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Item Indole-3-propionic acid mitigates chlorpyrifos-mediated neurotoxicity by modulating cholinergic and redox-regulatory systems, inflammatory stress, apoptotic responses and DNA damage in rats(Elsevier B.V., 2022) Owumi, S. E.; Adedara, I. A.; Oyelere, A. K.This study probed the neuroprotective influence of indole-3-propionic acid (IPA) in rats exposed to chlorpyrifos (CPF) alone at 5 mg/kg body weight or co-administered with IPA at 12.5 and 25 mg/kg for 14 days. Behavioral data indicated that IPA significantly (p < 0.05) abated CPF-mediated anxiogenic-like behaviors with concomitant improvement in the locomotor and exploratory behaviors as substantiated by track plots and heat maps data. Also, IPA mitigated CPF-mediated diminution in cholinergic and antioxidant defense systems whereas it mark- edly improved thioredoxin level and thioredoxin reductase activity in cerebral and cerebellar tissues of the animals. Co-administration of IPA significantly enhanced anti-inflammatory cytokine, interleukin-10 but sup- pressed oxidative and inflammatory stress, caspase-9 and caspase-3 activation with concomitant reduction in 8- hydroxy-2'-deoxyguanosine (8-OHdG) level and histological damage. Collectively, IPA-mediated neuro- protection involves modulation of cholinergic and redox-regulatory systems, inflammatory stress, apoptotic re- sponses and DNA damage in cerebrum and cerebellum of rats.Item Neuroprotective role of gallic acid in aflatoxin Bi-induced behavioral abnormalities in rats(Wiley Periodicals LLC, 2020) Adedara, I. A.; Owumi, S. E.; Oyelere, A. K.; Farombi, E. O.The neurotoxic impact of dietary exposure to aflatoxin Bi (AFBJ is documented in experimental and epidemiological studies. Gallic acid (GA) is a triphenolic phyto- chemical with potent anticancer, anti-inflammatory, and antioxidant activities. There is a knowledge gap on thè influence of GA on AFBi-induced neurotoxicity. This study probed thè influence of GA on neurobehavioral and biochemical abnormalities in rats orally treated with AFBi per se (75pg/kg body weight) or administered together with GA (20 and 40mg/kg) for 28 uninterrupted days. Behavioral endpoints obtained with video-tracking software demonstrated sig-nificant (p<.05) abatement of AFBrinduced anxiogenic-like behaviors (increased freezing, urination, and fecal bolus discharge), motor and locomotor inadequacies, namely increased negative geotaxis and diminished grip strength, absolute turn angle, total time mobile, body rotation, maximum speed, and total distance traveled by GA. The improvement of exploratory behavior in animals that received both AFBi and GA was confirmed by track plots and heat maps appraisal. Abatement of AFBj-induced decreases in acetylcholinesterase activity, antioxidant status and glutathione level by GA was accompanied by a marked reduction in oxidative stress markers in thè cerebellum and cerebrum of rats. Additionally, GA treatment abro- gated AFBi-mediated decrease in interleukin-10 and elevation of inflammatory in- dices, namely tumor necrosis factor-a, myeloperoxidase activity, interleukin-l|3, and nitric oxide. Further, GA treatment curtailed caspase-3 activation and histological injuries in thè cerebral and cerebellar tissues. In conclusion, abatement of AFBi-induced neurobehavioral abnormalities by GA involves anti-inflammatory, antioxidant, and antiapoptotic mechanisms in rats.Item Gallic acid enhances reproductive function by modulating oxidoinflammatory and apoptosis mediators in rats exposed to aflatoxin-B1(Society for Experimental Biology and Medicine, 2020) Owumi, S. E.; Adedara, I. A.; Akomolafe, A. P.; Farombi, E. O.; Oyelere, A. K.Aflatoxin B1 (AFB1) is reported to elicit adverse reproductive outcomes in animals. Gallic acid (GA) is known to exhibit antioxidant and inflammatory bioactivities. The impact of GA on AFB1-facilitated reproductive dysfunction is nonexistent in literature. This investigation elucidated GA protective effect on AFB1-induced reproductive toxicities in rats, exposed for 28 consecutive days to AFB1 (75 mg/kg), or co-treated with GA (20 or 40 mg/kg) body weight. AFB1 significantly (p<0.05) reduced testicular function biomarkers, serum hormonal levels, and functional sperm characteristics in experimental animals. GA abated AFB1-induced increases (p<0.05) in lipid peroxidation and reactive oxygen and nitrogen species, suppressed myeloperoxidase, interleukin-1b, nitric oxide, and tumor necrosis factor-a levels—inflammatory biomarkers—in testes, epididymis, and hypothalamus. Furthermore, GA improved antioxidant defenses and alleviated reduction in interleukin-10, caspase-3 activation, and histological variations in epididymis, testes, and hypothalamus of rats dosed with AFB1. Conclusively, GA enhanced reproductive function in AFB1-exposed rats by modulating inflammatory, oxidative stress, and apoptosis mediators.Item Protocatechuic acid modulates reproductive dysfunction linked to furan exposure in rats(Elsevier B.V., 2020) Owumi, S. E.; Adedara, I. A.; Farombi, E. O.; Oyelere, A. K.The reproductive toxicity associated with furan exposure in both animals and humans has been documented. Protocatechuic acid (PCA), a dietary polyphenolic chemical, reportedly elicits beneficial effects on the male reproductive system. However, the influence of PCA on the reproductive toxicity related to furan exposure is unavailable in the literature. The current study evaluated the effects of PCA on the dysfunctional reproductive axis caused by furan exposure in rats. Experimental animals were exposed to furan (8 mg/kg) or co-treated with furan (8 mg/kg) and PCA (25 or 50 mg/kg) for twenty-eight successive days. Results revealed that PCA treatment significantly alleviated furan-mediated declines in sperm production and characteristic qualities as well as in serum levels of prolactin, luteinizing hormone, follicle-stimulating hormone, and testosterone. Further, PCA attenuated furan-induced reduction in antioxidant enzyme activities and testicular function marker enzymes, namely lactate dehydrogenase, glucose-6-phosphate dehydrogenase, acid phosphatase, and alkaline phospha- tase. PCA effectively mitigated furan-mediated increases in myeloperoxidase activity, levels of reactive oxygen and nitrogen species, nitric oxide, tumour necrosis factor-alpha, and interleukin-1^ in testes, epididymis, and hypothalamus of rats. Moreover, PCA increased anti-inflammatory cytokine interleukin-10 but suppressed cas- pase-9 and caspase-3 activities and ameliorated injuries in the testes, epididymis, and hypothalamus of furan- treated rats. In conclusion, PCA ameliorated deficits in the hypothalamic-pituitary-gonadal axis function in furan-exposed rats by suppressing oxido-inflammatory stress and apoptosis.