2014, Number 3
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Med Int Mex 2014; 30 (3)
Oxidative and Nitrosative Stress as Mechanism of Hepatocyte Damage Produced by Ethanol Metabolism
Hernández-Rodríguez S, Gutiérrez-Salinas J, García-Ortíz L, Mondragón-Terán P, Ramírez-García S, Núñez-Ramos NR
Language: Spanish
References: 56
Page: 295-308
PDF size: 534.45 Kb.
ABSTRACT
Free radicals derived from reactive oxygen species (ROS) and reactive
nitrogen species (RNS) are highly reactive molecules, which usually reacts
with cell macromolecules producing irreversible cell damage. Ethanol is
oxidized to acetaldehyde within hepatocytes through three main systems:
a) by alcohol dehydrogenase (ADH), an enzymatic reaction carried out
in the cytosol;
b) by cytochrome P450 (CYP2E1) within endoplasmic
reticulum, and
c) by catalase enzyme within the peroxisomes. Acetaldehyde
is oxidized in the mitochondria by aldehyde dehydrogenase (ALDH)
producing acetate. The metabolic sub-products derived from ethanol
oxidation include an alteration of the redox balance; both at cytoplasm
and mitochondria level, thus generating a high ROS and RNS production
mainly at mitochondria’s electron transport chain (or respiratory chain).
ROS and RNS over-production can lead to oxidative/nitrosative stress with
a high potential to damage macromolecular cell components inducing
cell death through the activation of apoptosis mechanism.
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