Diethylnitrosamine（DEN）是一种肝致癌物，存在于多种烟熏和油炸食品中，并被报道在小鼠中具有肝毒性。羟基苯甲醚（BHT）是一种强效抗氧化剂，用于化妆品配方和作为食品添加剂和防腐剂。因此，BHT被研究作为在乙醇二乙氨基（DEN）诱导的HCC的早期阶段中的潜在抑制剂。雄性Wistar白化鼠（n=24）被均分为四组。第1组为阴性对照组；第2和3组分别接受BHT和DEN；第4组接受BHT后接受DEN。提取血样和大鼠肝脏进行生化和组织学检查。肝毒性通过增加肝酶和HCC指标以及降低抗氧化和前凋亡因子来评估。AFP、AFPL3、GPC3、GSH、SOD、MDA、CASP3和BAX的表达在DEN处理后显著增加。DEN还降低了GPx、CAT和CYP2E1活性以及BCl-2的表达。此外，DEN还引起了肝实质的组织学改变。BHT预处理增强了抗氧化状态，同时防止了大多数组织学和生化变化。BHT预处理通过降低氧化应激，触发内在有丝分裂凋亡并预防肝脏组织中的组织学改变，抑制了DEN引发的HCC。

Diethylnitrosamine (DEN), a hepatocarcinogen, is found in a variety of smoked and fried foods and was reported to be hepatotoxic in mice. Butylated hydroxytoluene (BHT) is a potent antioxidant used in cosmetic formulations and as a food additive and preservative. As a result, BHT was studied as a potential inhibitor in the early stages of diethylnitrosamine (DEN)-induced HCC. Male Wistar albino rats (n = 24) were equally subdivided. Group 1 was the negative control; Group 2 and 3 administered BHT and DEN, respectively; Group 4 received BHT followed by DEN. Blood samples and rat livers were taken for biochemical and histological investigation. Hepatotoxicity was assessed by increased liver enzymes and HCC indicators, along with reduced antioxidant and pro-apoptotic factors. AFP, AFPL3, GPC3, GSH, SOD, MDA, CASP3 and BAX expression increased significantly after DEN treatment. DEN also reduced GPx, CAT, and CYP2E1 activity, and BCl-2 expression. Moreover, in the hepatic parenchyma, the DEN caused histological alterations. Pretreatment with BHT enhanced antioxidant status while preventing histopathological and most biochemical alterations. BHT pretreatment suppresses DEN-initiated HCC by decreasing oxidative stress, triggering intrinsic mitotic apoptosis, and preventing histopathological changes in liver tissue.