Peroxiredoxin (Prx) II belongs to a recently discovered family of peroxidases that play important roles in antioxidation and signal transduction. In this study, we aimed to study the localization and expression of Prx II in the mouse ovary, oviduct, and uterus, and preimplantation embryos. Immunohistochemical staining analysis showed that, in the ovary, Prx II was expressed in the oocyte cytoplasm of the primary follicle, the secondary follicle, and the premature follicle; Prx II was expressed in germinal vesicle-intact oocytes (GV oocytes) and metaphase II eggs (MII eggs), as well as at various stages in early embryos. Reverse transcription polymerase chain reaction (RT-PCR) results indicated that the Prx II mRNA was expressed at a high level in GV eggs, slightly lower levels in MII eggs, and had no detectable expression in four-cell embryos and early blastocysts. In the oviduct, Prx II was expressed in the epithelia, while in the uterus Prx II was mainly distributed in the endometrial stroma. Taken together, our results suggest that Prx II plays a key antioxidation role in the maturation of oocytes and development of early embryos, thus providing crucial experimental evidence for further exploring the function of Prx II in the development of oocytes and preimplantation embryos. Anat Rec,[293][294][295][296][297]

The correlation between the early embryonic block to development and mitochondrial activity was investigated comparing two-cell embryos produced in vitro from Kunming (KM) and B6C3F1 mice. One-cell embryos were obtained from two species of hybrids (female KM mice mated with KM males and female B6C3F1 mice mated with KM males) and cultured for 84 hr in M16 media. The mitochondrial membrane potential, ATP content, and reactive oxygen species levels were measured in the resulting KM and B6C3F1 two-cell embryos. Mitochondrial membrane potential and ATP content were also determined in KM and B6C3F1 metaphase II eggs. The results showed that the two-cell block was observed in cultured KM embryos but not in B6C3F1 embryos. Mitochondrial membrane potential and ATP content of KM two-cell embryos were significantly lower than in B6C3F1 two-cell embryos (P < 0.01). Interestingly, the reactive oxygen species levels of KM two-cell embryos were significantly lower than their B6C3F1 counterparts (P < 0.01). There was no difference in mitochondrial membrane potential and ATP content between KM and B6C3F1 metaphase II eggs. It is concluded that KM mice have an early twocell embryo block and that a possible ''blocking'' mechanism is the lower mitochondrial membrane potential and ATP content in these embryos. The results suggest a new approach for overcoming early embryonic development block, that of manipulating mitochondrial activity. Anat Rec, 292:661-669, 2009. V V C 2009 Wiley-Liss, Inc.

ObjectivePrevious studies determined ovariectomy (OVX) induced cancellous bone loss and raised cage (RC) bipedal stance partially prevented OVX induced bone loss at red marrow bone sites in adult rats; however, these effects in the distal tibial metaphysis (DTM) with fatty marrow, a site similar to adult long bone metaphyses (non‐veterbral bone sites) with low risk of postmenopausal fracture, have yet to be determined.MethodsSix‐month‐old female S‐D rats were divided into basal, sham, OVX, RC and combination of OVX plus RC exercise for 4 and 8 weeks, cancellous bone histomorphometry on fluorescent labeled undecalcified cross sections of DTM were performed.ResultsIn DTM, OVX did not induce cancellous bone loss, but significantly increased bone turnover. RC exercise alone had no effect on cancellous bone mass, but significantly reduced bone resorption. Unlike in high turnover red marrow sites, the combination of RC exercise and OVX only partially prevented bone loss, but combining with raised cage exercise and OVX in DTM totally inhibited OVX induced cancellous bone loss by depressing bone resorption (reduced eroded perimeter).ConclusionsIn DTM, the inhibition of OVX induced bone loss can be attributing to a combination of fatty marrow content and increased mechanical loading with decreased resorption, which may partly explain why non‐vertebral bone sites are less at risk to fracture in postmenopausal patients.