난관상피세포와 그 배양액에서 분비된 고분자 분획이 소정자의 수정능력에 어떠한 영향을 미치는지 알아보고자 실시한 실험에서 다음과 같은 결론을 얻었다. 1. 난관상피세포배양액으로부터 MW 5 kDa cut-off bucket을 사용하여 탈염 및 농축을 실시, 단백질/고분자분획을 회수하고 이를 체외수정용 배양액에 첨가하고 난관상피세포 monolayer와 공배양을 통해 체외수정을 실시한 결과 고분자분획첨가 및 난관상피세포 공배양(OM+OEC)군이 고분자분획첨가

어수리의 미숙배로부터 체소포배 형성시 자엽의 수적변이에 미치는 cytokinin의 영향을 조사하하였다. 구상형배에 0.2mg/l의 BA, 2ip, kinetin을 각각 처리하여 2주간 배양하였을 때, 다자엽의 형성률은 각각 84.9, 42.6, 32.9%로서 대조구(25.2%)에 비하여 BA>2ip>kinein순으로 높았으며 특히 BA 처리시에 가장 높게 나타났다. 또한 BA를 농도별(0, 0.01, 0.05, 0.1mg/l)로 배발생세포괴에 2주간 처리하였을 때, 다자엽의 형성율은 각각 23.3, 39.7, 69.4, 74.4%로서 농도가 높을수록 증가하는 경향이었다. 0.2mg/l의 BA를 구상형, 심장형, 또는 어뢰형, 자엽시기의 배에 2주간 처리한 경우에 다자엽의 형성률은 각각 92.4, 84.4, 26.3%로서 배발생 초기에 처리될 경우에 더욱 높게 나타났다.

Prolactin (PRL) surge in cycling rats at proestrous afternoon has previously been reported as an inducer of apoptotic cell death of luteal cells. This death-inducing action of PRL seeins unusual, because PRL can he categorized as a cell-survival factor, if other known physiological functions of PRL are taken into account. In this study, the apoptotic action of PRL was assessed in cultured cells prepared from rat luteal tissue and underlying molecular /cellular mechanism of PRL-induced luteolysis was analyzed. The latest crop of corpora lutea (CLs) were enucleated from rat ovaries at 18:00 h on the proestrous day before the next ovulation. Donor rats were pretreated with CB154, a dopamine agonist, in order to he exempted from the endogenous PRL surge. The harvested GLs were dispersed and cultured with or without PRL (2g /ml) for 24 or 48 h. An addition of PRL to the culture medium changed the parameters indicative of cell death via apoptosis: a decrease in cell viability (MTT) and an increase in chromatin condensation. Most of the DNA breakdown in nuclei induced by PRL occurred in steroidogenic cells which were identified by 3-HSD activity staining, and the number of 3-HSD-positivecells were significantly decreased. Interestingly, most of the cells with an apoptotic nucleus adhered to one or more intact and seemingly non-steroidogenic cells. Because the expression of Fas has heen shown to be abundant in murine ovary, and Fas is known to have an exact physiological role in occurrence of apoptotic cell death, the membrane form-Fas ligand (rnFasL) was quantified in the cell lysate. An addition of PRL increased expression of mFasL. Moreover, an addition of concanavalin A (ConA), a T-cell specific activator, in place of PRL, enhanced the apoptotic parameters. Cumulatively, the apoptotic PRL action was addressed to cells unknown than steroidogenic lute~ cells. The most prohable candidate for the direct target cells is Tcells in the luteal tissue that can express mFasL in response to PRL.