Ethanol (EtOH) binge drinking is characterized by high EtOH intake during few hours followed by withdrawal. Protection\nstrategies against the damages generated by this binge are poorly explored. Thus, this study is aimed at investigating the\nprotective role of treadmill physical exercise (PE) on the damage caused after repeated cycles of binge-like EtOH exposure in the\noxidative biochemistry, morphology, and cerebellar function of rats from adolescence to adulthood. For this, animals were\ndivided into four groups: control group (sedentary animals with doses of distilled water), exercised group (exercised animals\nwith doses of distilled water), EtOH group (sedentary animals with doses of 3 g/kg/day of EtOH, 20% w/v), and exercised+EtOH\ngroup (exercised animals with previous mentioned doses of EtOH). The PE occurred on a running treadmill for 5 days a week\nfor 4 weeks, and all doses of EtOH were administered through intragastric gavage in four repeated cycles of EtOH in a\nbinge-like manner. After the EtOH protocol and PE, animals were submitted to open field and beam walking tests. In sequence,\nthe cerebellums were collected for the biochemical and morphological analyses. Biochemical changes were analyzed by\nmeasurement of Trolox equivalent antioxidant capacity (TEAC), reduced glutathione content measurements (GSH), and\nmeasurement of nitrite and lipid peroxidation (LPO). In morphological analyses, Purkinje cell density evaluation and\nimmunohistochemistry evaluation were measured by antimyelin basic protein (MBP) and antisynaptophysin (SYP). The present\nfindings demonstrate that the binge drinking protocol induced oxidative biochemistry misbalance, from the decrease of TEAC\nlevels and higher LPO related to tissue damage and motor impairment. In addition, we have shown for the first time that\ntreadmill physical exercise reduced tissue and functional alterations displayed by EtOH exposure.
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