Abstract
The senescence accelerated mouse prone (SAMP) mice with a shortened life span show accelerated changes in many of the signs of aging and have a shorter reproductive life span than SAM resistant (SAMR) controls. The reproductive senescence of SAMP is more accelerated than that of SAMR. In the present study, we found abnormal accumulation of luteal bodies (LBs) only in the ovaries of SAMP mice and, we examined the mechanism of abnormalities in luteal cell regression in the ovaries of SAMP mice. No significant changes were detected in serum progesterone or 17β-estradiol levels during estrus cycle between SAMP and SAMR mice. In abnormally accumulated LBs of SAMP mice, extremely high levels of activity of 20α-hydroxysteroid dehydrogenase, which catalyzes conversion of progesterone to the inactive form, 20α-hydroxyprogesterone were demonstrated histochemically. However, no marked differences in activity of 17β-hydroxysteroid dehydrogenase were detected histochemically. Moreover, no apoptotic cells were detected in the abnormally accumulated LBs of SAMP mice. Extremely weak immunohistochemical reactivity for endothelial nitric oxide synthase (eNOS) was noted in the abnormally accumulated LBs of SAMP mice, but no differences were seen in inducible NOS (iNOS). No marked differences in expression of eNOS- or iNOS-mRNA were seen during the estrus cycle in the ovaries of SAMP mice. However, high levels of expression of eNOS-mRNA at estrus stage and of iNOS-mRNA at estrus and metestrus stages were noted in the ovaries of SAMR mice. SAMP mice may be a useful model in which to examine the mechanism of regression of LBs in mammalian ovaries.
