Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Department of Medical Biochemistry, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Toxicol Mech Methods. 2021 Jul;31(6):467-475. doi: 10.1080/15376516.2021.1916667. Epub 2021 May 23.
The major sources for human exposure to Benzo [] pyrene (B[a]P) are contaminated food, water, and inhalation of polycyclic aromatic hydrocarbon. B[]P is a well-known human genotoxic carcinogen (IARC Group 1). It has a tumorigenic potential in virtually all experimental animal model systems. The study aimed to evaluate the effect of catechin hydrate (CH) against B [] P-induced toxicity in the lung of adult albino rats. Thirty-six adult male albino rats (150-200 g) were divided into six groups, three control groups, and three experimental groups: B[] P-treated group, (CH)-treated group, and B[a] P+(CH)-treated group. At the end of the fourth week of the study, blood samples and lung tissues were obtained for the biochemical and genotoxicity, RT-PCR, histopathological, and immunohistochemical investigations, respectively. Our results clarified that B[] P exposure caused a subsequent decrease in the activities of antioxidant enzymes (SOD, CAT), and conversely (MDA) levels elevated markedly. Also, B[] P induced DNA damages and activated the apoptotic pathway, presented by upregulated Bax, caspase-3, and downregulated Bcl-2 gens. However, treatment with CH increased antioxidant enzymes as well as regulated apoptosis. Discernible histological changes in the lung also supported the protective effects of CH. These findings suggested that CH is an effective natural product that attenuates Benzo [] pyrene-induced lung toxicity.
人类接触苯并[a]芘（B[a]P）的主要来源是受污染的食物、水和多环芳烃吸入。B[a]P 是一种众所周知的人类遗传毒性致癌物质（IARC 组 1）。它在几乎所有的实验动物模型系统中都具有致癌潜力。本研究旨在评估儿茶素（CH）对成年白化大鼠肺中 B[a]P 诱导毒性的影响。将 36 只成年雄性白化大鼠（150-200g）分为六组，三组对照组和三组实验组：B[a]P 处理组、（CH）处理组和 B[a]P+（CH）处理组。在研究的第四周结束时，分别采集血液样本和肺组织，用于生化和遗传毒性、RT-PCR、组织病理学和免疫组织化学研究。我们的结果表明，B[a]P 暴露导致抗氧化酶（SOD、CAT）的活性随后下降，而（MDA）水平显著升高。此外，B[a]P 诱导了 DNA 损伤并激活了凋亡途径，表现为 Bax、caspase-3 上调和 Bcl-2 下调。然而，CH 的治疗增加了抗氧化酶并调节了凋亡。肺的明显组织学变化也支持 CH 的保护作用。这些发现表明 CH 是一种有效的天然产物，可减轻苯并[a]芘引起的肺毒性。
