Proceedings of The Physiological Society
University of Oxford (2011) Proc Physiol Soc 23, PC223
Chronic exercise in the absence of ovarian hormones enhances stress-induced gastric and colonic oxidative damage by a glucocorticoid receptor-dependent mechanism
G. Memi1, B. . Yegen1
1. Physiology, Marmara University School of Medicine, Istanbul, Turkey.
Multiple studies have shown that physical exercise, which may be a stressful stimulus in activating the hypothalamic-pituitary-gonadal axis and elevating circulating glucocorticoids (GC), is also a strong inducer of lipid peroxidation that is likely to occur after moderate to exhaustive exercise. Postmenopausal women with higher fitness levels were shown to have higher antioxidant enzyme activity and lower levels of lipid peroxidation (Pialoux et al. 2009), but their responses to stressful events are not well studied. In the present study, the effect of moderate exercise (30 min/day 5 days/week swimming for 9 weeks) on the gastric and colonic tissues of female Sprague-Dawley rats (2-3-month-old; n=80) with intact ovaries or ovariectomy (OVX) that were exposed to a painless psychological stress (30 min) for 3 days was investigated. OVX or sham operation was conducted under ketamine and chlorpromazine (100 and 2 mg/kg, respectively, i.p.) anesthesia and rats were injected with either saline or glucocorticoid receptor antagonist (RU486, 10 mg/kg; i.p.) during stress exposure. At the end of the last stress procedure, rats were decapitated and trunk blood samples were obtained for the measurement of serum levels of cortisol, IL-1β and TNF-α, while malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activity were studied in the gastric and colonic tissue samples. Values are means ± S.E.M. compared by ANOVA. Although the applied stress did not result in significant elevations in serum cortisol levels in either sham or OVX rats, GC blockade elevated serum cortisol levels (p<0.01). In sedentary OVX rats, TNF-α and IL-1β levels were increased in response to stress with respect to control levels (p<0.05) and they were reduced in the trained OVX rats (p<0.01). Colonic and gastric MDA levels, indicating lipid peroxidation, were not changed in sham-operated sedentary groups with stress exposure, but they were significantly increased in the trained OVX rats (p<0.001), while RU486 treatment further enhanced MDA levels in the trained OVX groups (p<0.01). Exposure to stress in neither exercised nor sedentary groups with intact ovaries did not alter MPO activities in the gastric or colonic tissues, while increased gastric and colonic MPO activities in the exercised rats with OVX were increased more by GC blockade (p<0.001). Antioxidant GSH levels in gastric and colonic tissues were increased in the exercised rats with OVX (p<0.01), but not in the sedentary rats. However, RU486 treatment abolished exercise-induced elevations in GSH levels (p<0.01). In conclusion, the results demonstrate that in the absence of ovarian hormones, moderate exercise depresses stress-induced cytokine response and improves antioxidant status, but augments lipid peroxidation by a glucocorticoid receptor-dependent mechanism.
Where applicable, experiments conform with Society ethical requirements