Sandoval Cristian, Mella Luciana, Godoy Karina, Adeli Khosrow, Farías Jorge
Escuela de Tecnología Médica, Facultad de Salud, Universidad Santo Tomás, Los Carreras 753, Osorno 5310431, Chile.
Departamento de Ingeniería Química, Facultad de Ingeniería y Ciencias, Universidad de La Frontera, Temuco 4811230, Chile.
Antioxidants (Basel). 2022 May 23;11(5):1033. doi: 10.3390/antiox11051033.
One of the key routes through which ethanol induces oxidative stress appears to be the activation of cytochrome P450 2E1 at different levels of ethanol intake. Our aim was to determine if oral β-carotene intake had an antioxidant effect on gene expression in mice that had previously consumed ethanol. C57BL/6 mice were used and distributed into: control (C), low-dose alcohol (LA), moderate-dose alcohol (MA), β-carotene (B), low-dose alcohol+β-carotene (LA + B), and moderate-dose alcohol+β-carotene (MA + B). Animals were euthanized at the end of the experiment, and liver tissue was taken from each one. was measured using qPCR to detect liver damage. The relative expression level of each RNA was estimated using the comparative threshold cycle (Ct) technique (2 method) by averaging the Ct values from three replicates. The LA+B (2267 ± 0.707) and MA+B (2.307 ± 0.384) groups had the highest fold change values. On the other hand, the C (1.053 ± 0.292) and LA (1.240 ± 0.163) groups had the lowest levels. These results suggest that ethanol feeding produced a fold increase in protein in mice as compared to the control group. Increased activity was found to support the hypothesis that β-carotene might be dangerous during ethanol exposure in animal models. Our findings imply that β-carotene can increase the hepatic damage caused by low and high doses of alcohol. Therefore, the quantity of alcohol ingested, the exposure period, the regulatory mechanisms of alcoholic liver damage, and the signaling pathways involved in the consumption of both alcohol and antioxidant must all be considered.
乙醇诱导氧化应激的关键途径之一似乎是在不同乙醇摄入量水平下细胞色素P450 2E1的激活。我们的目的是确定口服β-胡萝卜素对先前摄入乙醇的小鼠基因表达是否具有抗氧化作用。使用C57BL/6小鼠并将其分为：对照组（C）、低剂量酒精组（LA）、中等剂量酒精组（MA）、β-胡萝卜素组（B）、低剂量酒精+β-胡萝卜素组（LA + B）和中等剂量酒精+β-胡萝卜素组（MA + B）。在实验结束时对动物实施安乐死，并从每只动物身上获取肝脏组织。使用qPCR检测肝脏损伤来测量[具体指标未给出]。通过对三个重复样本的Ct值求平均值，使用比较阈值循环（Ct）技术（2−ΔΔCt方法）估计每个RNA的相对表达水平。LA+B组（2.267±0.707）和MA+B组（2.307±0.384）具有最高的[具体指标未给出]倍数变化值。另一方面，C组（1.053±0.292）和LA组（1.240±0.163）水平最低。这些结果表明，与对照组相比，给小鼠喂食乙醇使[具体指标未给出]蛋白增加了[倍数未明确]。发现[具体指标未给出]活性增加支持了β-胡萝卜素在动物模型乙醇暴露期间可能有害的假设。我们的研究结果表明，β-胡萝卜素会增加低剂量和高剂量酒精引起的肝脏损伤。因此，必须考虑摄入的酒精量、暴露时间、酒精性肝损伤的调节机制以及酒精和抗氧化剂摄入所涉及的信号通路。
