Zuretti M F, Gravela E
Cancer Lett. 1987 Jul;36(1):35-43. doi: 10.1016/0304-3835(87)90100-5.
A strong ornithine decarboxylase (ODC)-inactivating capacity has been previously shown (M.F. Zuretti and E. Gravela (1983) Biochim. Biophys. Acta, 742, 269-277) to be bound to rat liver microsomes. Present results show that in 2 fast-growing transplantable tumors, the 3924A Morris hepatoma and the AH 130 Yoshida ascites hepatoma, microsomes are endowed with a greatly enhanced ODC-inactivating capacity, and, concurrently, ODC displays an extreme in vitro liability and an unusual thiol-dependency (most of the activity requires dithiothreitol supply to be determined). These data are at variance with those previously obtained in hepatomas induced by N-2-fluorenylacetamide (E. Gravela et al., (1983) Cancer Res., 42, 2298-2300). The possibility that ODC liability in the 2 hepatomas here studied may result from in vivo exposure to a strong microsomal activity is considered.
先前已表明(M.F. 祖雷蒂和E. 格拉韦拉(1983年)《生物化学与生物物理学报》,742卷,269 - 277页),强大的鸟氨酸脱羧酶(ODC)失活能力与大鼠肝脏微粒体相关。目前的结果表明,在两种快速生长的可移植肿瘤中,即3924A莫里斯肝癌和AH 130吉田腹水肝癌,微粒体具有大大增强的ODC失活能力,同时,ODC在体外表现出极强的不稳定性和不寻常的硫醇依赖性(大部分活性需要二硫苏糖醇供应才能测定)。这些数据与先前在N - 2 - 芴基乙酰胺诱导的肝癌中获得的数据(E. 格拉韦拉等人,(1983年)《癌症研究》,42卷,2298 - 2300页)不一致。本文研究的两种肝癌中ODC不稳定性可能是由于体内暴露于强大的微粒体活性这一可能性也被考虑在内。