Resveratrol Ameliorates Testicular Histopathology of Mice Exposed to Restraint Stress.

We evaluated immobilization stress and resveratrol supplementation in immature male mice at 30 days of age for 15 consecutive days. Fifty Swiss mice were divided into five groups (10 mice each): Controls, restraint stress (RS), restraint stress + vehicle (RS + V), RS + 2 mg/kg, and RS + 20 mg/kg. We determined results on the basis of hematoxylin and eosin (H&E), "Periodic acid-Schiff" staining, and TUNEL assay. The results indicated that immobilization stress significantly decreased body weight, testis weight, and water/food intake compared to the control; while resveratrol ameliorated these effects. The quantitative histologic evaluation of the seminiferous tubule diameter, luminal diameter, area of seminiferous tubules, area of tubule lumen, epithelial height, Leydig cell number, and the width of the tunica albuginea were similarly decreased after exposure to RS. These parameters recovered back to normal in the RS + 2 mg/kg group. The development of spermatogenesis was significantly delayed in the RS, RS + V, and RS + 20 mg groups based upon our evaluation score system. However, we observed no significant differences in the RS + 2 mg group compared with the control group. The number of TUNEL-positive cells also significantly decreased in the RS + 2 mg/kg group. In conclusion, we found that the administration of 2 mg/kg was an effective dose against immobilization stress in mice.

Sweet taste receptor agonists alter ovarian functions and ovarian cycles in aged mice.

Saccharine sodium and rebaudioside A are low-calorie sweeteners, and the biologic effects of these sweeteners in rat ovaries are related to the activity of sweet taste receptors. Data on the impact and regulatory mechanisms underlying such sweeteners on the reproduction of aged animals are currently lacking. In the present study we assessed how the consumption of sweeteners affects the ovarian cycle, ovulation, biochemical indices, and other biologic functions. Thirty-six 1-year-old mice were randomly divided into 3 groups: a control (C) group receiving regular water, a saccharin sodium group receiving a 7.5 mM solution, and the rebaudioside A group receiving a 2.5 mM solution for 30 days. We observed no significant changes in body weights in any group. However, uterine weight in the rebaudioside A group significantly increased in diestrus, and we recorded a significant increase in the percentage of abnormal estrous cycles and the number of corpora lutea in the treatment groups. TUNEL staining and Immunoreactivity for the apoptosis-inducing factor (AIF) confirmed apoptosis in granulosa cells, oocyte, and corpus luteum. Serum glucose increased significantly in both treatment groups and there was a significant increase in cholesterol in the rebaudioside A group. Furthermore, the saccharin sodium-treated group exhibited elevated serum progesterone levels compared with the other groups. In conclusion, sweeteners manifested deleterious effects on reproductive indices in aged mice.

Sodium Arsenite Injection Induces Ovarian Oxidative Stress and Affects Steroidogenesis in Rats.

Oxidative stress is involved in the regulation of mammalian reproduction. The present study was conducted to detect the sodium arsenite-induced oxidative stress and alterations in the structure and steroidogenesis in rat ovary. Twenty female adult rats were injected i.p. with sodium arsenite (8 mg/kg BW, T) or 0.9% saline (C) for 16 days. The oxidative stress indexes and morphology of the liver, kidney, and ovary were detected using commercial kits and HE staining, respectively. The serum progesterone and estradiol were detected by RIA, and the ovarian steroidogenic gene expressions were detected by real-time PCR. Results showed that the ovarian activities of SOD and GSH-PX decreased (P < 0.05), while the ROS activity and MDA level increased (P < 0.05) in the T group. HE staining results showed that treatment with sodium arsenite damaged the ovarian morphology, resulting in reduced large and medium follicles and increased atretic follicles. Nonetheless, neither the liver nor kidney showed evident changes in the oxidative stress indexes or morphology after sodium arsenite treatment. The serum progesterone and estradiol levels decreased (P < 0.05) with the reduced expressions in the ovarian steroidogenic genes (StAR, P450scc, and 3ß-HSD) (P < 0.05). In conclusion, sodium arsenite injection can induce ovarian oxidative stress in rats which set up an appropriate model for future studies of ovarian diseases as well as the toxic mechanism of arsenic in the reproduction.