Bio

Honors & Awards


  • International Investigator Opportunity Grants, American Association for Cancer Research (2009)
  • Undergraduate Scholar, Shell Petroleum Development Company (1996- 2000)

Professional Education


  • Predoctoral Fellow, Indiana University Purdue University, Indianapolis, Chemical carcinogenesis (2007)
  • Doctor of Philosophy, University Of Ibadan (2009)

Stanford Advisors


Research & Scholarship

Current Research and Scholarly Interests


Acetaminophen – N-acetyl-p-amino-phenol (APAP) , Tylenol™ - is an over the counter drug used for its analgesic, antipyretic and peripheral anti-inflammatory effects. APAP is the most widely studied of all drugs known to have hepatotoxic potentials. Its regioisomer N-acetyl-m-amino-phenol (AMAP) cause no injury to the liver and appears to be relatively safe. APAP overdose has been reported to cause liver injury, necrosis acute liver failure and over 450 deaths yearly in the United State. Implicated in these series of adverse effect is N-acetyl-p-benzoquinone imine (NAPQI) the reactive metabolite formed from a fraction of APAP metabolism by cytochrome p450 enzymes. Conjugation of NAPQI with glutathione (GSH) leads to its biliary excretion. Subsequent GSH depletion and accumulation of NAPQI, results in NAPQI preferential binding to cellular proteins and other macromolecules. NAPQI -protein binding is implicated in APAP toxicity. Consequently, activation of Kupffer cells (KC) and neutrophil recruitment exacerbate these situation. N-acetyl cysteine (NAC) from inception in the 1970’s as a antidote of APAP toxicity, still finds relevance in the management of accidental or suicidal APAP overdose.

Projects


  • HIV Studies, Stanford University (12/5/2011 - Present)

    Glucose transporter-1 (Glut-1), a receptor for human T-cell leukemia virus (HTLV). HTLV is similar to the human immunodeficiency virus-1 (HIV-1). We show that Glut-1 (an isotope of the glucose carrier) is up-regulated in PBMC treated with Tat and this is much so evident at 5% oxygen tension (physiologic oxygen) compared to 20% oxygen tension (normoxic conditions). Glut-1 induction may be a mechanism for viral entry into T-cells in HIV infection and disease pathogenesis.

    CD3-expressing human null cells. We are currently phenotyping a previously unidentified subset of CD3+ve lymphocytes (null cells) that emerge from CD3-ve population when stimulated with Tat. Upon Tat treatment, these ''Null cells" tend to appear after 16-24 hours and disappear at 48hrs

    Location

    Stanford

Lab Affiliations


Teaching

Graduate and Fellowship Programs


Publications

Journal Articles


  • Protective effect of Juglans nigra on sodium arsenite-induced toxicity in rats. Pharmacognosy research Owumi, S. E., Odunola, O. A., Gbadegesin, M. A., Nulah, K. L. 2013; 5 (3): 183-188

    Abstract

    Consumption of arsenic contaminated water has been implicated in metalloid-induced carcinogenesis. Dietary intake of certain plant products with chemoprotective properties may protect against the onset of diseases and promote maintenance of health.We investigated the outcome of black walnut Juglans nigra (JN) consumption on sodium arsenite (SA)-induced toxicity in rats.WISTER ALBINO RATS WERE TREATED AS FOLLOWS: Control, SA only (positive control) (2.5 mg/kg body weight), JN only (100 mg/kg weight), and JN+SA coadministered. After 5 weeks animals were sacrificed whole blood, femur, liver and testis harvested were assessed for hepatic transaminases and clastogenicity. Histology of the liver, sperm morphology and quality were also assessed. Data were analyzed (ANOVA) and expressed as means ±SD.SA treatment elevated hepatic transaminases level in serum (P < 0.05), induced histological changes in liver: fibroplasia and periportal hepatocytes infiltration by mononuclear cells. These changes were ameliorated by JN (P < 0.05) coadministration. SA induced micronuclei formation (P < 0.05). Again JN decreased (P < 0.05) micronuclei formation by 50%. Sperm count and motility decreased (P < 0.05) in all groups compared to control.JN showed no protection against arsenite effect on sperm quality. Hepatoprotective and anticlastogenic effects were apparent suggesting a chemopreventive potential active against arsenite genotoxicity and chromosomal instability which have implication for metalloid-induced carcinogenesis.

    View details for DOI 10.4103/0974-8490.112425

    View details for PubMedID 23901214

  • Toxicity associated with repeated administration of artemether-lumefantrine in rats. Environ Toxicol. Owumi, S. E., Gbadegesin, M. A., Odunola, O. A., Adegoke, A. M., Uwaifo, A. O. 2013: 7

    View details for DOI 10.1002/tox.21907

  • Co-administration of sodium arsenite and ethanol: Protection by aqueous extract of Aframomum longiscapum seeds. Pharmacognosy research Owumi, S. E., Odunola, O. A., Aliyu, M. 2012; 4 (3): 154-160

    Abstract

    Human exposure to arsenicals, its toxicity, subsequent adverse effects on health has been widely reported and implicated in the etiology of several cancers.We investigated the effect of Aframomum longiscapum (AL) extracts on sodium arsenite (SA) and ethanol (EtOH)-induced toxicities in rats.Male rats were fed SA, EtOH, and SA + EtOH, with or without AL for 5 weeks. Hepatic transaminases were assessed in serum, micronucleated polychromatic erythrocytes (mPCEs) from bone marrow, liver histopathology, and semen quality from caudal epididymis were assessed, respectively, and data were represented as mean ± SD, analyzed by ANOVA.SA, SA + EtOH, and AL alone induced mPCEs formation in rat bone marrow (P < 0.05). A decrease (P < 0.05) in mPCEs in AL + SA + EtOH-treated rats compared with SA, and SA + EtOH was observed. SA and EtOH treatment increased serum hepatic transaminases (P < 0.05) relative to control, while AL treatment resulted in a decrease (P < 0.05). AL, SA, and SA + EtOH treatment decreased sperm count and motility (P < 0.05) with no effect on viability compared with control. Semen morphological abnormalities showed no difference (P > 0.05) across the treated groups. Hepatic histopathology indicated mild mononuclear cellular infiltration in the control group. Necrotic hepatocyte were observed in SA, SA + EtOH treated groups, with no visible lesions seen in the AL treated group. Mild hepatocyte congestion of the portal vessels was observed in AL + SA + EtOH-treated groups.The AL extract exhibited anticlastogenic and hepatoprotective potentials, reduced sperm count, motility, with no effect on viability and morphology. Our findings suggest that AL may mitigate the effect of arsenicals-induced clastogenicity implicated in chemical carcinogenesis.

    View details for DOI 10.4103/0974-8490.99078

    View details for PubMedID 22923953

  • Induction of micronuclei in bone marrow cells and hepatotoxicity of one of the most common over-the-counter pyrethriod insecticide products in Nigeria Toxicological and Environmental Chemistry Oyeronke A. Odunola, Michael A. Gbadegesin, Solomon E. Owumi, Oluwatobi T. Somade 2012; 94 (9): 1822-1831
  • Depletion of Kupffer cells modulates ethanol-induced hepatocyte DNA synthesis in C57Bl/6 mice. Environmental toxicology Owumi, S. E., Corthals, S. M., Uwaifo, A. O., Kamendulis, L. M., Klaunig, J. E. 2012

    Abstract

    Kupffer cells (KCs) are important in hepatic homeostasis and responses to xenobiotics. KCs are activated on interaction with endotoxin, releasing cytokines, and reactive oxygen species normally associated with increased gene expression, cellular growth, or hepatic injury. Ethanol-induced endotoxemia is one means of KC activation. We propose that KC depletion attenuates the effect of EtOH-induced endotoxemia to impact the hepatic growth response. Hepatic DNA synthesis was examined in KC competent (KC+) or KC-depleted (KC-) C57BL/6 mice fed EtOH-containing diet in the presence or absence of polyphenol-60 antioxidant. KC depletion was assessed by F4/80 antigen, and DNA synthesis was assessed by 5-bromo-2'-deoxyuridine incorporation. Tumor necrosis factor alpha (TNF-?) messenger RNA released was quantified by RT-PCR/electrophoresis. ERK1/2 phosphorylation was evaluated by Western blotting, and Nrf2 and CYP2E1protein were also assayed. Apoptosis and hepatic injury were examined by the Tunnel assay and hepatic transaminases in serum, respectively. Hepatic transaminases in serum (AST and ALT) were within normal range. Over 90% of KC was depleted by clodronate treatment. KC depletion decreased TNF-? mRNA release, ERK1/2 phosphorylation, and hepatocyte DNA synthesis. KC depletion is associated with increased numbers of apoptotic cells bodies in KC- mice. Antioxidant treatment decreased DNA synthesis, Nrf2, and CYP2E1 protein expression in EtOH-consuming mice. Our data indicate that upon ethanol exposure, KC participates in hepatic DNA synthesis and growth responses. Collectively, these observations suggest that KC depletion attenuates the downstream effect of ethanol-induced endotoxemia by reduced cytokine and reactive oxygen species production with its concomitant effect on MAPK-signaling pathway on hepatocyte DNA synthesis. © 2012 Wiley Periodicals, Inc.

    View details for PubMedID 22996800

  • Aflatoxin B-1 and ethanol co-exposure induces hepatic oxidative damage in mice TOXICOLOGY AND INDUSTRIAL HEALTH Adedara, I. A., Owumi, S. E., UWAIFO, A. O., Farombi, E. O. 2010; 26 (10): 717-724

    Abstract

    The present study investigated the effects of aflatoxin B? (AFB?) and ethanol co-exposure on biomarkers of hepatic damage in mice. Four groups of adult male mice were treated for 7 consecutive days. Control mice received corn oil alone at a dose of 2 mL/kg bw. One group was treated with ethanol at a dose of 500 µL/kg bw and another group administered 9 mg/kg bw of AFB? dissolved in corn oil. The fourth group was co-administered with ethanol and AFB?. The body and liver weights of treated mice decreased significantly when compared with corresponding control. Alone, ethanol and AFB(1) treatment separately increased serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT) and alkaline phosphatase (ALP). Alcohol dehydrogenase (ALD) activity was markedly elevated in ethanol-treated mice but was unaffected by AFB? treatment. Co-exposure of AFB? and ethanol escalated the activities of these serum enzymes. Administration of ethanol and AFB? separately resulted in significant decrease in both non-enzymatic antioxidant glutathione (GSH) level and enzymatic antioxidant catalase (CAT) and glutathione-S-transferase (GST) activities, whereas lipid peroxidation was markedly elevated. Superoxide dismutase activity and vitamin C level remained unaffected in all treatment groups. Co-exposure of animals to ethanol and AFB? showed additive effects on the activities of GST and CAT as well as on the GSH level. Histopathological study revealed that these compounds interact together to exacerbate their individual effects on the liver. In summary, the data presented showed that AFB? and ethanol co-exposure induced severe oxidative damage to the liver of mice and as such humans consuming excessive amount of ethanol and diets contaminated with AFB? simultaneously may be at greater risk of the hepatotoxic effects of these compounds.

    View details for DOI 10.1177/0748233710377772

    View details for Web of Science ID 000283438900009

    View details for PubMedID 20837563

  • Petroleum Refining Chemicals Enhance Aflatoxin B1-induced Toxicities in Wistar Rats Journal of Medical Sciences Oyeronke A. Odunola, Michael A. Gbadegesin , Solomon E. Owumi, Anthony O. Uwaifo 2007; 7 (4): 615 -619

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