Benzo(a)pyrene (BaP), an important environmental pollutant, is produced as the result of incomplete combustion of organic materials in many industries and food cooking process. It has been purposed that BaP induces hepatotoxicity through oxidative stress and apoptosis. Several studies have shown that melatonin can protect against chemical-induced apoptosis through autophagy pathway. In this study, we assessed the modulating effect of melatonin, a well-known antioxidant, on BaP-induced hepatotoxicity through induction of autophagy. Thirty male mice were treated daily for 28 consecutive days. BaP (75 mg/kg; oral gavage) and melatonin (10 and 20 mg/kg, i.p.) were administered to mice. The liver histopathology and the levels of apoptosis and autophagy proteins as well as the expression of miR-34a were determined. The BaP exposure induced severe liver histological injury and markedly enhanced AST, ALT and MDA level. Also, apoptosis proteins and hepatic miR-34a expression increased. However, the level of Sirt1 and autophagy markers such as LC3 II/I ratio and Beclin-1 reduced. The co-administration of melatonin reversed all changes caused by BaP. In summary, melatonin appears to be effective in BaP-induced hepatotoxicity maybe through the miR-34a/Sirt1/autophagy molecular pathway.

苯并（a）re（BaP）是一种重要的环境污染物，是许多行业和食品烹饪过程中有机材料不完全燃烧的结果。目的是BaP通过氧化应激和凋亡诱导肝毒性。几项研究表明，褪黑激素可以通过自噬途径防止化学诱导的细胞凋亡。在这项研究中，我们评估了褪黑素（一种著名的抗氧化剂）通过自噬诱导对BaP诱导的肝毒性的调节作用。每天治疗三十只雄性小鼠，连续28天。将BaP（75 mg / kg;口服管）和褪黑激素（10和20 mg / kg，腹膜内）给予小鼠。测定肝脏的组织病理学，凋亡和自噬蛋白的水平以及miR-34a的表达。BaP暴露可导致严重的肝脏组织学损伤，并显着增强AST，ALT和MDA水平。而且，凋亡蛋白和肝miR-34a表达增加。但是，Sirt1和自噬标志物如LC3 II / I比和Beclin-1的水平降低。褪黑激素的共同给药逆转了由BaP引起的所有变化。总之，褪黑激素可能通过miR-34a / Sirt1 /自噬分子途径对BaP诱导的肝毒性有效。