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Regular exercise improves learning and memory, including during aging process. Interestingly, the imbalance of epigenetic mechanisms has been linked to age-related cognitive deficits. However, studies about epigenetic alterations after exercise during the aging process are rare. In this preliminary study we investigated the effect of aging and exercise on DNA methyltransferases (DNMT1 and DNMT3b) and H3-K9 methylation levels in hippocampus from 3 and 20-months aged Wistar rats. The animals were submitted to two exercise protocols: single session or chronic treadmill protocol. DNMT1 and H3-K9 methylation levels were decreased in hippocampus from aged rats. The single exercise session decreased both DNMT3b and DNMT1 levels in young adult rats, without any effect in the aged group. Both exercise protocols reduced H3-K9 methylation levels in young adult rats, while the single session reversed the changes on H3-K9 methylation levels induced by aging. Together, these results suggest that an imbalance on DNMTs and H3-K9 methylation levels might be linked to the brain aging process and that the outcome to exercise seems to vary through lifespan.

These results suggest that both stimulation protocols exert a neuroprotective effect against the cognitive impairment and the reduction of biomarkers for oxidative damage caused by chronic cerebral hypoperfusion.

Objectives: It is know that repeated exposure to opiates impairs spatial learning and memory and that the hippocampus has important neuromodulatory effects after drug exposure and withdrawal symptoms. Thus, the aim of this investigation was to assess hippocampal levels of BDNF, oxidative stress markers associated with cell viability, and TNF-alpha in the short, medium and long term after repeated morphine treatment in early life. Methods: Newborn male Wistar rats received morphine (morphine group) or saline (control group), 5 ug in the mid-scapular area (s.c.), starting on postnatal day 8 (P8), once daily for 7 days, and neurochemical parameters were assessed in the hippocampus on postnatal days 16 (P16), 30 (P30), and 60 (P60). BDNF and TNF-alpha levels were analyzed through ELISA. Cell viability and cell damage were analyzed in dissected hippocampus with or without H2O2 damage. Superoxide dismutase (SOD) activity was determined using RANSOD kit; Glutathione peroxidase (GPx) activity was determined as described by Wendel (1981), with some modifications; reactive species production by chemical oxidation of Dichlorodihydrofluorescein (DCFH) was evaluated in according method described by Sriram et al (1987); total Thiol level was evaluated in according method described by Aksenov and Markesbery (2001). The data analysis and interactions were evaluated using two-way ANOVA (morphine, age, morphine*age) followed by the Student-Newman-Keuls (SNK) method when indicated. The between group differences were considered significant at P<0.05. The number of animals was 4-7/group/age for each assay. Results: The two way ANOVA showed no effect of age (P = 0.327), but there is effect of morphine (P = 0.042), and interaction between age and morphine treatment (P = 0.049) in BDNF levels. In the TNFalpha levels, showed effects of age (P = 0.036), of morphine treatment (P = 0.011), and no interaction between age and morphine treatment (P = 0.275). There is effect of morphine treatment (P = 0.01), no effect of age (P = 0.127) and no interaction between age and morphine treatment in the superoxide dismutase activity (P = 0.144); effect of age (P<0.001), no effects of morphine treatment (P = 0.624) and no interactions between age and morphine treatment in the glutathione peroxidase activity (P = 0.164); in the thiol levels was also observed effect of age (P = 0.041), no effects of morphine treatment (P = 0.178) and no interactions between age and morphine treatment (P = 0.254); there is effect of age (P<0.001), no effects of treatment (P = 0.541) and no interactions between age and morphine treatment in the analysis of reactive species production (P = 0.715). In the MTT assay, there are no interactions between age and morphine treatment and H2O2-induced cellular damage (P = 0.887), between morphine and age (P = 0.880) and between morphine and H2O2-induced cellular damage (P = 0.200). However, there is effect of H2O2-induced cellular damage (P<0.001), and interaction between age and H2O2-induced cellular damage (P = 0.034), and no eff...

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