Obesity (Silver Spring). 2011 (May 19) [Epub ahead of print]
Savory LA, Kerr CJ, Whiting P, Finer N, McEneny J, Ashton T.
Department of Sport and Exercise Sciences,
University of Bedfordshire,
Selenium Reduces Oxidative Stress Induced by Exercise
Until the late 1950s, selenium was thought to be toxic. Although it can be toxic at high doses, it is now recognized as an important nutritional trace mineral. Selenium plays important roles in detoxification and antioxidant defense mechanisms in the body. Selenium is an antioxidant and because of this antioxidant activity it is believed to be responsible in protecting against heart attacks and strokes while supporting overall cardiovascular health. The symptoms of selenium deficiency include: destructive changes to the heart and pancreas, sore muscles, increased red blood cell fragility, and a weakened immune system.
Oxidative stress is caused when there is increased oxidant production in animal cells characterized by the release of free radicals resulting in cellular damage. In humans, oxidative stress is involved in many diseases, such as cancer, Parkinson's disease, heart failure, Alzheimer's disease, and chronic fatigue syndrome, but short-term oxidative stress may also be important in the prevention of aging.
This new study suggests that selenium supplementation may reduce markers of oxidative stress especially in overweight adults who exercise. The randomized, double-blind study included 10 normal weight and 10 overweight adults who received either placebo or 200 micrograms of selenium daily for three weeks. At the end of three weeks, both groups received placebo for three more weeks and then crossed over to the opposite group. The results revealed that the overweight participants taking selenium supplements experienced a 0.25 micromole per liter decrease in lipid hydroperoxide levels immediately following exercise. It was also noted that the overweight participants had low selenium levels at the start of the study. In the overweight group, selenium supplementation was effective at increasing plasma selenium levels to near recommended levels which in turn decreased lipid hydroperoxide responses at rest and after high-intensity exercise.
The reason that selenium supplementation may not have had an impact in normal weight individuals could be because they already had sufficient levels of selenium to support levels of oxidative stress caused by exercise. Based on these findings, it appears that overweight individuals who embark on an exercise program may benefit from selenium supplementation to reduce levels of oxidative stress.
Both obesity and acute high-intensity exercise increase oxidant stress levels. This study investigates whether selenium (Se) supplementation could be a potential effective therapy to reduce obesity-associated oxidant stress and exercise-induced oxidant stress. Ten normal-weight (NW) (22.80 ± 0.41 kg/m(2)) and ten overweight (OW) healthy subjects (28.00 ± 0.81 kg/m(2)) were assessed during a randomized double-blind Se supplementation study (200 µg sodium selenite/day for 3 weeks) with a 3-week placebo control and inversion of treatment periods. Blood levels of lipid hydroperoxide (LH), superoxide dismutase (SOD), erythrocyte glutathione (GSH), and total antioxidant status (TAS), were measured at rest, pre-, and postexercise (30 min 70% VO(2) max before and after treatment (pretreatment (week 0 and 12) and post-treatment (week 3 or 15)). At rest, compared to placebo, Se supplementation had no significant effect on LH, SOD, GSH, and TAS levels. However, Se supplementation decreased LH levels in the OW group, immediately postexercise (-0.25 ± 0.12 µmol/l, P = 0.05) compared to placebo treatment. Postexercise, with or without Se supplementation, no changes in TAS, SOD, and GSH levels were observed in both the NW and OW group. This study has highlighted a potential benefit of Se in reducing LH levels postexercise in OW individuals. Given that oxidant stress is a predictor of coronary events, it is imperative to better understand oxidant stress-related responses to lifestyle factors (in particular "high-risk" population groups) and potential antioxidant therapy.
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