OXIDATIVE DAMAGE

IN YOUNG ALCOHOL
DRINKERS.
A PRELIMINARY
STUDY
RendnRamrez
A.

INTRODUCTION

Alcohol use is the third-highest risk factor

for disease or injury in developed countries,
and the greatest risk factor in developing
countries with low child and low adult
mortality, as classified by WHO (WHO, 2002).

INTRODUCTION
Most studies on alcohol biomarkers include
participants with evident chronic effects of
alcohol abuse such as liver inflammation,
gastritis, delirium tremens, or behavioral
disorders (Brien, Ronksley, Turner, Mukamal, & Ghali,
2011; Hingson, Heeren, Winter, & Wechsler, 2005).

The acute effects are seen in the central nervous

system, while chronic effects are mediated by
oxidative damage in the liver (Castaeda, 2009).

Questions:
How long does an individual have to be exposed
to
alcohol to show detectable chronic effects?

At which stage is it possible to know if an

individual will exhibit effects from chronic alcohol
exposure?

Could a biomarker be detected in early stages

before greater damage is caused by chronic
toxicity?

Previusly
Studies on chronic effects of
alcohol on human populations
have been conducted in patients
with several years of alcohol
intake, i.e., when clinical signs of
impaired hepatic function are
evident.
However, an obvious choice
for biomarkers in early stages
of alcohol toxicity are the ODsensitive biomarkers, since
OD is part of the mechanism
of chronic toxicity.

If so, LPO would be an excellent

biomarker for early stages of
chronic alcohol toxicity, i.e.
Within a time interval before greater
damage is observed.

DISCUSSION
The ADH increase may indicate an induction of the
enzyme which could appear at early stages of chronic alcohol
abuse. This is probably due to an increase in the ADH3
isozyme, which has been shown to be up-regulated by
alcohol (Haseba & Ohno, 2010).

Ethanol metabolism itself alters the cell redox state and

can produce reactive oxygen species that may play an
important role in the noxious effects of alcohol via oxidative
stress (Haorah et al., 2008).

DISCUSSION
The results demonstrate that the YEA group
has oxidative stress. Since GSH-Px is involved in the
antioxidant mechanism, some antioxidant responses could be
inferred from changes in its levels.

In the present work, participants have fewer years of

alcohol intake and a lower age. In spite of these differences,
a similar effect on GSH-Px activity was observed. Possibly,
less than 5 years of alcohol exposure are sufficient to induce
a decrease in GSH-Px activity.

DISCUSSION

Whatever the regulatory mechanism is, our GSH-Px results

could be explained as a part of the antioxidant response.
As a part of the cell response, GSH-Px activity is increased
when an organism is under oxidative stress (Dlugosz,
Pruss, & Lembas Bogaczyk, 2010; Tseng et al., 2008).

DISCUSSION
Thus, we can expect a positive correlation between OD
biomarkers and GSH-Px. In the present work, the LPO
biomarker TBARS correlates with GSH-Px activity (r 2=
0.3529).
There are other mechanisms by which cells could avoid
oxidative stress. In the case of alcoholism, oxidative
stress is not induced by ethanol itself.

Rather, the oxidative stress results when ethanol is

metabolized by enzymes other than ADH.

DISCUSSION

When ADH activity is able to efficiently metabolize

ethanol, a lower level of oxidative damage might be
expected, and hence a lower GSH-Px level. Thus, an
inverse correlation between ADH activity and GSH-Px
activity is to be expected. Indeed, in our work, higher
GSH-Px activity correlates with lower ADH activity (r 2=
0.4030).

DISCUSSION
In the present work, the YEA group -with few years
of alcohol intake- showed a similar effect on GSH-Px, but
no clinical differences in red blood count or any other
hematological parameter were found, compared to
controls.

This is the first work indicating that oxidative

damage could be observed at early stages of alcohol
dependence.

The oxidative damage in young subjects

exposed to alcohol is evident; this could be used to
evaluate effects of alcohol and prospective risks for
young people.

PERSPECTIVES
Before using oxidative biomarkers to diagnose and
evaluate early alcohol abuse, further studies are
needed to:
1.Identify additional biomarkers.
2.Determine the dependence of OD biomarkers on
duration of ethanol exposure, and
3.Determine the correlation of OD biomarkers with
other biomarkers of ethanol susceptibility (such
as polymorphisms).

Oxidativedamagein young alcohol drinkers

: A preliminary study.
Rendn-Ramrez A, Corts-Couto M, MartnezRizo AB, Muiz-Hernndez S, VelzquezFernndez JB.
Alcohol. 2013 Nov;47(7):501-4. doi:
10.1016/j.alcohol.2013.08.002. Epub 2013
Sep 27.

http://
www.ncbi.nlm.nih.gov/pubmed/24
080163

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