Publications by authors named "Oluwakemi A Rotimi"

7 Publications

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A Review of Cancer Genetics and Genomics Studies in Africa.

Front Oncol 2020 15;10:606400. Epub 2021 Feb 15.

Department of Translational Genomics, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.

Cancer is the second leading cause of death globally and is projected to overtake infectious disease as the leading cause of mortality in Africa within the next two decades. Cancer is a group of genomic diseases that presents with intra- and inter-population unique phenotypes, with Black populations having the burden of morbidity and mortality for most types. At large, the prevention and treatment of cancers have been propelled by the understanding of the genetic make-up of the disease of mostly non-African populations. By the same token, there is a wide knowledge gap in understanding the underlying genetic causes of, and genomic alterations associated with, cancer among black Africans. Accordingly, we performed a review of the literature to survey existing studies on cancer genetics/genomics and curated findings pertaining to publications across multiple cancer types conducted on African populations. We used PubMed MeSH terms to retrieve the relevant publications from 1990 to December 2019. The metadata of these publications were extracted using R text mining packages: RISmed and Pubmed.mineR. The data showed that only 0.329% of cancer publications globally were on Africa, and only 0.016% were on cancer genetics/genomics from Africa. Although the most prevalent cancers in Africa are cancers of the breast, cervix, uterus, and prostate, publications representing breast, colorectal, liver, and blood cancers were the most frequent in our review. The most frequently reported cancer genes were , , and . Next, the genes reported in the reviewed publications' abstracts were extracted and annotated into three gene ontology classes. Genes in the class were mostly associated with , while those in and classes were mainly associated with cell process, biological regulation, and binding, and catalytic activity, respectively. Overall, this review highlights the paucity of research on cancer genomics on African populations, identified gaps, and discussed the need for concerted efforts to encourage more research on cancer genomics in Africa.
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http://dx.doi.org/10.3389/fonc.2020.606400DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7917259PMC
February 2021

Early Life Exposure to Aflatoxin B1 in Rats: Alterations in Lipids, Hormones, and DNA Methylation among the Offspring.

Int J Environ Res Public Health 2021 01 12;18(2). Epub 2021 Jan 12.

Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI 48109, USA.

Aflatoxins are toxic compounds produced by molds of the species that contaminate food primarily in tropical countries. The most toxic aflatoxin, aflatoxin B1 (AFB1), is a major cause of hepatocellular carcinoma (HCC) in these countries. In sub-Saharan Africa, aflatoxin contamination is common, and perinatal AFB1 exposure has been linked to the early onset of HCC. Epigenetic programming, including changes to DNA methylation, is one mechanism by which early life exposures can lead to adult disease. This study aims to elucidate whether perinatal AFB1 exposure alters markers of offspring health including weight, lipid, and hormone profiles as well as epigenetic regulation that may later influence cancer risk. Pregnant rats were exposed to two doses of AFB1 (low 0.5 and high 5 mg/kg) before conception, throughout pregnancy, and while weaning and compared to an unexposed group. Offspring from each group were followed to 3 weeks or 3 months of age, and their blood and liver samples were collected. Body weights and lipids were assessed at 3 weeks and 3 months while reproductive, gonadotropic, and thyroid hormones were assessed at 3 months. Prenatal AFB1 (high dose) exposure resulted in significant 16.3%, 31.6%, and 7.5% decreases in weight of the offspring at birth, 3 weeks, and 3 months, respectively. Both doses of exposure altered lipid and hormone profiles. Pyrosequencing was used to quantify percent DNA methylation at tumor suppressor gene and growth-regulator in DNA from liver and blood. Results were compared between the control and AFB1 exposure groups in 3-week liver samples and 3-week and 3-month blood samples. Relative to controls, DNA methylation in both low- and high-dose exposed rats was significantly decreased in liver samples and increased in the blood ( < 0.05 in linear mixed models). methylation was higher in the liver from low- and high-exposed rats and decreased in 3-month blood samples from the high exposure group ( < 0.05). Further research is warranted to determine whether such hormone, lipid, and epigenetic alterations from AFB1 exposure early in life play a role in the development of early-onset HCC.
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http://dx.doi.org/10.3390/ijerph18020589DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7828191PMC
January 2021

Bisphenol A in Africa: A review of environmental and biological levels.

Sci Total Environ 2021 Apr 9;764:142854. Epub 2020 Oct 9.

Department of Biochemistry, Covenant University, Nigeria.

Bisphenol A (BPA) is a synthetic ubiquitous environmental toxicant present in many industrial and consumer products. BPA is recognized as an endocrine-disrupting chemical (EDC), and its mechanisms of perturbation of the physiological process include interference with hormone pathways and epigenetic modifications. An increase in industrial productions and food packaging across Africa has resulted in increased utilization of BPA-containing products with a concomitant increase in environmental bioaccumulation and human exposure. In order to assess the extent of this bioaccumulation, we identified, collated, and summarized the levels of BPA that have been reported across Africa. To achieve this aim, we performed a systematic search of four indexing databases to identify articles and extracted the necessary data from the selected articles. Of the 42 publications we retrieved, 42% were on water samples, 22% on food, 20% on human biological fluids, 10% on sediments, soils, and sludge and 6% on consumer and personal care products (PCPs). The highest level of BPA reported in literature across Africa was 251 ng/mL, 384.8 ng/mL, 937.49 ng/g, 208.55 ng/mL, 3,590 μg/g, and 154,820 μg/g for water, wastewater, food, biological fluids, consumer and PCPs, and semisolids, respectively. This review presented a comparative perspective of these levels relative to regulatory limits and levels reported from other continents. Finally, this review highlighted critical needs for the regulation of BPA across Africa in order to stem its environmental and toxicological impact. We hope that this review will stimulate further research in understanding the impact of BPA on health outcomes and wellbeing across Africa.
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http://dx.doi.org/10.1016/j.scitotenv.2020.142854DOI Listing
April 2021

Time-Course Effects of Acute Aflatoxin B1 Exposure on Hepatic Mitochondrial Lipids and Oxidative Stress in Rats.

Front Pharmacol 2019 7;10:467. Epub 2019 May 7.

Department of Biochemistry and Molecular Biology Research Laboratory, Covenant University, Ota, Nigeria.

Aflatoxins are secondary metabolites of certain species, that contaminate staple foods, particularly in developing countries. Aflatoxin B1 (AFB1) is the most toxic and common of the major types of aflatoxins. AFB1 is hepatotoxic and has been implicated in increasing the risk of hepatocellular carcinoma (HCC). We have previously shown that subacute exposure to AFB1 for 7 days disrupts hepatic lipids; therefore, this study determined the time-course effects of acute aflatoxin exposure on hepatic mitochondrial lipids and oxidative stress. To achieve this, thirty male albino rats were randomly assigned to six groups. The groups received an oral dose of 1 mg/kg body weight AFB1 or vehicle only (controls) for one, four, or seven days, respectively. Twenty-four hours after the last dose, the animals were sacrificed and liver excised. Mitochondria and cytosolic fractions were obtained from the liver after which lipids (cholesterol, triacylglycerols) were determined in the mitochondria while biomarkers of oxidative stress (glutathione, glutathione transferase (GST), glutathione peroxidase (GPx), glutathione reductase, nitric oxide (NO), malonaldehyde (MDA), thioredoxin reductase (TR), and superoxide dismutase (SOD) were determined spectrophotometrically in the mitochondria and cytosolic fractions. The expression of genes (, , , and ) were determined using quantitative RT-PCR. Results showed that AFB1 significantly increased mitochondrial cholesterol at day seven (treatment vs. control, = 0.016). It also increased the concentrations of NO and MDA at day one and day seven while the activity of GPx and concentration of GSH were increased at day seven ( = 0.030) and day one ( = 0.025) alone, respectively, compared to control. The activities of cytosolic GR ( = 0.014), TR ( = 0.046) and GST ( = 0.044) were increased at day seven. AFB1 significantly increased the expression of ( = 0.029) and decreased the expression of ( = 0.005) at day one. This study revealed that AFB1 disrupts hepatic mitochondrial lipids and antioxidant capacity. These changes were dependent on the timing of exposure and did not follow a linear time-course trend. These alterations could be part of the hepatic mitochondria response mechanism to acute AFB1 toxicity.
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http://dx.doi.org/10.3389/fphar.2019.00467DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6514194PMC
May 2019

Oxidative Stress in Extrahepatic Tissues of Rats Co-Exposed to Aflatoxin B1 and Low Protein Diet.

Toxicol Res 2018 Jul 15;34(3):211-220. Epub 2018 Jul 15.

Department of Biochemistry, University of Ilorin, Ilorin, Nigeria.

Early life exposure to aflatoxin B1 (AFB1) and low protein diet through complementary foods during weaning is common in parts of Africa and Asia. This study evaluated the effect of co-exposure to AFB1 and low protein diet on the extrahepatic tissues of rats. Twenty-four three-week old weanling male albino rats were used for this study and were randomly assigned into four groups: group 1 served as control and was fed normal protein diet (20% protein), group 2 was fed low protein diet (5% protein), group 3 was fed normal protein diet + 40 ppb AFB1 while group 4 received low protein diet + 40 ppb AFB1, all for eight weeks. Afterward, biomarkers of anemia (packed cell volume (PCV), hemoglobin) and kidney function (urea, uric acid, and creatinine) were determined in the blood while biomarkers of oxidative stress were determined in the tissues spectrophotometrically. Co-exposure to AFB1 and low protein diet significantly ( < 0.05) decreased body weight gain and PCV, increased biomarkers of kidney functions and induced oxidative stress in the tissues studied. There was significant ( < 0.05) reduction in glutathione concentration while TBARS was significantly increased in the tissues. Co-exposure to AFB1 and low protein diet had additive effects on decreasing the weight gain and potentiation effect of kidney dysfunction in the rats. The co-exposure also decreased antioxidant enzymes and increased oxidant status in the tissues. Our results demonstrate that this co-exposure has deleterious health effects on extrahepatic tissues and should be a public health concern especially in developing countries where AFB1 contamination is common.
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http://dx.doi.org/10.5487/TR.2018.34.3.211DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057291PMC
July 2018

Coexistence of Aflatoxicosis with Protein Malnutrition Worsens Hepatic Oxidative Damage in Rats.

J Biochem Mol Toxicol 2016 Jun 25;30(6):269-76. Epub 2016 Jan 25.

Department of Biochemistry, University of Ilorin, Ilorin, Nigeria.

To investigate the effects of the coexistence of aflatoxin B1 (AFB1) and protein malnutrition in rat liver, weanling rats were fed either normal protein diet (20% protein), low-protein (PEM) diet (5%), normal protein diet + 40 ppb AFB1, or low-protein diet + 40 ppb AFB1. After 8 weeks, biomarkers of hepatic functions and oxidative stress, caspase-3 activity, and tumor suppressor protein 53 (p53) were determined spectrophotometrically. Randomly amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) was employed to determine genomic alterations among the groups. Coexistence of aflatoxicosis and PEM significantly decreased glutathione, glutathione-S-transferase, glutathione peroxidase, and superoxide dismutase, while it increased peroxidase and catalase. RAPD-PCR showed genomic alterations that were associated with significant increases in p53 level and caspase-3 activity in rats fed PEM diet + AFB1. In conclusion, the coexistence of aflatoxicosis and protein malnutrition induced oxidative stress with concomitant genomic alterations in the liver of weanling rats.
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http://dx.doi.org/10.1002/jbt.21787DOI Listing
June 2016

Persistence of acidosis in alloxan-induced diabetic rats treated with the juice of Asystasia gangetica leaves.

Pharmacogn Mag 2011 Jan;7(25):25-30

Biochemistry Unit, Department of Biological Sciences, Covenant University, Ota, Nigeria.

Background: Diabetes mellitus is gradually becoming a global health burden leading to an increase in the search for herbal hypoglycemic agents as alternatives to synthetic ones. Asystasia gangetica is one of the herbs used in folklore system of medicine for managing hypoglycaemia associated with diabetes.

Materials And Methods: The influence of the juice of A. gangetica leaf on alloxan-induced diabetic rats was assessed by treating diabetic rats with 25%, 50% and 75% fresh juice and glibenclamide for 5 weeks. Afterwards, the plasma concentrations of glucose, triacylglycerols, total cholesterol, high-density lipoprotein (HDL) cholesterol, thiobarbituric acid reactive substances and bicarbonate were assayed spectrophotometrically.

Results: Treatment of the diabetic rats with the juice significantly (P < 0.05) reduced the elevated plasma levels of glucose to a level not significantly (P > 0.05) different from that of glibenclamide. The juice also significantly (P < 0.05) reduced the plasma lipid peroxidation and improved the lipid profile, as indicated by a significant (P < 0.05) reduction in the total cholesterol: HDL cholesterol ratio. However, there was a significant (P < 0.05) rise in the level of bicarbonate as result of the juice treatment from 28.15 ± 2.82 mmol/l in normal control to 60.83 ± 17.46 mmol/l in diabetic control and to 122.20 ± 34.68 mmol/l, 120.95 ± 35.09 mmol/l and 115.85 ± 11.79 mmol/l in 25%, 50% and 75% juice, respectively.

Conclusion: Therefore, this inability of A. gangetica to prevent acidosis detracts from the potential of its usefulness in managing diabetes.
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http://dx.doi.org/10.4103/0973-1296.75887DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065152PMC
January 2011