Oxidative stress and signal transduction pathways in alcoholic liver disease.

摘要: Ethanol is linked to several pathologies like alcohol liver injury, neurotoxicity, cardiomyopathy, fetal alcoholic syndrome or cancer. It generally accepted that oxidative stress plays a central role in their pathogenesis. After chronic and excessive consumption, may accelerate mechanisms both directly via increased production of reactive oxygen species indirectly by impairing protective against them. Ethanol, its metabolites arising during metabolic degradation as well novel compounds formed ethanol induced stress, especially the action inducible microsomal cytochrome CYP2E1, apart from direct damage biological structures affect signal transduction pathways thus modulating potentiating damage. Alteration redox status cells following misuse have profound effects on cellular function viability lead cell death tissue These changes pathologic processes organism, are related alteration intracellular signaling associated with protein kinases transcription factor activation. Mainly mitogen activated kinase (MAPK) family, factors-nuclear KB (NF-KB) activating 1 (AP-1) involved deterioration organs. The response cell-type specific depends dose ethanol. Oxido-reduction balance, regulatory disturbances cascades responsible for been partially described, nevertheless, further studies required allow future diagnostic therapeutical strategies. We only at beginning...