To evaluate the effect of reactive oxygen species in human corpus luteum function, we investigated whether hydrogen peroxide (H2O2) affects the in vitro luteal cell production of steroids. H2O2 treatment (1.0-100 microM) of mid and late luteal cell cultures elicited a dose-dependent decrease in basal progesterone production. However, treatment of mid luteal cells with a low concentration of H2O2 (0.01 microM) significantly stimulated progesterone secretion (P < 0.05). In addition, H2O2 (100 microM) markedly inhibited human chorionic gonadotropin (hCG)-stimulated progesterone and estradiol secretion. cAMP production was enhanced (2.4-fold, P < 0.05) by hCG treatment of luteal cells. The addition of H2O2 (0.1-100 microM) to hCG-stimulated luteal cell cultures elicited a decrease in cAMP concentration (P < 0.05) and in the specific binding of radiolabeled hCG by luteal cells. Progesterone and estradiol production stimulated by dibutyryl cAMP were significantly inhibited by H2O2 (P < 0.05). These findings suggest that H2O2 interferes with basal steroid production and, in hCG-stimulated conditions, it may inactivate the gonadotropin-receptor complex. The anti-steroidogenic action of H2O2 therefore raises the possibility of a modulatory role of H2O2 in human luteal steroidogenesis.
The effect of the menstrual cycle on the thermic effect of food (TEF) was examined in eight healthy, normal-weight [mean +/- SD: 56.1 +/- 5.6 kg and body mass index (in kg/m2) 21.3 +/- 1.8] women aged 22-38 y. Their lean body mass and fat mass were 39.4 +/- 2.7 kg and 16.9 +/- 6.5 kg, respectively. TEF was measured on 4 separate days selected to match the four phases of a menstrual cycle: early follicular, follicular, luteal, and late luteal. The volunteers consumed a 3138-kJ liquid meal (54.5% carbohydrate, 14.0% protein, and 31.5% fat) on each test day. Resting metabolic rate was measured for 55 min before the meal and every 30 min after the start of the meal for 205 min. Although resting metabolic rate remained unchanged, there was a significant difference (P < 0.01 by ANOVA) in mean (+/- SEM) values for TEF among the four phases of the cycle: 0.94 +/- 0.05 kJ/min during the early follicular phase, 0.86 +/- 0.09 kJ/min during the follicular phase, 0.70 +/- 0.10 kJ/min during the luteal phase, and 0.76 +/- 0.07 kJ/min during the late luteal phase. TEF decreased significantly (P < 0.025 by paired t test) during postovulation (average of luteal and late luteal phases), when it was 0.73 +/- 0.07 kJ/min, compared with preovulation (average of early follicular and follicular phases), when it was 0.90 +/- 0.06 kJ/min. In conclusion, TEF decreased during the luteal phase of the menstrual cycle, possibly as a result of impairment of glucose uptake and slower transit of food through the upper gastrointestinal tract.
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