Previous studies have shown that rats subjected to subchronic treatment with nicotine experience changes in
COX-2 (a marker of pro-inflammatory systems) and accumulate lipid hydroperoxides (a marker of oxidative stress) in the
CNS (CNSMC, 2010; 10:180-206) (hippocampus, frontoparietal cortex and cerebellar cortex). Such changes are specific
to each region since each contains different types of neuronal and glial cells with different nicotine receptors. They also
differ in animals exposed to a source of oxidative stress, such as D-amphetamine. This paper discusses the changes in
other markers of oxidative stress - the isozymes of superoxide dismutase Mn-SOD and Cu/Zn-SOD - in nicotine- and
nicotine + D-amphetamine-treated rats. The biochemical and histochemical changes observed were specific to each region
(in general very marked in the frontoparietal cortex and the hippocampus but less so in the cerebellar cortex) and each
type of neuronal and glial cell. The SODs induced by nicotine may exert a neuroprotective effect via the reduction of
oxidative stress. This might be beneficial in the treatment of neurodegenerative diseases. The fact that nicotine did not
greatly increase the SODs in the rats treated with D-amphetamine may indicate that the effect of nicotine is partially or
totally abolished in situations of oxidative stress. However, since ROS and lipid hydroperoxide levels are also reduced
when nicotine is administered to such animals, it could be argued that nicotine is beneficial.
Keywords: Cu/Zn-SOD, D-amphetamine, Mn-SOD, nicotine, oxidative stress.
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