Change-Laboratory, Cancer Research and Molecular Biology Laboratories, Department of Biochemistry, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria.
Nutritional and Industrial Biochemistry Research Laboratories, Department of Biochemistry, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria.
Andrologia. 2022 Feb;54(1):e14248. doi: 10.1111/and.14248. Epub 2021 Sep 20.
We assessed the individual and combined consequence of 3-indolepropionic acid on aflatoxin B1-induced reproductive toxicity in rats. The experimental cohorts were dosed for four consecutive weeks with aflatoxin B1 (50 μg/kg), 3-indolepropionic acid (50 mg/kg), and both (aflatoxin B1: 50 μg/kg + 3-indolepropionic acid: 25 or 50 mg/kg), and the untreated control. Following sacrifice, biomarkers of testicular, epididymal and hypothalamic oxidative status, lipid peroxidation, reactive oxygen and nitrogen species, nitric oxide levels and myeloperoxidase activity were determined. Besides, tumour necrosis factor-alpha, Bcl-2 and Bax proteins were also assessed. Aflatoxin B1-induced testicular, epididymal and hypothalamic oxidative stress was significantly alleviated with 3-indolepropionic acid co-treatment. Also, increases in biomarkers of oxidative stress and reduced levels of antioxidants were abated significantly in rats co-treated with 3-indolepropionic acid. Aflatoxin B1-mediated increase in tumour necrosis factor-alpha, Bax, nitric oxide and myeloperoxidase activity in the examined organs was decreased significantly in aflatoxin B1 and 3-indolepropionic acid co-treated rats. Also, 3-indolepropionic acid dose dependently reduced Bcl-2 levels in the treated rats. The degree of aflatoxin B1-induced histopathological injuries was minimised in rats co-treated with 3-indolepropionic acid. Our results demonstrated that 3-indolepropionic acid protected experimental rats from aflatoxin B1-induced oxido-inflammatory stress and apoptotic response in the examined organs.
我们评估了 3-吲哚丙酸对黄曲霉毒素 B1 诱导的大鼠生殖毒性的个体和联合影响。实验组连续四周给药,分别给予黄曲霉毒素 B1(50μg/kg)、3-吲哚丙酸(50mg/kg)和两者(黄曲霉毒素 B1:50μg/kg+3-吲哚丙酸:25 或 50mg/kg),以及未处理的对照组。处死动物后,测定睾丸、附睾和下丘脑氧化应激、脂质过氧化、活性氧和氮物种、一氧化氮水平和髓过氧化物酶活性的生物标志物。此外,还评估了肿瘤坏死因子-α、Bcl-2 和 Bax 蛋白。3-吲哚丙酸共同处理显著减轻了黄曲霉毒素 B1 引起的睾丸、附睾和下丘脑氧化应激。此外,用 3-吲哚丙酸共同处理的大鼠,氧化应激生物标志物的增加和抗氧化剂水平的降低也显著减轻。黄曲霉毒素 B1 介导的肿瘤坏死因子-α、Bax、一氧化氮和髓过氧化物酶活性在检查器官中的增加在黄曲霉毒素 B1 和 3-吲哚丙酸共同处理的大鼠中显著降低。此外,3-吲哚丙酸剂量依赖性地降低了处理大鼠中 Bcl-2 的水平。在用 3-吲哚丙酸共同处理的大鼠中,黄曲霉毒素 B1 诱导的组织病理学损伤的程度最小化。我们的结果表明,3-吲哚丙酸保护实验大鼠免受黄曲霉毒素 B1 诱导的氧化炎症应激和检查器官中的细胞凋亡反应。