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Background Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age and has a prevalence of 1 in 15 women worldwide. This study aims to investigate the role of lncRNA SRA in the pathological processes of polycystic ovary syndrome (PCOS). Methods Twenty five-day old female C57BL/6 mice received subcutaneous injection of 60 mg/kg dehydroepiandrosterone for 20 days to induce PCOS. Lentivirus containing lncRNA SRA-specific shRNA was subcapsularly injected into the ovaries of PCOS mice. Granulosa cell was primary cultured to explore the mechanism of DHEA-induced inflammatory responses. H&E staining was used to examine the histological changes of ovaries. ELISA was used to assess serum insulin level and proinflammatory cytokines and angiogenetic factors contents in ovary tissue. The expression levels of LncRNA SRA and proteins involved in the NF-κB signaling pathway were detected through Quantitative real-time PCR and Western blot. The nuclear translocation of NF-κB was observed by immunofluorescence and the activity of NF-κB-DNA binding was detected using EMSA. Results Silencing of lncRNA SRA changed insulin release, attenuated ovary injury and reduced the production of angiogenetic factors in the PCOS mice. In addition, shRNA targeting lncRNA SRA inhibited DHEA-induced pro-inflammatory cytokines production and NF-κB nuclear translocation in the ovary of PCOS mice and primary granulosa cells. Conclusion Silencing of lncRNA Steroid Receptor RNA Activator (SRA) attenuates polycystic ovary syndrome (PCOS) in mice. LncRNA SRA plays important roles in the development of PCOS.

Formaldehyde (FA), a ubiquitous environmental pollutant, is extensively used in hospitals, laboratories, and industrial settings. Previous studies showed that FA exerts adverse effects on testicular function and as epididymis is known to play an important role in the maturation and storage of sperm, the effects of FA were examined on epididymis. In particular, this study was designed to investigate the influence of FA on structure and function of epididymis in adult male rats using histological and biochemical methods. Sprague-Dawley adult rats were randomly allotted to three groups and exposed to FA at a 0 (control), 0.5, or 10 mg m−3 by inhalation for 28 days. The results indicated that epididymal toxicity of FA was concentration dependent. Epdididymal structure and function in rats of 0.5 mg m−3 FA exposure group showed no apparent difference from control. However, epididymal weight, sperm count and motility, the activities of superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were signifi...

Formaldehyde (FA), a ubiquitous environmental pollutant, is extensively used in hospitals, laboratories and many industrial settings. Previous studies have showed that short-term, high-dose FA exposure is toxic to male reproduction of mammals. In this paper, we evaluated the male reproductive toxicity of long-term, low-dose formaldehyde exposure in rats, and explored the potential mechanisms. A total of 30 Sprague-Dawley male rats were randomly allotted to three groups, rats were exposed to FA at a dose of 0 (control), 0.5, 2.46 mg/m3 respectively by inhalation for consecutive 60 days. The results indicated that the reproductive toxicity of FA is dose-dependent. Testicular, epididymal structure and function in rats of 0.5 mg/m3 FA exposure group showed no obvious difference compared with those in control group. However, sperm quantity and quality, testicular seminiferous tubular diameter, the activities of superoxide dismutase and glutathione peroxidase was significantly decreased whereas the level of malondialdehyde was significantly increased in rats of 2.46 mg/m3 FA exposure group compared with those in control group. Moreover, histopathological results showed atrophy of seminiferous tubules, decreases of spermatogenic cells and the lumina were oligozoospermic in testes of 2.46 mg/m3 FA exposure rats. In conclusion, the level of 0.5 mg/m 3 can be considered as a safe level for FA exposure, but long-term FA exposure at a dose of 2.46 mg/m3 has a harmful effect on male reproduction by inducing oxidative stress in male rats.

Di-n-butyl phthalate (DBP) is a ubiquitous environmental pollutant, extensively used as a plasticizer in many products including plastics, cosmetics, and medical devices. Some studies have shown that DBP has potential testicular toxicity. However, the mechanism of action of DBP on male reproduction is not clear. The present study was designed to further investigate the potential male reproductive toxicity of DBP . Oxidative stress was assessed in rat testes as an underlying mechanism. Forty SD adult rats were randomly allotted to four groups, and DBP was administered to each group by oral gavage at doses of 0 (control), 100, 250, and 500 mg/kg/d for 2 consecutive weeks. The results indicated that the reproductive toxicity of DBP is dose-dependent. Body and testicular weight was significantly decreased in rats of DBP exposure at a dose of 500 mg/kg/d. Sperm count and motility were significantly decreased at doses of 250 and 500 mg/kg/d. The same two doses significantly inhibited the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) while the level of malondialdehyde (MDA) was significantly increased in testes of rats. Microscopy with hematoxylin and eosin (HE) staining showed that seminiferous tubules atrophy and seminiferous epithelial cells disintegrated and shed in rats of DBP exposure at doses of 500 mg/kg/d. In conclusion, DBP alters the testicular structure and function, at least partly, by inducing oxidative stress in testes of adult rats.

Di-n-butyl phthalate (DBP) is a ubiquitous environmental pollutant, extensively used as a plasticizer in many products including plastics, cosmetics and medical devices. Previous studies have shown that DBP has potential testicular toxicity. Epididymis is known to play an important role in the maturation and storage of sperm. However, the effect and mechanism of action of DBP on epididymis is unclear. The present study was designed to investigate the effect of DBP on structure and function of epididymis in adult male rats by histological and biochemical study. Oxidative stress was also assessed in rat epididymis as an underlying mechanism. Forty SD adult rats were randomly allotted to four groups, and DBP was administered to each group by oral gavage at doses of 0 (control), 100, 250 and 500 mg/kg/day for 2 consecutive weeks. The results indicated that the epididymal toxicity of DBP is dose-dependent. Epididymal weight, activities of epididymal alpha-glucosidase and glutathione peroxidase (GSH-Px) was significantly decreased in rats of 500 mg/kg DBP exposure group compared to the control. The activity of superoxide dismutase (SOD) was significantly decreased while the level of malondialdehyde (MDA) was significantly increased in the epididymal tissue of the 250 and 500 mg/kg DBP exposure groups compared with the control group. Moreover, microscopy with hematoxylin and eosin (HE) staining showed that atrophy of epididymal tubules, the interstitial vascular was hyperemia and the lumina were oligozoospermic in rats of 500 mg/kg DBP exposure group. In conclusion, DBP exposure alters the epididymal structure and function by inducing oxidative stress in epididymis of adult rats.

The results of several recent studies indicated that free radicals are involved in the biochemical mechanisms that underlie neuropsychiatric disorders. In the present study, we evaluated changes in oxidative stress and human 8-hydroxyguanine glycosylase1 gene (hOGG1) expression in depressive patients with acute leukemia. Ninety two cases were assessed using the Zung self-rating depression scale (SDS) and multiple-item questionnaires. We measured total antioxidant capacity (T-AOC) and the concentrations of reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) during a pre-treatment period. The steady-state expression of hOGG1 mRNA transcripts was monitored. The incidence of depression was 47.83%. There was a significant decrease in serum T-AOC and SOD concentrations in depressive patients compared to the control subjects, whereas the opposite was the case for serum concentrations of ROS, NO and MDA. Real-time polymerase chain reaction (PCR) revealed that hOGG1 mRNA expression was greater in depressive patients than in the controls. Person correlation analysis revealed that depression was correlated positively with sex, the course of the disease and hOGG1 mRNA expression; depression was correlated negatively with T-AOC. Based on these results, we conclude that the antioxidant system is impaired in leukemic patients with affective disorders. Therefore, oxidative stress may play an important role in the pathophysiology of depression.