OMOTOSO GABRIEL OLAIYA
@unilorin.edu.ng
Professor, Faculty of Basic Medical Sciences
University of Ilorin
RESEARCH, TEACHING, or OTHER INTERESTS
Developmental Biology, Neuroscience, Cell Biology, Anatomy
Scopus Publications
Scopus Publications
Fatimo Ajoke Sulaimon, Ruqayyah Yetunde Ibiyeye, Aminu Imam, Aboyeji Lukuman Oyewole, Abubakar Lekan Imam, Monsur Shehu, Sikiru Abayomi Biliaminu, Risikat Eniola Kadir, Gabriel Olaiya Omotoso, and Moyosore Salihu Ajao
Korean Association of Anatomists
Parkinson’s disease (PD) affects about 8.5 million individuals worldwide. Oxidative and inflammatory cascades are implicated in the neurological sequels, that are mostly unresolved in PD treatments. However, proper nutrition offers one of the most effective and least costly ways to decrease the burden of many diseases and their associated risk factors. Moreover, prevention may be the best response to the progressive nature of PD, thus, the therapeutic novelty of honey and levodopa may be prospective. This study aimed to investigate the neuroprotective role of honey and levodopa against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced oxidative stress. Fifty-four adult male Swiss mice were divided into control and PD model groups of 27 mice. Each third of the control mice either received phosphate buffered saline, honey, or levodopa for 21 days. However, each third of the PD models was either pretreated with honey and levodopa or not pretreated. Behavioral studies and euthanasia were conducted 2 and 8 days after MPTP administration respectively. The result showed that there were significantly (P<0.05) higher motor activities in the PD models pretreated with the honey as well as levodopa. furthermore, the pretreatments protected the midbrain against the chromatolysis and astrogliosis induced by MPTP. The expression of antioxidant markers (glutathione [GSH] and nuclear factor erythroid 2-related factor 2 [Nrf2]) was also significantly upregulated in the pretreated PD models. It is thus concluded that honey and levodopa comparably protected the substantia nigra pars compacta neurons against oxidative stress by modulating the Nrf2 signaling molecule thereby increasing GSH level to prevent MPTP-induced oxidative stress.
Nathaniel Amedu, Rodiat Adeleye, Habeebullahi Abdur-Rahman, Patrick Abolarin, and Gabriel Omotoso
Apex Publishing
Gabriel Olaiya Omotoso, , Ridwan Adeniyi Olanrewaju, Nathaniel O. Amedu, Rhoda Mama Kolo, Ismail Temitayo Gbadamosi, , , , and
Negah Scientific Publisher
Introduction: The neurotoxic effects of aluminum exposure during the critical period of neurodevelopment have been well documented. This study investigated the known protective effects of calcium supplementation on the cerebellum of juvenile Wistar rats following aluminum-induced neurotoxicity during lactation. Methods: Four groups of juvenile rats were exposed via lactation to distilled water (control group), aluminum (40 mg/kg/d), calcium supplement (50 mg/kg/d), and a combination of both aluminum and calcium from postnatal day 4 to day 28. The cerebella of the animals were excised to access the levels of antioxidant enzymes (superoxide dismutase [SOD], glutathione peroxidase [GPx]), lipid peroxidation (malondialdehyde), histomorphological alterations (hematoxylin and eosin staining), Nissl profile (cresyl fast violet staining), and glial activation (glial fibrillary acidic protein immunohistochemistry). Results: Lactational aluminum significantly decreased the activities of superoxide dismutase and glutathione peroxidase while exacerbating lipid peroxidation and reactive astrocyte in cerebellar lysates. Lactational calcium supplementation normalized the activities of SOD and GPx, thereby preventing excessive lipid peroxidation and glial activation. Despite no apparent changes in the general histology of the cerebellum, aluminum-induced chromatolysis changes in the Purkinje cell layer, which was counteracted by the antioxidant propensities of calcium supplementation. Conclusion: These findings support that calcium supplementation significantly protects the cerebellum against aluminum-induced oxidative stress, chromatolysis, and neuroinflammation.
Eniola Risikat Kadir, , Lekan Sheriff Ojulari, Taiye Abdullah Gegele, Ismail Adetayo Lawal, Lukman Sulu-Gambari, Fatimo Ajoke Sulaimon, Gabriel Olaiya Omotoso, , ,et al.
Negah Scientific Publisher
Background: Bisphenol-A (BPA) is a pervasive environmental toxin that is used in the production processes of many consumables and equipment that are in daily application. The aim of this study was to determine the effects of BPA on the structural and functional integrity of the reproductive system in male Wistar rats and its interaction with melatonin. Methods: Adult female rats in pro-estrus phases were mated with adult male rats and the conception determined. The male pups were divided into two groups of A and B. These groups were further subdivided into six subgroups each. They were administered varying low doses of BPA (25 or 50mg/kg) and melatonin (10mg/kg) at neonatal and adolescent ages. The testes, epididymis and blood samples were collected for histological, semen and biochemical investigations, respectively. Results: The results show that BPA caused histological alterations, reduced quality and quantity of sperm cells, and induced oxidative stress at birth and adolescence. Conclusion: Bisphenol A exposure, even at low dose, is toxic to the male reproductive system, and melatonin administration did not significantly improve the alterations caused by the BPA.
Gabriel Olaiya Omotoso, Fatimah Adeola Abdulsalam, Nafisat Yetunde Mutholib, Abdulkabir I. Bature, and Ismail Temitayo Gbadamosi
Elsevier BV
Nathaniel Ohiemi Amedu and Gabriel Olaiya Omotoso
Springer Science and Business Media LLC
Nathaniel Ohiemi Amedu and Gabriel Olaiya Omotoso
Springer Science and Business Media LLC
Nathaniel Ohiemi Amedu and Gabriel Olaiya Omotoso
The Korean Society of Environmental Health and Toxicology
This study was aimed at investigating the neuroprotective effect of Vitexin against lead (Pb) induced neurodegenerative changes in the dorsolateral prefrontal cortex (DLPFC) and working memory in mice. Thirty-two adolescent male albino mice were divided into four groups (n=8). Control group received 0.2 mL of normal saline; Pb group received 100 mg/kg of Pb acetate for 14 days, Vitexin group received 1mg/kg of Vitexin for 14 days, and Pb+Vitexin group received 100 mg/kg of Pb acetate and 1 mgkg of Vitexin for 14 days. Barnes maze test and novel object recognition test were done to ascertain working memory. Histoarchitectural assessment of DLPFC was done with haematoxylin and eosin (H&E), cresyl fast violet and congo red stains. Furthermore, cell count and other morphometric measurements were done. There was significant decline in working memory in the Pb group, but a combination of Pb+Vitexin improved the working memory. Vitexin significantly reduced neuronal death and chromatolysis caused by Pb. Amyloid aggregation was not observed in any of the groups. This study has shown that concurrent administration of Vitexin and Pb will significantly reduce neurodegeneration and improve working memory. However, Pb treatment or Pb+Vitexin treatment does not have any effect on intercellular distance, neuronal length and the cross-sectional area of neurons in layer III of DLPFC.
Gabriel Olaiya Omotoso, Nafisat Yetunde Mutholib, Fatimah Adeola Abdulsalam, and Abdulkabir I Bature
Korean Association of Anatomists
Prolonged separation of pups from their mother in early postnatal period can interfere with normal growth and development, resulting in different behavioral changes similar to features of schizophrenia in man. This study explored the cytoprotective action of kolaviron, a biflavonoid, on the prefrontal cortex and hippocampus of maternally deprived Wistar rats. Eight months old female rats were time-mated, and after delivery their pups were randomly assigned into four groups; group A received 0.5 ml of normal saline, group B received kolaviron orally (200 mg/kg/bw) on postnatal days (PND) 21–35, group C were maternally deprived on PND 9 for 24 hours, while group D were also maternally deprived on PND 9 for 24 hours, and then received kolaviron orally (200 mg/kg/bw) on PND 21–35. Behavioral studies (open field test, Morris water test, and Y-maze test) were conducted after the experiment prior to sacrifice. Some of the rats were anesthetized with ketamine and perfusion-fixed with 0.1 M phosphate buffered saline and 4% paraformaldehyde, while others were sacrificed by cervical dislocation for enzyme studies. The hippocampus and prefrontal cortex were excised from the brain and processed for tissue histology, histochemistry, and enzymatic analysis. Results revealed behavioral deficits, oxidative stress, degenerative changes, and astrocytosis in the prefrontal cortex and hippocampus of maternally deprived rats, but intervention with kolaviron caused significant improvement in neurobehavior, morphology, and neurochemistry in these brain areas. We concluded that kolaviron could protect the brain against neurological consequences of nutritional and environmental insults arising from maternal separation in early postnatal period.
Adelaja Akinlolu, Mubarak Ameen, Tobilola Quadri, Kayode Odubela, Gabriel Omotoso, Rahmat Yahya, Sikiru Biliaminu, Muinat Adeyanju, Gabriel Ebito, and Jubril Otulana
African Journals Online (AJOL)
This study evaluated the neuroprotective effects of MOF6 (isolated from Moringa oleifera leaves) and Trimyristin (isolated from Myristica fragrans seeds) on Acetylcholinesterase concentrations in cerebral cortices of rats with Sodium arsenite-induced neurotoxicity. Sixty-five adult male rats (150 g-250 g) were randomly divided into thirteen groups comprising of five rats per group. Groups 1 and 3 received physiological saline and 1 ml/200 g bodyweight of Olive oil respectively for 9 weeks. Group 2 received 20 mg/kg bodyweight of Sodium arsenite (SA) for 6 weeks and left untreated for another 3 weeks. Groups 4-5 received 20 mg/kg bodyweight of SA for 3 weeks followed by treatments with 5.0 and 7.5 mg/kg bodyweight of MOF6 respectively for 6 weeks. Groups 6-7 received 20 mg/kg bodyweight of SA for 3 weeks followed by treatments with 15 and 30 mg/kg bodyweight of Trimyristin respectively for 6 weeks. Groups 8-11 received 5.0 and 7.5 mg/kg bodyweight of MOF6; 15 and 30 mg/kg bodyweight of Trimyristin respectively for 9 weeks. Groups 12-13 received 7.5 mg/kg bodyweight of MOF6 and 30 mg/kg bodyweight of Trimyristin respectively for 6 weeks followed by co-administration of each extract dose with 20 mg/kg bodyweight of SA for another 3 weeks. Histological examination of cerebral cortices and biochemical analyses of Acetylcholinesterase concentrations were carried out in all rats. Computed data were analyzed using Microsoft Excel 2016 with statistical significance at p≤0.05. Histo-pathological evaluations revealed normal histo-architecture of cerebral cortices of all rats. Results showed statistically significant (p≤0.05) increases in Acetylcholinesterase concentrations in rats of Groups 1-10 and 12 compared with Group 2 (2.78±1.76 𝜇mole/min/g). 7.5 mg/kg bodyweight of MOF6 showed the best therapeutic and neuro-regenerative potential against SA-induced neurotoxicity.Conclusions: Our findings implied that MOF6 and Trimyristin reversed downregulation of Acetylcholinesterase concentrations in SA-induced neurotoxicity in rats; and possess neuro-protective and neuro-regenerative potentials.
Gabriel Omotoso, Olajumoke Oloyede, Shakirah Lawal, Ismail Gbadamosi, Nafisat Mutholib, Fatimah Abdulsalam, Abdulkabir Bature, Abulsalam Babalola, Busola Ayeni, and Nathaniel Amedu
The Korean Society of Environmental Health and Toxicology
This study investigated the neurotoxic effects of permethrin on the cerebellum, hippocampus and prefrontal cortex of Wistar rats and its effects on some behavioral patterns. Fifteen adult male Wistar rats were grouped into three categories: Group A received 0.1 mL normal saline (control), and Groups B and C received mixed feed with 500 mg/kg and 1,000 mg/kg of 0.6% permethrin, respectively, for 14 days. The animals were assessed for memory, anxiety and exploratory locomotion and thereafter anesthetized and transcardially perfused with normal saline and 4% paraformaldehyde (PFA). Cerebellum, hippocampus and prefrontal cortex were excised from the whole brain and processed for tissue histology, histochemistry and immunohistochemistry. Oxidative status and lipid peroxidation were also assessed using catalase, glutathione peroxidase, superoxide dismutase and malondialdehyde as biomarkers. Results revealed dosedependent decrease in body weights but increase in cerebellar and prefrontal weights, depletion of endogenous antioxidant markers, cognitive deficits, reduced locomotor activities, degenerative changes in the microarchitecture at high doses and presence of chromatolytic cells at both low and high doses of permethrin. Astrocytes were activated while synaptophysin expression was downregulated. Permethrin causes dose-dependent neurotoxicity on the morphology, neurochemistry and oxidative status of different brain regions, and these could affect behavioral performance and other neurologic functions.
Burcu BİTERGE SÜT and Ayşe İKİNCİ KELEŞ
Walter de Gruyter GmbH
G.O. Omotoso, O.J. Olajide, I.T. Gbadamosi, J.O. Adebayo, B.U. Enaibe, O.B. Akinola, and B.V. Owoyele
Elsevier BV
Gabriel Olaiya Omotoso, Ileje Inelo Ukwubile, Leviticus Arietarhire, Fatima Sulaimon, and Ismail Temitayo Gbadamosi
Elsevier BV
Gabriel Olaiya Omotoso, Ismail Temitayo Gbadamosi, Theresa Titilayo Afolabi, Ahmad Bolakale Abdulwahab, and Adelaja Abdulazeez Akinlolu
Korean Association of Anatomists
Cuprizone is a neurotoxin with copper-chelating ability used in animal model of multiple sclerosis in which oxidative stress has been documented as one of the cascade in the pathogenesis. Moringa oleifera is a phytomedicinal plant with antioxidant and neuroprotective properties. This study aimed at evaluating the ameliorative capability of M. oleifera in cuprizone-induced behavioral and histopathological alterations in the prefrontal cortex and hippocampus of Wistar rats. Four groups of rats were treated with normal saline, cuprizone, M. oleifera and a combination of M. oleifera and cuprizone, for five weeks. The rats were subjected to Morris water maze and Y-maze to assess long and short-term memory respectively. The animals were sacrificed, and brain tissues were removed for histochemical and enzyme lysate immunosorbent assay for catalase, superoxide dismutase, and nitric oxide. Cuprizone significantly induced oxidative and nitrosative stress coupled with memory decline and cortico-hippocampal neuronal deficits; however, administration of M. oleifera significantly reversed the neuropathological deficits induced by cuprizone.
Gabriel Olaiya : Omotoso, , Olayemi Joseph Olajide, Ismail Temitayo Gbadamosi, Mikail Abiodun Rasheed, Chiazokam Tochukwu Izuogu, , , , ,et al.
Penerbit Universiti Sains Malaysia
Background This study explored the efficacy of kolaviron—a biflavonoid complex isolated from the seeds of Garcinia kola—in protecting against cuprizone (CPZ)-induced demyelination in both the prefrontal cortex and the hippocampus of Wistar rats. Methodology Thirty rats were treated to receive 0.5 mL phosphate-buffered saline (group A, control), 0.5 mL corn oil (group B), 0.2% CPZ (group C), for 6 weeks, 0.2% CPZ for 3 weeks and then 200 mg/kg of Kv for 3 weeks (group D), or 200 mg/kg of Kv for 3 weeks followed by 0.2% CPZ for 3 weeks (group E). Rats were assessed for exploratory functions and anxiety-like behaviour before being euthanised and perfused transcardially with 4% paraformaldehyde. Prefrontal and hippocampal thin sections were stained in hematoxylin and eosin and cresyl fast violet stains. Results CPZ-induced demyelination resulted in behavioural impairment as seen by reduced exploratory activities, rearing behaviour, stretch attend posture, center square entry, and anxiogenic characteristics. Degenerative changes including pyknosis, karyorrhexis, neuronal hypertrophy, and reduced Nissl integrity were also seen. Animals treated with Kv showed significant improvement in behavioural outcomes and a comparatively normal cytoarchitectural profile. Conclusion Kv provides protective roles against CPZ-induced neurotoxicity through prevention of ribosomal protein degradation.
Gabriel Olaiya Omotoso, Ismail Temitayo Gbadamosi, Olayemi Joseph Olajide, Shakirat Opeyemi Dada-Habeeb, Tolulope Timothy Arogundade, and Emmanuel Olusola Yawson
Elsevier BV
Gabriel Olaiya Omotoso, , Risikat Eniola Kadir, Fatima A. Sulaimon, Rukayat Jaji-Sulaimon, Ismail Temitayo Gbadamosi, , , , and
Penerbit Universiti Sains Malaysia
Background and aim This study aimed to determine the effect of gestational nicotine exposure before neurodevelopment on the morphology and histology of the prefrontal cortex (PFC) in rats. Methodology Adult female Wistar rats were time-mated and grouped into three categories: (a) control–given 0.1 mL of normal saline, (b) low-dose nicotine–given 6.88 mg/ kg/d/0.05 mL, and (c) high-dose nicotine–given 13.76 mg/kg/d/0.1 mL in two divided doses. Treatment was given intraperitoneally from gestational days 2 to 6. On postnatal day 15 (P15), the pups were separated from their mothers, anaesthetised and sacrificed, followed by intracardial perfusion with 4% paraformaldehyde. PFC was excised from the brain and processed for tissue histology, histochemistry, and morphology of brain cells. Results Gestational nicotine exposure during the first week of gestation in rats significantly reduced birth weights in nicotine-treated groups compared with control; it, however, accelerated body weights, altered neuronal morphology, and elevated astrocytic count significantly, while oligodendroglial count was slightly increased in the PFC of juvenile rats examined at P15. Conclusion These alterations revealed that gestational nicotine exposure before the commencement of the cellular processes involved in brain development negatively affects neurodevelopment, and this could result in neurological dysfunctions in later life.
Abdulazeez Adelaja Akinlolu, Olaide Kamal Ghazali, Oloduowo Mubarak Ameen, Seunayo Comfort Oyebanji, Gabriel Olaiya Omotoso, and Bernard Ufuoma Enaibe
SciELO Agencia Nacional de Investigacion y Desarrollo (ANID)
Se puso a prueba la hipotesis que Moringa oleifera altera la morfologia y funcion del rinon en ratas. Fueron utilizadas 24 ratas Wistar macho adultas. El grupo control recibio suero fisiologico mientras que los Grupos II a IV recibieron 250, 500 y 750 mg/kg peso corporal del extracto metanolico de Moringa oleifera respectivamente, durante 21 dias. No se observaron anomalias en el comportamiento en ratas de los Grupos I - IV. En las ratas del grupo de control se registro un aumento de peso corporal estadisticamente significativo, mientras que las ratas de los grupos II - IV experimentaron una disminucion no significativa de peso corporal durante el procedimiento experimental (P0,05). No se observaron diferencias estadisticamente significativas (P0,05) en el analisis de los pesos relativos en rinones de las ratas de los grupos I - IV. Los examenes histologicos mostraron citoarquitectura normal de los rinones de las ratas del grupo I, mientras que en ratas de los grupos II IV los espacios capsulares de los rinones aparecian mas amplios que los del Grupo I. Los analisis estadisticos mostraron niveles superiores significativos ( P 0,05 ) de la alanina y aspartato aminotransferasa, y de urea en suero en ratas de los Grupos II - IV no dependiente de la dosis, en comparacion con las ratas del Grupo I. Estos resultados coinciden con la hipotesis planteada.