Abnormal accumulation of corpora lutea in ovaries of the senescence accelerated mouse prone (SAMP1)

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 SAMP1 mice and examined the mechanism of abnormality in luteal cell regression in the ovaries of SAMP1 mice. No significant changes were detected in serum progesterone or 17β-estradiol levels during the estrus cycle between SAMP1 and SAMR1 mice. In abnormally accumulated LBs of SAMP1 mice, extremely high levels of 20α-hydroxysteroid dehydrogenase, which catalyzes the conversion of progesterone to the inactive form, 20α-hydroxyprogesterone, were demonstrated histochemically. However, no marked differences in the activity of 17β-hydroxysteroid dehydrogenase activity were detected histochemically. Moreover, no apoptotic cells were detected in the abnormally accumulated LBs of SAMP1 mice. The SAMP1 mouse may be a useful model in which to examine the mechanism of regression of LBs in mammalian ovaries.