Alcohol metabolism takes place primarily in the liver. Initial exposures to ethanol have a major impact on the hepatic redox state and intermediary metabolism as a consequence of ethanol metabolism via alcohol dehydrogenase. However, upon continued exposure to ethanol, the progression of liver injury involves ethanol metabolism via CYP2E1 and consequent oxidant stress, as well as potential direct effects of ethanol on membrane proteins that are independent of ethanol metabolism. Multiple organ systems contribute to liver injury, including the innate immune system and adipose tissue. In response to ethanol exposure, specific signal transduction pathways, including NFkappaB and the mitogen-activated protein kinase family members ERK1/2, JNK, and p38, are activated. These complex responses to ethanol exposure translate into activation of nuclear transcription factors and altered gene expression within the liver, leading to the development of steatosis and inflammation in the early stages of alcohol-induced liver injury.

中文翻译：

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酒精代谢的分子方面：参与早期乙醇诱导的肝损伤的转录因子。

酒精代谢主要发生在肝脏中。由于乙醇通过乙醇脱氢酶的代谢，最初暴露于乙醇会对肝脏的氧化还原状态和中间代谢产生重大影响。但是，继续暴露于乙醇后，肝损伤的进展包括经由CYP2E1的乙醇代谢和随之而来的氧化应激，以及乙醇对独立于乙醇代谢的膜蛋白的潜在直接作用。多器官系统导致肝损伤，包括先天免疫系统和脂肪组织。响应乙醇暴露，包括NFkappaB和有丝分裂原激活的蛋白激酶家族成员ERK1 / 2，JNK和p38在内的特定信号转导途径被激活。