Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage

被引:112
|
作者
Hernandez, Jose A. [1 ]
Lopez-Sanchez, Rosa C. [1 ]
Rendon-Ramirez, Adela [2 ,3 ]
机构
[1] Escuela Nacl Med, Tecnol Monterrey, Monterrey 64710, NL, Mexico
[2] Univ Basque Country, UPV EHU, Unidad Biofis CSIC, Apartado 644, E-48080 Bilbao, Spain
[3] Univ Basque Country, Dept Bioquim, Apartado 644, E-48080 Bilbao, Spain
关键词
PRENATAL ALCOHOL EXPOSURE; PROTEIN-KINASE-C; N-ACYLETHANOLAMINE; RAT-BRAIN; METABOLIZING ENZYMES; CELL-DEATH; MITOCHONDRIAL DYSFUNCTION; ENVIRONMENTAL-INFLUENCES; TRYPTOPHAN AVAILABILITY; ALDEHYDE DEHYDROGENASE;
D O I
10.1155/2016/1543809
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页数:15
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