Alcohol abuse has reached massive proportions, associated with a number of
adverse consequences, becoming one of the most widespread phenomena of recent
decades and therefore alcohol, alcoholic disease agent of a public health problem.
Young people are under physiological and social transition, with the curiosity, the
pressure of the social group, the family model, propaganda and lack of public
policies, the main risk factors which lead to early alcohol consumption. The teenager
once is maturing presents its central nervous system (CNS) vulnerable to aggression
caused by the consumption of this drug. It is known that alcohol promotes a series of
motor change the point of view of clinical and physiological concurrently. These
amendments are consequential action of alcohol sore CNS, specifically on the
Cerebellum, and by chronic use of the drug suffer (like other organs of the CNS)
some changes. The aim of this study was to evaluate the cerebellar changes
resulting from exposure to ethanol from adolescence to adulthood in rats, on the
morphometric patterns observed in the organ, tissue response and investigation of
oxidative balance the body against the injury caused by toxic. Mice received from the
35th day of postnatal life (puberty period) by gavage at a dose of EtOH 6.5g/kg/day
for 90 days (adulthood). To view the injury caused to the fabric was made
morphometric biochemical research and analysis through oxidative stress. The
results show that cerebellar mass is not changed, but there is a reduction in organ
size and an increase in the density of the cell population in the molecular and
granular layers, however a decrease in neuronal cells, with all the changes occurred
were not morphohistologics accompanied by alterations in the biochemical oxidation.
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