Abstract
We investigated changes in oxidative biomarkers in brain regions such as brainstem, cerebellum, and cerebral cortex of 3-, 6-, 18-, 24-, and 30-month-old rats. We also assessed the effects of low-intensity exercise on these biomarkers in these regions of 6-, 18-, and 24-month-old rats that started exercise on a treadmill at 3, 15, and 21 months of age, respectively. Radiographic images of the femur were taken for all rats. A total of 25 rats (age: twelve 6-, ten 18-, ten 24-, and three 30-month-old rats) were used. Lipid hydroperoxide levels increased in cerebellum at 18 months. Total antioxidant activity exhibited lowest values in brainstem at 3 months. Superoxide dismutase activity did not exhibit significant changes during aging. Total thiol content exhibited lowest values in brain regions of 24- and 30-month-old rats. Exercise reduced total thiol content in brainstem at 6 months, but no change occurred in other regions and other ages. Femur increased its length and width and cortical thickness with advancing age. No change occurred in medullary width. Radiolucency increased and sclerosis was found in cortical and medullary bone with advancing age. Exercise reduced radiolucency and medullary sclerosis. Therefore, aging differentially changed oxidative biomarkers in different brain regions and radiographic measures of the femur. Low-intensity exercise only ameliorated some radiographic measurements of femur. Since the present study possessed limitations (small number of rats per group), a beneficial effect of regular low-intensity exercise on oxidative markers in brain cannot be ruled out.
Highlights
The world population is progressively getting older
Lipid hydroperoxide levels A significant difference was found in lipid hydroperoxide levels between brain region (F(2,76)=3.478, P=0.034) but not age (F(2,76)=1.843, P=0.126)
Post hoc test revealed a significant increase in superoxide dismutase (SOD) activity in cerebellum of sedentary 18-month-old rats compared to brainstem of exercise 18-month-old rats (Figure 3B)
Summary
The number of older people aged 60 or more will grow from 962 million to nearly 2.1 billion by 2050 [1,2]. Evidence has shown that oxidative stress is one of the most important factors contributing to biochemical impairments of the brain during aging [3]. Oxidative stress may be defined as an excessive amount of reactive oxygen species (ROS), which is the net result of an imbalance between production and destruction of these species [5]. The thiol moiety is sensitive to redox reactions and is an established redox sensor that interacts with a variety of oxidants to form in many cases a reversible covalent modification that includes disulfide bond formation, a major mechanism by which protein function can be controlled [6]
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