Past Issue

Volume 9, Supplement 1, Summer 2015 (Presented at 16th Congress on Reproductive Biomedicine and 10th Royan Nursing and Midwifery Seminar) Pages: 50-51

P-18: Protective Effect of Selenium- Enriched Saccharomyces Cerevisiae Cytoplasm and Cell Wall on Chronic Immobilization Stress-Induced Damages in Testis; Evidence for Apoptosis


Background
Previous reports showed that immobilization stress (IMS) results in severe damages at spermatogenesis level. Present study was performed in order to evaluate the protective effect of selenium-enriched yeast fragments on IMS-induced derangements.
Materials and methods
For this purpose, 42 mature male Wister rats were assigned into 6 groups (7 rats in each group) including; control, stress-induced and SE-enriched saccharomyces cerevisiae fragments-treated groups. The animals in treatment groups subdivided into 4 groups as; SE-enriched yeast cytoplasm (SEC)+stress, SE-enriched saccharomyces cerevisiae cell wall+stress (SECW), SEC alone-treated and SECW alone-treated groups. In order to induce stress, the rats were immobilized by keeping them into transparent plastic jars with 5 holes for 2 hours a day. All animals received the chemicals (5×108 CFU/ml, in one mL for day) orally for 42 days. At the end of day 42. The testicles were dissected out, fixed in formaldehyde. The expression of bcl-2 and p53 were investigated by using immnohistochemical and RT-PCR techniques. Moreover, the TUNEL staining was performed in order to evaluate apoptosis.
Results
Observations demonstrated that co-administrating cytoplasm+cell wall in SECW group significantly (P<0.05) reduced p53 at both protein and mRNA levels and remarkably (P<0.05) enhanced bcl-2 protein and mRNA. Estimating apoptotic cells distribution between experimental groups illustrated a significant reduction more significantlyin SEC and SECW-treated groups.
Conclusion
Our data suggested that co-administrating SEenriched yeast cytoplasm with SE-enriched yeast cell wall reduces IMS-induced apoptosis by up-regulating bcl-2 mRNA and protein contents and by down-regulating p52 expression.