Hernández José A, López-Sánchez Rosa C, Rendón-Ramírez Adela
Tecnologico de Monterrey, Escuela Nacional de Medicina, 64710 Monterrey, NL, Mexico.
Unidad de Biofísica (CSIC, UPV/EHU) and Departamento de Bioquímica, Universidad del País Vasco, Apartado 644, 48080 Bilbao, Spain.
Oxid Med Cell Longev. 2016;2016:1543809. doi: 10.1155/2016/1543809. Epub 2016 Jan 5.
The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.
过量饮酒是一个严重的公共卫生问题,尤其是考虑到慢性或产前接触酒精所引发的严重损害,这种损害会影响许多生理过程,如记忆、运动功能和认知能力。这种损害与大脑中的乙醇氧化有关。乙醇代谢为乙醛然后再代谢为乙酸的过程与活性氧的产生有关,活性氧会加剧细胞的氧化状态。乙醇的这种代谢会诱导磷脂中脂肪酸的氧化,已知所产生的生物活性醛与神经毒性和神经退行性变有关。因此,在这里我们将综述脂质在乙醇相关氧化应激诱导的神经元损伤中的作用,以及脂质在相关补偿或防御机制中所起的作用。