE-treated rats. Kolaviron and vitamin E significantly inhibited induction of stress proteins and germ cell apoptosis in EGEE-treated rats. Overall, kolaviron by virtue of its antioxidant and anti-apoptotic properties prevented EGEE-induced reproductive toxicity in rats.Item Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether-induced pituitary-thyroid axis toxicity in male rats(Blackwell Verlag GmbH, 2012) Adedara, I. A.; Farombi, E. O.Endocrine disrupting chemicals cause reproductive dysfunction by interacting with intricate regulation and cellular processes involve in spermatogenesis. This study investigated the probable mechanism of action of ethylene glycol monoethyl ether (EGEE) as an antiandrogenic compound as well as the effects of kolaviron upon co-administration with EGEE in rats. Adult male rats were exposed to EGEE (200 mg kg_1 bw) separately or in combination with either kolaviron [100 (KV1) and 200 (KV2) mg kg_1 bw] or vitamin E (50 mg kg_1bw) for 14 days. Western blot analysis revealed that the administration of EGEE adversely affected steroidogenesis in experimental rats by decreasing the expression of steroid acute regulatory (StAR) protein and androgen-binding protein (ABP). EGEE significantly decreased the activities of 3b-hydroxysteroid dehydrogenase (3b-HSD) and 17b-hydroxysteroid dehydrogenase (17b-HSD) but markedly increased sialic acid concentration in rat testes. EGEE-treated rats showed significant decreases in plasma levels of luteinising hormone (31%), testosterone (57.1%), prolactin (80.9%), triiodothyronine (65.3%) and thyroxine (41.4%), whereas follicle-stimulating hormone was significantly elevated by 76.9% compared to the control. However, co-administration of kolaviron or vitamin E significantly reversed the EGEE-induced steroidogenic dysfunction in rats. This study suggests that kolaviron may prove promising as a chemoprotective agent against endocrine pathology resulting from EGEE exposure.Item Chemoprotection of ethylene glycol monoethyl ether-induced reproductive toxicity in male rats by kolaviron, isolated biflavonoid from Garcinia kola seed(Sage Publishers, 2012) Adedara, I. A.; Farombi, E. O."The present study investigated the protective effect of kolaviron, a biflavonoid from the seed of Garcinia kola, on ethylene glycol monoethyl ether (EGEE)–induced reproductive toxicity in male rats. The protective effect of kolaviron was validated using vitamin E, a standard antioxidant. EGEE was administered at a dose of 200 mg/kg. Other groups of rats were simultaneously treated with kolaviron (100 and 200 mg/kg) and vitamin E (50 mg/kg) for 14 days. EGEE treatment resulted in significant decrease in glutathione (GSH) level, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities but markedly increased the glutathione-Stransferase (GST) and lactate dehydrogenase (LDH) activities in the testes. In the spermatozoa, administration of EGEE caused significant decrease in the activities of CAT, GPx, GST and LDH as well as in the level of GSH but significantly increased SOD activity with concomitant increase in hydrogen peroxide and malondialdehyde levels in both testes and spermatozoa. EGEE-exposed rats showed marked testicular degeneration with concomitant decrease in spermatozoa quantity and quality. Overall, EGEE causes reproductive dysfunction in rats by altering antioxidant systems in the testes and spermatozoa. Kolaviron or vitamin E exhibited protective effects against EGEE-induced male reproductive toxicity by enhancement of antioxidant status and improvement in spermatozoa quantity and quality.