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Long term running biphasically improves methylglyoxal-related metabolism, redox homeostasis and neurotrophic support within adult mouse brain cortex.

Falone S, D'Alessandro A, Mirabilio A, Petruccelli G, Cacchio M, Di Ilio C, Di Loreto S, Amicarelli F - PLoS ONE (2012)

Bottom Line: Oxidative stress and neurotrophic support decline seem to be crucially involved in brain aging.This research investigated whether a long-term, forced and moderate running initiated in adult age may affect the interplay between the redox-related profile and the oxidative-/MG-dependent molecular damage patterns in CD1 female mice cortices; as well, we investigated possible exercise-induced effects on the activity of the brain derived neurotrophic factor (BDNF)-dependent pathway.Our findings suggested that after a transient imbalance in almost all parameters investigated, the lately-initiated exercise regimen strongly reduced molecular damage profiles in brains of adult mice, by enhancing activities of the main ROS- and MG-targeting scavenging systems, as well as by preserving the BDNF-dependent signaling through the transition from adult to middle age.

View Article: PubMed Central - PubMed

Affiliation: Department of Basic and Applied Biology, University of L'Aquila, L'Aquila, Italy.

ABSTRACT
Oxidative stress and neurotrophic support decline seem to be crucially involved in brain aging. Emerging evidences indicate the pro-oxidant methylglyoxal (MG) as a key player in the age-related dicarbonyl stress and molecular damage within the central nervous system. Although exercise promotes the overproduction of reactive oxygen species, habitual exercise may retard cellular aging and reduce the age-dependent cognitive decline through hormetic adaptations, yet molecular mechanisms underlying beneficial effects of exercise are still largely unclear. In particular, whereas adaptive responses induced by exercise initiated in youth have been broadly investigated, the effects of chronic and moderate exercise begun in adult age on biochemical hallmarks of very early senescence in mammal brains have not been extensively studied. This research investigated whether a long-term, forced and moderate running initiated in adult age may affect the interplay between the redox-related profile and the oxidative-/MG-dependent molecular damage patterns in CD1 female mice cortices; as well, we investigated possible exercise-induced effects on the activity of the brain derived neurotrophic factor (BDNF)-dependent pathway. Our findings suggested that after a transient imbalance in almost all parameters investigated, the lately-initiated exercise regimen strongly reduced molecular damage profiles in brains of adult mice, by enhancing activities of the main ROS- and MG-targeting scavenging systems, as well as by preserving the BDNF-dependent signaling through the transition from adult to middle age.

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Antioxidant enzymatic defense in brains of mice undergoing a long-term moderate treadmill running.Specific activities of superoxide dismutase (SOD) (panel a), catalase (CAT) (panel b) and glutathione peroxidase (GPX) (panel c) in brain cortices of adult CD1 female mice undergoing a two- or four-month moderate and regular treadmill-based exercise program (E2 or E4, respectively); age-matched sedentary animals (S2, S4) were used as controls (n = 6 per group). No major age-dependent variation of tSOD and CAT specific activities was revealed; however, a significant increase in GPX activity was detected when comparing S4 and S2. Two-month physical activity reduced specific activities of tSOD, CAT and GPX catalytic capacities (E2 vs S2), whereas four-month exercise triggered a significant elevation of tSOD and CAT (E4 vs S4). Values were given as means ± std. dev. The level of statistical significance was computed by using two-way ANOVA and post-hoc Newman-Keuls test: * P<0.05; ** P<0.01; *** P<0.001. Experiments were performed in triplicate.
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pone-0031401-g002: Antioxidant enzymatic defense in brains of mice undergoing a long-term moderate treadmill running.Specific activities of superoxide dismutase (SOD) (panel a), catalase (CAT) (panel b) and glutathione peroxidase (GPX) (panel c) in brain cortices of adult CD1 female mice undergoing a two- or four-month moderate and regular treadmill-based exercise program (E2 or E4, respectively); age-matched sedentary animals (S2, S4) were used as controls (n = 6 per group). No major age-dependent variation of tSOD and CAT specific activities was revealed; however, a significant increase in GPX activity was detected when comparing S4 and S2. Two-month physical activity reduced specific activities of tSOD, CAT and GPX catalytic capacities (E2 vs S2), whereas four-month exercise triggered a significant elevation of tSOD and CAT (E4 vs S4). Values were given as means ± std. dev. The level of statistical significance was computed by using two-way ANOVA and post-hoc Newman-Keuls test: * P<0.05; ** P<0.01; *** P<0.001. Experiments were performed in triplicate.

Mentions: Spectrophotometric analyses of the catalytic activities of the main antioxidant enzymes revealed no major age-dependent variations of total superoxide dismutase (tSOD) and catalase (CAT) specific activities (Fig. 2a and b), whereas a significant age-dependent increase in GPX activity was observed (P<0.001, S4 vs S2) (Fig. 2c). Significant age-related changes in glutathione reductase (GR) activity could not be detected (Fig. 3a). After two months of regular exercise, marked reductions in brain cortex enzymatic activities of tSOD, CAT and GPX (P<0.05, E2 vs S2) were revealed (Fig. 2a, b and c), together with a marked increase in GR activity (P<0.001, E2 vs S2) (Fig. 3a). On the contrary, four-month exercise caused a significant enhancement of specific activities of tSOD (P<0.05) and CAT (P<0.01), in comparison to the age-matched sedentary group (Fig. 2a and b). No statistical differences were found when comparing GPX and GR specific activities between E4 and S4 (Fig. 2c and 3a).


Long term running biphasically improves methylglyoxal-related metabolism, redox homeostasis and neurotrophic support within adult mouse brain cortex.

Falone S, D'Alessandro A, Mirabilio A, Petruccelli G, Cacchio M, Di Ilio C, Di Loreto S, Amicarelli F - PLoS ONE (2012)

Antioxidant enzymatic defense in brains of mice undergoing a long-term moderate treadmill running.Specific activities of superoxide dismutase (SOD) (panel a), catalase (CAT) (panel b) and glutathione peroxidase (GPX) (panel c) in brain cortices of adult CD1 female mice undergoing a two- or four-month moderate and regular treadmill-based exercise program (E2 or E4, respectively); age-matched sedentary animals (S2, S4) were used as controls (n = 6 per group). No major age-dependent variation of tSOD and CAT specific activities was revealed; however, a significant increase in GPX activity was detected when comparing S4 and S2. Two-month physical activity reduced specific activities of tSOD, CAT and GPX catalytic capacities (E2 vs S2), whereas four-month exercise triggered a significant elevation of tSOD and CAT (E4 vs S4). Values were given as means ± std. dev. The level of statistical significance was computed by using two-way ANOVA and post-hoc Newman-Keuls test: * P<0.05; ** P<0.01; *** P<0.001. Experiments were performed in triplicate.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3275619&req=5

pone-0031401-g002: Antioxidant enzymatic defense in brains of mice undergoing a long-term moderate treadmill running.Specific activities of superoxide dismutase (SOD) (panel a), catalase (CAT) (panel b) and glutathione peroxidase (GPX) (panel c) in brain cortices of adult CD1 female mice undergoing a two- or four-month moderate and regular treadmill-based exercise program (E2 or E4, respectively); age-matched sedentary animals (S2, S4) were used as controls (n = 6 per group). No major age-dependent variation of tSOD and CAT specific activities was revealed; however, a significant increase in GPX activity was detected when comparing S4 and S2. Two-month physical activity reduced specific activities of tSOD, CAT and GPX catalytic capacities (E2 vs S2), whereas four-month exercise triggered a significant elevation of tSOD and CAT (E4 vs S4). Values were given as means ± std. dev. The level of statistical significance was computed by using two-way ANOVA and post-hoc Newman-Keuls test: * P<0.05; ** P<0.01; *** P<0.001. Experiments were performed in triplicate.
Mentions: Spectrophotometric analyses of the catalytic activities of the main antioxidant enzymes revealed no major age-dependent variations of total superoxide dismutase (tSOD) and catalase (CAT) specific activities (Fig. 2a and b), whereas a significant age-dependent increase in GPX activity was observed (P<0.001, S4 vs S2) (Fig. 2c). Significant age-related changes in glutathione reductase (GR) activity could not be detected (Fig. 3a). After two months of regular exercise, marked reductions in brain cortex enzymatic activities of tSOD, CAT and GPX (P<0.05, E2 vs S2) were revealed (Fig. 2a, b and c), together with a marked increase in GR activity (P<0.001, E2 vs S2) (Fig. 3a). On the contrary, four-month exercise caused a significant enhancement of specific activities of tSOD (P<0.05) and CAT (P<0.01), in comparison to the age-matched sedentary group (Fig. 2a and b). No statistical differences were found when comparing GPX and GR specific activities between E4 and S4 (Fig. 2c and 3a).

Bottom Line: Oxidative stress and neurotrophic support decline seem to be crucially involved in brain aging.This research investigated whether a long-term, forced and moderate running initiated in adult age may affect the interplay between the redox-related profile and the oxidative-/MG-dependent molecular damage patterns in CD1 female mice cortices; as well, we investigated possible exercise-induced effects on the activity of the brain derived neurotrophic factor (BDNF)-dependent pathway.Our findings suggested that after a transient imbalance in almost all parameters investigated, the lately-initiated exercise regimen strongly reduced molecular damage profiles in brains of adult mice, by enhancing activities of the main ROS- and MG-targeting scavenging systems, as well as by preserving the BDNF-dependent signaling through the transition from adult to middle age.

View Article: PubMed Central - PubMed

Affiliation: Department of Basic and Applied Biology, University of L'Aquila, L'Aquila, Italy.

ABSTRACT
Oxidative stress and neurotrophic support decline seem to be crucially involved in brain aging. Emerging evidences indicate the pro-oxidant methylglyoxal (MG) as a key player in the age-related dicarbonyl stress and molecular damage within the central nervous system. Although exercise promotes the overproduction of reactive oxygen species, habitual exercise may retard cellular aging and reduce the age-dependent cognitive decline through hormetic adaptations, yet molecular mechanisms underlying beneficial effects of exercise are still largely unclear. In particular, whereas adaptive responses induced by exercise initiated in youth have been broadly investigated, the effects of chronic and moderate exercise begun in adult age on biochemical hallmarks of very early senescence in mammal brains have not been extensively studied. This research investigated whether a long-term, forced and moderate running initiated in adult age may affect the interplay between the redox-related profile and the oxidative-/MG-dependent molecular damage patterns in CD1 female mice cortices; as well, we investigated possible exercise-induced effects on the activity of the brain derived neurotrophic factor (BDNF)-dependent pathway. Our findings suggested that after a transient imbalance in almost all parameters investigated, the lately-initiated exercise regimen strongly reduced molecular damage profiles in brains of adult mice, by enhancing activities of the main ROS- and MG-targeting scavenging systems, as well as by preserving the BDNF-dependent signaling through the transition from adult to middle age.

Show MeSH
Related in: MedlinePlus