Gallic acid enhances reproductive function by modulating oxido-inflammatory and apoptosis mediators in rats exposed to aflatoxin-B1

• Published in: Experimental biology and medicine (Maywood, N.J.) Vol. 245; no. 12; pp. 1016 - 1028
• Main Authors: Owumi, Solomon E, Adedara, Isaac A, Akomolafe, Ayomide P, Farombi, Ebenezer O, Oyelere, Adegboyega K
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01-06-2020
• Subjects: Aflatoxin B1 - adverse effects; Animals; Antioxidants - physiology; Apoptosis - drug effects; Apoptosis Regulatory Proteins - metabolism; Biomarkers - metabolism; Epididymis - drug effects; Epididymis - metabolism; Gallic Acid - pharmacology; Hypothalamus - drug effects; Hypothalamus - metabolism; Inflammation - drug therapy; Inflammation - metabolism; Male; Original Research; Oxidation-Reduction - drug effects; Oxidative Stress - drug effects; Rats; Rats, Wistar; Reproduction - drug effects; Spermatozoa - drug effects; Spermatozoa - metabolism; Testis - drug effects; Testis - metabolism; Aflatoxin B1; inflammation; gallic acid; reproductive deficits; oxidative stress; caspase-3
• ISSN: 1535-3702; 1535-3699
• DOI: 10.1177/1535370220936206

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 µg/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-1β, nitric oxide, and tumor necrosis factor-α 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.
Impact statement
Infertility resulting from reproductive deficiency can be stressful. Exposure to aflatoxin B1, a dietary mycotoxin prevalent in improperly stored grains, is reported to elicit reproductive insufficiencies and infertility. We, therefore, examined the likely beneficial effect of gallic acid (GA) a phytochemical, recognized to exhibit in vitro and in vivo pharmacological bioactivities against oxidative stress and related inflammatory damages in rats, since AFB1 toxicities are predicated on oxidative epoxide formation, in a bid to proffer new evidence to advance the field of nutriceutical application from plant-derived chemopreventive agents. Our findings will advance the field of chemoprevention by presenting data absent in the literature on GA. Our results demonstrate further evidence for GA conferred protection against AFB1-mediated histological lesions in testes, epididymis, and hypothalamus of treated rats; suppresses oxidative damages, relieved inflammatory and apoptotic responses, restored sperm functional characteristics, and hormonal levels relevant for reproductive integrity and function.