I Medical Clinic, Sapienza University, Rome, Italy.
Vascul Pharmacol. 2012 Sep-Oct;57(2-4):69-71. doi: 10.1016/j.vph.2012.06.005. Epub 2012 Jul 4.
Alcoholic (ethanol-containing) beverages are consumed by most societies in the world. Low-to-moderate levels of ethanol consumption have been shown to reduce the risk of cardiovascular diseases and atherosclerosis. The decreased risk is likely due to alcohol's favorable pleiotropic effects on lipids, adhesion molecules, platelet activation and oxidative stress. However, there is also an abundance of clinical, experimental and epidemiological evidence showing that chronic high-dose ethanol consumption increases mortality, cardiovascular complications and also the progression of atherosclerosis. This last phenomenon appears to be due to the metabolism of ethanol, that leads to the formation of acetaldehyde, which is oxidized to acetate, leading to the generation of reactive oxygen species (ROS) and a toxic effect of ethanol on the formation of the atherosclerosis plaque. We will here briefly review the mechanisms through which high intakes of ethanol induce the formation of atherosclerotic plaque, focusing on increased oxidative stress as the main underlying mechanism.
酒精（含乙醇）饮料在世界上大多数社会中都有消费。低至中度的乙醇摄入已被证明可降低心血管疾病和动脉粥样硬化的风险。这种风险降低可能是由于酒精对脂质、黏附分子、血小板激活和氧化应激的有利多效性作用所致。然而，也有大量的临床、实验和流行病学证据表明，慢性高剂量乙醇摄入会增加死亡率、心血管并发症，以及动脉粥样硬化的进展。后一种现象似乎是由于乙醇的代谢导致乙醛的形成，乙醛被氧化为醋酸盐，导致活性氧（ROS）的产生和乙醇对动脉粥样硬化斑块形成的毒性作用。在这里，我们将简要回顾乙醇摄入引起动脉粥样硬化斑块形成的机制，重点关注增加氧化应激作为主要潜在机制。
