Regional responses in antioxidant system to exercise training and dietary Vitamin E in aging rat brain

Abstract

We have evaluated the effect of exercise, Vitamin E and a combination of both on the antioxidant enzymes (AOEs)-superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) along with the products of lipid peroxidation (LP)-malondialdehyde (MDA) and lipofuscin-like auto fluorescent substances (LF-like AFS) in discrete brain regions of rats of 4 (young adults), 8 (old adults), 12 (middle-age) and 22 months (mos) old of age. Hippocampus (HC) showed greater increase in GSH-Px activity than cerebral cortex (CC) to exercise and Vitamin E and was irrespective of the age. A combination of both was effective in the CC of all age groups but not in the supplemented sedentary of 12-and 22-mo-olds. CAT activity increased significantly in the HC of supplemented and trained rats but not in the combination group of any age. SOD increased in both the regions of supplemented trainees. However, old were more benefited in terms of maximal elevation in the HC. Vitamin E reduced MDA content in both regions of adult. LF-like AFS decreased significantly in supplemented sedentary and trainees of all ages. Our results demonstrate that an age-related deficit in AOEs in the CC and HC can be overcome through Vitamin E plus exercise, and further suggests the rationale for looking at these markers of oxidative stress in several age-related neuronal diseases.

Comparison of lifelong and late life exercise on oxidative stress in the cerebellum

“…The difference may relate to a stress from forced swimming which can decrease brain antioxidants [42] and increase superoxides in the cerebellum [34]. In fact, other studies indicate that milder swimming exercise (30 min/day) has age-sensitive effects that are region specific [7,21]. Similar to the results of the current study, these researchers observed that aging was associated with an increase in cerebellar lipid peroxidation, which was reduced by exercise or vitamin E treatment in aged animals [21].…”

Exercise Training Normalizes Sympathetic Outflow by Central Antioxidant Mechanisms in Rabbits With Pacing-Induced Chronic Heart Failure

“…19 Other studies have provided evidence for an EX-induced increase in SOD activity in the striatum 42 and an increase in glutathione peroxidase in the hippocampus and cerebral cortex. 43 We realize that the results of the present study cannot necessarily be extrapolated to the clinical situation; however, the data from the present study do provide useful information relevant to therapy in CHF patients. In the present study, the beneficial effects of exercise training in the CHF state were, at least in part, dependent on the enhanced central antioxidative activity, which induced normalization of sympathetic nerve activity.…”

Protein oxidation inhibits NO-mediated signaling pathway for synaptic plasticity

“…Actually, numerous studies have demonstrated various correlations between age and the accumulation of oxidative damage to cellular macromolecules (Floyd and Hensley, 2002;Stadtman, 2001). For example, enhanced lipid peroxidation (Calabrese et al, 2004;Devi and Kiran, 2004;Gupta et al, 1991;Murray and Lynch, 1998;O'Donnell and Lynch, 1998 ) and protein oxidation (Cini and Moretti, 1995;Forster et al, 1996;Sohal et al, 1994;Sultana et al, 2009;Vaishnav et al, 2007) are observed in the brains of aged rodents. Furthermore, several studies have shown that behavioral deficits of aged animals are associated with increases in oxidative stress Cantuti-Castelvetri et al, 2000;Carney et al, 1991;Forster et al, 1996;Fukui et al, 2001).…”