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.

中文翻译：

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没食子酸通过调节暴露于黄曲霉毒素B1的大鼠中的氧化炎症和细胞凋亡介质来增强生殖功能。

据报道黄曲霉毒素B1（AFB1）会引起动物不利的生殖结果。没食子酸（GA）表现出抗氧化剂和炎症生物活性。在文献中不存在GA对AFB1促进的生殖功能障碍的影响。这项研究阐明了GA对AFB1诱导的大鼠生殖毒性的保护作用，该毒性连续28天暴露于AFB1（75 µg / kg），或与GA（20或40 mg / kg）体重共同治疗。AFB1显着（p  <  0.05）降低了实验动物的睾丸功能生物标志物，血清激素水平和功能性精子特征。GA减轻了AFB1引起的增加（p  < 0.05）的脂质过氧化和活性氧和氮物种，抑制了睾丸，附睾和下丘脑的髓过氧化物酶，白介素-1β，一氧化氮和肿瘤坏死因子-α水平（炎性生物标志物）。此外，GA改善了抗氧化剂防御能力，并减轻了补充AFB1的大鼠白细胞介素10，胱天蛋白酶3活化以及附睾，睾丸和下丘脑组织学变化的减少。结论是，GA通过调节炎症，氧化应激和凋亡介体，增强了AFB1暴露大鼠的生殖功能。

影响陈述

生殖不足引起的不孕症可能会令人压力大。据报道，暴露于黄曲霉毒素B1（一种在食物中储存不当的饮食中的霉菌毒素）会引起生殖功能不全和不育。因此，我们检查没食子酸（GA）的植物化学，识别为表现出的可能有益作用的体外和体内由于AFB1的毒性取决于氧化环氧化物的形成，因此针对大鼠氧化应激和相关炎症损害的药理生物活性，旨在提供新的证据来促进植物来源的化学预防剂在营养领域的应用。我们的发现将通过介绍GA文献中缺少的数据来推进化学预防领域。我们的研究结果进一步证明了GA可以保护AFB1介导的大鼠睾丸，附睾和下丘脑的组织学损伤。抑制氧化损伤，缓解炎症和凋亡反应，恢复精子功能特性以及与生殖完整性和功能有关的激素水平。