This study strengthens the current literature associating sperm quality with recurrent pregnancy loss, and emphasizes the important of evaluating male factor by tests such as SCD in addition to conventional sperm parameters.

Objective This study evaluated the protective effect of betacarotene (BC) on titanium oxide nanoparticle (TNP) induced spermatogenesis defects in mice. Materials and methods Thirty-two NMRI mice were randomly divided into four groups. BC group received 10 mg/kg of BC for 35 days. TNP group received 300 mg/kg TNP for 35 days. TNP+BC group initially received 10 mg/kg BC for 10 days and was followed by concomitant administration of 300 mg/kg TNP for 35 days. Control group received only normal saline for 35 days. Epididymal sperm parameters, testicular histopathology, spermatogenesis assessments and testosterone assay were performed for evaluation of the TNP and BC effects on testis. Results Serum testosterone levels were markedly decreased in TNP-intoxicated mice. Epididymal sperm parameters including sperm number, motility and percentage of abnormality were significantly changed in TNP-intoxicated mice (p < 0.01). Histopathological criteria such as epithelial vacuolization, sloughing of germ cells and detachment were significantly increased in TNP-intoxicated mice (p<0.001). BC+TNP treatment significantly prevented these changes (p<0.05). BC also significantly elevates testosterone levels in BC+TNP group compared to TNP-treated mice (p<0.01). Discussion and conclusion The results of this study demonstrated that BC improved the spermatogenesis defects in TNPtreated mice. BC had a potent protective effect against the testicular toxicity and might be clinically useful.

The aim of the study was to characterise the alterations in expression of some apoptosis regulators in unilaterally and bilaterally heat-treated mouse testes at different time intervals to 42 days after surgery. Cryptorchidism was induced in immature mice by returning the testis to the abdominal cavity via a surgical procedure. Transcript levels of Bax, Bcl-2 proper, p53 and survivin mRNA and protein were determined in normal and cryptorchid testes using reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. RT-PCR data verified the elevation of p53 expression and decrease of Bax and Bcl-2 proper mRNA in the cryptorchid testis in a time-dependent manner. The expression of survivin 140 and 40 variants strongly decreased in the bilateral groups compared with unilateral and control groups. These changes were significantly different in the bilateral groups in comparison with the unilateral groups. Immunohistochemistry data showed that the intensity of p53 and Bax expression mainly increased in the remainder cells in the cryptorchid testis and the rates of Bcl-2 proper and survivin expression decreased mainly in the bilateral groups. These observations suggest that multiple molecular pathways participate in the germ cell apoptosis induced by cryptorchidism.

Background: Hydrogen sulfide (H2S) has been shown to have a protective role in various kidney disorders. Objectives: This study investigated the molecular mechanism of NaHS (a H2S donor) in treating on the renal damage induced by cisplatin (CP).Materials and Methods: Thirty-two male rats were randomly divided into 4 groups: Normal control group (group A)‚ NaHS group (group B) which received 200 µg/kg/d (intraperitoneal injection; i.p.) for 15 days‚ CP group (group C) which rats were injected with CP (5 mg/kg, single dose, i.p.), and CP + NaHS group (group D) (5 mg/kg and 200 µg/kg, respectively, i.p.). Samples of urine and serum, tissue of kidney were collected for analysis after treatments for 15 days. Morphological changes were elevated under light microscope‚ protein expression of desmin and nephrin were determined by immunohistochemistry and western blotting and also malondialdehyde (MDA) level was determined by spectrophotometer. Results: Compared to the CP group, NaHS treatment mitigated histological damages, decreased 24-hour urine protein excretion, serum urea and creatinine as well as MDA level. NaHS treatment increased protein levels of nephrin. Moreover, NaHS treatment decreased protein levels of desmin. Conclusions: NaHS can ameliorate CP -induced renal damage in rats which is associated with the increase in nephrin protein expression, and the decrease in MDA level and desmin protein expression.