O-32: Quinazolinone Exposure Induces Apoptosis and Upregulation of Fas/FasL Expression in the Testis of Mice Embryonic (Pages: 33-33)

Sarhadi M *, Shams Lahijani M , Farivar S ,


Objective: Quinazolinones represent a class of drugs with variety of biological activities (antimicrobial,antiinflamatory,diuretic,antiallergic,anticancer and many others).Previousreports demonstrated the ability of quinazolinones-based compounds to suppress prostate tumor growth via apoptosis.Apoptosis is very common in embryos of normal and injured mammalian testes as well as in adults.Spermatogenic cell degeneration in mature mammalian testis occurs spontaneously during normal spermatogenesis and in response to cytotoxic agents.The aim of the present study is to investigate gene expression involved in the signal pathway of death signal receptor pathway of fas/fasl in quinazolinone induced apoptosis of testicular germ cells during different developmental days (15.5, 18.5). Materials and Methods: Pregnant Balb/C mice were divided into control,sham and experimental groups.Experimental groups were given intraperitoneal injection of QEPE at the most effective dose (100 mg/kg / body weight). The sham groups received 0/05% methyl cellulose (the solvent). Testes of 15.5 and 18.5 days old embryos were removed 48 hour after QEPE administration.The presence of apoptosis within seminiferous tubules of mouse foetal testis was determined by H&E staining,terminal deoxynucleotidyl transferase-mediated dUTP nick-endlabelling(TUNEL)was applied to detect the highlights of in situ DNA fragmentation and finally, changes in the expression levels of Fas and FasL detected by RT-PCR. Results: After QEPE administration,TUNEL positive cells and expression levels of Fas/FasL increased compared with sham and control groups.Our results showed quinazolinone as a significant inducer of apoptosis in foetal testicular germ cells Conclusion: Previouse studies suggested that the death receptor signaling pathway may be a mechanism through wich toxicant materials mediates germ cell apoptosis. The mechanism of germ cell apoptosis induced by quinazolinone associated with the activation of Fas/FasL.