Riboflavin recovery of spermatogenic dysfunction via a dual inhibition of oxidative changes and regulation of the PINK1-mediated pathway in arsenic-injured rat model.

Arsenic trioxide (As2O3) poisoning and associated potential lesions are of a global concern. Inversely, riboflavin (vitamin B2, VB2) as a component of flavoproteins could play a vital role in the spermatogenic enzymatic reactions. Thus, this research aimed to explore potential beneficial roles of VB2 during As2O3-injured-toxicity. Rats were randomly allocated into 4 groups (n=8/group) and challenged as follows (for 30 days continuously): Group 1 received normal saline; Group 2 was treated with 3 mg As2O3/L; Group 3 received 40 mg VB2/L; Group 4 received 3 mg As2O3/L + 40 mg VB2/L. Both As2O3 and VB2 were dissolved in deionized water. Malondialdehyde (MDA), Glutathione Peroxidase (GSH-Px), Superoxide dismutase (SOD), and Catalase (CAT) were assessed for the oxidative profile, while TAS (Total Antioxidative Status) levels were evaluated for the antioxidant system, in both serum and testicular tissue. P<0.05 was considered statistically significant. The results show that As2O3 significantly decreased the body weight, testicular weight and testis volume, semen quality and testicular cell count (p<0.05). Furthermore, MDA content in the testicular tissue of the As2O3 group rats was significantly higher in comparison to the vehicle group (p<0.05). Likewise, TAS and the activities of GSH-Px, CAT and SOD were reduced (p<0.05) when compared to the control. As(2)O(3) induced testicular damage and seminiferous tubular atrophy. Monodansylcadaverine assays mirrored the histopathology observations. Meanwhile, As2O3 upregulated the expression of mitophagy-related genes including PINK1, Parkin, USP8, LC3-I, Fis1 and Mfn2. The p38 gene, responsible to stress stimuli, was also upregulated by As2O3 administration. Meanwhile, exposure to VB2 led to a significant decrease of the expression levels of mitophagy related genes. Our study revealed that VB2 supplementation protected testicular structures against As2O3-induced injury via a dual inhibition of oxidative changes and a regulation of the PINK1-mediated pathway.

The effects of sericin in recovering spermatogenesis and sexual hormone levels in diabetic rats.

Sericin-S (a hydrolysate from the silk protein sericin) is a natural antioxidant, which may improve spermatogenesis while having high biological safety, thus potentially useful for the treatment of male infertility. Our objective was to determine the effects of sericin-S on the sperm parameters and sexual hormone levels in a diabetic rat model. Thirty-six adult male rats were randomly divided in two groups, inducing diabetes in one of them by intraperitoneal administration of streptozotocin (STZ; 65 mg/kg). Both groups were randomly assigned to three subgroups, receiving oral gavage of saline, 1% or 2% sericin extract for 60 days. Therefore, the experimental design was a 2 × 3 factorial design of STZ and sericin treatments. One day after the last treatment, the rats were euthanized, weighed, the testes were processed (weigh, volume, and histology), and serum samples were processed for measuring sex hormone levels [testosterone, follicle-stimulating hormone, and luteinizing hormone (LH)]. STZ treatment decreased LH concentration and counts of spermatogonia, spermatocytes, and spermatids. Body and testis weights were significantly (p < 0.05) lower in the control group (non-diabetic saline) compared to the treated groups. In non-diabetic rats, sericin treatments increased (p < 0.05) the number of testicular cells (spermatogonia, spermatocytes, spermatids, Sertoli, and Leydig cells) and sex hormone concentrations. In diabetic rats, administration of sericin significantly (p < 0.05) improved sperm cell number and sex hormones levels. In nutshell, sericin can clearly modify sperm parameters and overall sex hormone function, and could improve spermatogenesis in normal and diabetic rats.