DOI 10.1095/biolreprod.104.031278 Effects of Acid Sphingomyelinase Deficiency on Male Germ Cell Development and

Deficiency of acid sphingomyelinase (ASM), an enzyme re-sponsible for producing a pro-apoptotic second messenger cer-amide, has previously been shown to promote the survival of fetal mouse oocytes in vivo and to protect oocytes from che-motherapy-induced apoptosis in vitro. Here we investigated the effects of ASM deficiency on testicular germ cell development and on the ability of germ cells to undergo apoptosis. At the age of 20 weeks, ASM knock-out (ASMKO) sperm concentrations were comparable with wild-type (WT) sperm concentrations, whereas sperm motility was seriously affected. ASMKO testes contained significantly elevated levels of sphingomyelin at the age of 8 weeks as detected by high-performance, thin-layer chromatography. Electron microscopy revealed that the testes started to accumulate pathological vesicles in Sertoli cells an