Thymoquinone ameliorates bleomycin-induced reproductive toxicity in male Balb/c mice.

Bleomycin (BL) is a powerful chemotherapy drug that has devastating effects on spermatogenic function and may make cancer survivors at risk of infertility. Protective effects of thymoquinone (TQ), a phytochemical compound with antioxidant and anticancer influences, were investigated on sperm parameters, testicular structures, and sexual hormones in BL-treated mice. Forty-eight adult male Balb/c mice were randomly divided into six groups. Control group received normal saline; BL group received 10 mg/kg BL; TQ7.5 group received 7.5 mg/kg TQ; TQ15 group received 15 mg/kg TQ; BL+TQ7.5 group received 10 mg/kg BL and 7.5 mg/kg TQ; BL + TQ15 group received 10 mg/kg BL and 15 mg/kg TQ. BL was intraperitoneally used every day through 35 days, and TQ was intraperitoneally injected 3 days before administration of BL and continued twice per week for 35 days. Results showed that BL significantly decreased count, viability, morphology, maturity, and progressive movement of sperm, testosterone, seminiferous tubule diameters, the ratio of testis weight to body weight, number of spermatogonia, spermatocytes, spermatids, and Sertoli cells per tubule, and expression of Bcl2l1 and Bcl2l1/Bax ratio, and increased the non-progressive movement and immotile sperm, intermediate and immature sperm, LH, FSH, and malondialdehyde levels, and tunica albuginea thickness compared to the control group (p < .05). TQ at a level of 7.5 mg/kg ameliorated BL-induced toxicity on measured parameters and returned most of them to the level of the control group. These data suggested TQ in a dose-dependent manner may have positive effects on BL-induced toxicity of the testis in mice model.

The effect of docetaxel on survival, fertilization rate and apoptosis-related genes mRNA expression in mouse metaphase II oocytes following vitrification.

BACKGROUND: Docetaxel is beneficial in oocyte cryopreservation. AIMS: The effect of docetaxel, on the survival, fertilization rate and mRNA expression of apoptosis-related genes of vitrified mature oocytes was investigated. METHODS: Mature oocytes were divided into eight experimental groups, including I) control, II) docetaxel, III) docetaxel + cryoprotectant agent 1 (CPA1), IV) docetaxel + CPA2, V) docetaxel + vitrification 1 (Vit1), VI) docetaxel + Vit2, VII) Vit1, and VIII) Vit2. The survival and fertilization rates, and the mRNA expression level of Bcl-xl, Bax and caspase-3 as apoptosis-related genes were evaluated. RESULTS: The survival rates in Vit1, and Vit2 groups were significantly lower than in the control group (P<0.05). The fertilization rates in docetaxel + Vit1, docetaxel + Vit2, Vit1, and Vit2 were significantly lower than the control, docetaxel, and related groups using docetaxel and CPAs. Bax expression was significantly increased in groups which oocytes vitrified. Also, its expression in the Vit2 group increased significantly in comparison to the docetaxel + Vit2 group. The expression of the Bcl-xl gene was downregulated in docetaxel + CPA2, docetaxel + Vit2 and Vit2 compared to docetaxel group. The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group. Caspase-3 expression significantly increased in all six groups in comparison to the control, and docetaxel groups. Its expression significantly increased in the Vit1 and Vit2 groups in comparison with docetaxel + Vit1, and docetaxel + Vit2, respectively. CONCLUSION: Docetaxel ameliorates the damages to oocytes during vitrification by altering the expression of apoptosis-related genes and its effects are dependent on the vitrification solution used in cryopreservation of oocytes.

The effect of exercise training on osteocalcin, adipocytokines, and insulin resistance: a systematic review and meta-analysis of randomized controlled trials.

Recently, it has been reported that osteocalcin (OC), in particular its undercarboxylated (ucOC) form, is not only a bone remodeling marker but also an active hormone that intercedes glucose metabolism in humans. This study aimed to determine the impact of an exercise intervention on ucOC, adiponectin, leptin, and insulin resistance (measured by HOMA-IR). PubMed, CINAHL, Medline, Google Scholar, and Scopus databases and reference lists of included studies were searched. Twenty-two randomized controlled trials (RCTs) of exercise training impact in adults were included in the analysis. Results showed an overall significant increase in serum ucOC (MD: 0.15 ng/ml; 95% CI: 0.05 to 0.25) and adiponectin (MD: 2.83 mg/ml; 95% CI: 1.67 to 3.98), a significant decline in leptin (MD: - 4.89 pg/ml; 95% CI: - 6.94 to - 2.84), fasting glucose (MD: - 2.29 mg/dl; 95% CI: - 4.04 to - 0.54), fasting insulin (MD, - 8.90 µIU/ml; 95% CI: - 13.81 to - 3.98), and HOMA-IR (MD: - 1.96; 95% CI: - 3.11 to - 0.80). However, after removal of studies that had prescribed a balanced diet along with exercise intervention, total OC (TOC) levels also increased in the exercise group compared with the control group (MD: 0.36 ng/ml; 95% CI: 0.07 to 0.65). Our findings demonstrate that exercise-induced increases in ucOC are the probable cause of increased adiponectin. Additionally, increases in ucOC itself are probably due to changes in leptin levels and other factors, rather than its direct impact on bone and its osteoblastic activity. Further studies are required to clarify the mechanisms underlying the impact of exercise training on ucOC, adipocytokines, and insulin resistance.