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

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.
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.
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.