Hepatoprotective effect of 17ß-estradiol as antioxidant modulators against stress damage.

BACKGROUND: Liver is one of the most important organs affected by exercise. According to the literature a few study to date has investigated the effects of estrogen supplementation on exercise-induced oxidative stress in liver tissue of rats. OBJECTIVES: We aimed to investigate the effects of estrogen supplementation on oxidative stress markers in liver tissue of exercised rats. MATERIALS AND METHODS: Male rats (n = 35) were divided as estrogen supplemented (n = 18) and non-supplemented groups (n = 17); these groups were further divided as rest and eccentric exercised groups. Eccentric exercise groups were further divided as rats killed after 1 hour and 48 hours of eccentric exercise. Estrogen (10 mg/kg) was administered subcutaneously for 30 days. Eccentric exercise was applied as treadmill run (15° downhill, 20 m/min) consisting of periods of "5 min" run and 2 min rest repeated 18 times. The rat liver was examined biochemically and histologically. Activities of GST, GSH-Px, CAT, SOD and MDA concentration were also measured spectrophotometrically. RESULTS: Some disruptions were detected in experimental groups compared with the control group. Additionally, exercise training caused an increase in SOD and decrease in GSH-Px activities in some experimental groups. SOD activities increased significantly in group 3 (Estrogen (-), eccentric exercise (+) killed (after 1 h), compared with group 5 (Estrogen (-), eccentric exercise (+) killed (after 48 h). On the other hand, GSH-Px activities were also significantly decreased in groups 3, 4 and 5 compared with the control group. Leukocyte infiltration in liver increased after 48 hours compared with after 1 hour and estrogen supplementation was not able to prevent this infiltration. CONCLUSIONS: Estrogen seemed to be not very effective to prevent eccentric exercise-induced liver damage.

Melatonin reduces oxidative stress in the rat lens due to radiation-induced oxidative injury.

PURPOSE: The aim of this study was to evaluate the antioxidant role of melatonin against radiation-induced cataract in the rat lens after total cranial irradiation with a single 5 Gray (Gy) dose of gamma irradiation. MATERIALS AND METHODS: Twenty-eight Sprague-Dawley rats were used for the experiment.The rats were randomly divided into four equal groups. The control group did not receive melatonin or irradiation but received both 0.1 ml physiological saline intraperitoneally and sham irradiation. The irradiation (IR) group received 5 Gy gamma irradiation to the total cranium as a single dose plus 0.1 ml physiological saline intraperitoneally. The melatonin plus IR group received irradiation to the total cranium plus 5 mg/kg/day melatonin intraperitoneally. The melatonin group received only 5 mg/kg/day melatonin plus sham-irradiation. Biochemical parameters measured in murine lenses were carried out using spectrophotometric techniques. RESULTS: Lens antioxidant capacity, as measured by levels of total superoxide scavenger activity (TSSA), non-enzymatic superoxide scavenger activity (NSSA) and glutathione reductase (GRD) activity, significantly increased in melatonin, control and melatonin plus IR groups when compared with the IR group. Lens glutathione-S-transferase (GST) activity significantly increased in control and melatonin groups when compared with the IR group. Lens malondialdehyde (MDA) levels significantly increased in the IR group when compared with control, melatonin and melatonin plus IR groups. Lens TSSA and NSSA activities significantly decreased in control and melatonin plus IR groups when compared with the melatonin group. Lens GST activity significantly increased in the control group when compared with melatonin plus IR group. Lens GRD activity significantly increased in melatonin and melatonin plus IR groups when compared with control group. CONCLUSIONS: Melatonin reduces oxidative stress markers and augments anti-oxidant capacity in the rat lens.

Protective effect of melatonin on experimental otitis media with effusion in guinea pigs.

The aims of this study were: (a) to assess whether the increased oxidative stress in otitis media with effusion (OME) induced in guinea pigs by histamine injection into the middle ear cavity is reflected by lipid peroxidation in erythrocytes, plasma, and middle ear effusion fluid; (b) to survey the alterations of oxidant and antioxidant enzyme activities in experimental OME; and (c) to determine the effects of melatonin and methylprednisolone on this oxidative stress. Malondialdehyde (MDA) level, erythrocyte total (enzymatic plus non-enzymatic) superoxide scavenger activity (TSSA), non-enzymatic superoxide scavenger activity (NSSA), superoxide dismutase (SOD), catalase (CAT), and xanthine oxidase (XO) activities were measured in 4 groups of 7 guinea pigs at 3 hr after injection of 0.1 ml of histamine (or saline) into the middle ear. Group I was the control group, Group II was an experimental group with OME induced by histamine, Group III was a melatonin-pretreated OME group, and Group IV was a methylprednisolone-pretreated OME group. In erythrocyte, plasma, and middle ear effusion samples, MDA levels were significantly increased in guinea pigs with OME (Group II), compared to controls (Group I); erythrocyte TSSA and SOD activities were lower and erythrocyte XO activity was increased in guinea pigs with OME (Group II) compared to controls (Group I). No significant differences were found in erythrocyte NSSA and CAT activities. In Group III, pretreatment of guinea pigs with i.p. melatonin at 1 hr prior to histamine induction of OME decreased the erythrocyte, plasma, and effusion MDA levels, compared to Group II; erythrocyte XO activity was diminished and erythrocyte TSSA, SOD, and CAT activities were increased in Group III compared to Group II. In Group IV, pretreatment of guinea pigs with i.p. methylprednisolone at 1 hr prior to histamine induction of OME decreased the plasma and effusion MDA levels and increased the erythrocyte TSSA and SOD activities, compared to Group II. These results suggest that reactive oxygen species (ROS) play a role in histamine-induced OME. Pretreatment with i.p. melatonin or methylprednisolone both decrease the ROS generated by experimental OME, but melatonin appears to be more effective than methylprednisolone.