Zinc-deficient rat embryos have increased caspase 3-like activity and apoptosis
Zinc-deficient rat embryos have increased caspase 3-like activity and apoptosis
复制标题
DOI：
10.1006/bbrc.2000.2608
复制
发表时间：
2000-04-29
影响因子：
3.1
通讯作者：
Keen, CL
中科院分区：
文献类型：
--
作者：
Jankowski-Hennig, MA;Clegg, MS;Keen, CL
半胱氨酸氨基转移酶活性是细胞凋亡的标志。鉴于母体缺锌会导致大鼠胚胎细胞凋亡，我们评估了缺锌胚胎中caspase的活性。取孕中期大鼠胚胎，随机饲喂缺锌饲料(0.5微克锌/克)，或自由饲喂锌充足饲料(25微克锌/克)，或成对喂饲低锌饲料。饲喂适锌饲料的母鸡胚胎细胞死亡水平正常，而饲喂缺锌饲料的母鸡胚胎细胞死亡水平要么增加，要么正常。缺锌胚胎表现为细胞死亡增加，caspase活性增加。细胞死亡水平正常的胚胎，无论母亲的饮食如何，都有类似的半胱氨酸酶活性。因此，体内缺锌诱导的细胞凋亡与caspase活性增加有关，(C)2000学术出版社。
Caspase activity is a hallmark of apoptosis. Given that maternal zinc (Zn) deficiency results in apoptosis in the rat embryo, we assessed caspase activity in Zn-deficient embryos. Mid-gestation rat embryos were collected from dams fed either a Zn-deficient (0.5 mu g Zn/g) diet ad libitum, or a Zn-adequate (25 mu g Zn/g) diet ad libitum or pair fed to dams fed the Zn-deficient diet. Embryos from dams fed the Zn-adequate diet had a normal level of cell death, while embryos from the dams fed the Zn-deficient diet had either increased or normal levels of cell death. Zn-deficient embryos displaying increased cell death had increased caspase activity. Embryos with normal levels of cell death, regardless of maternal diet, had similar caspase activities. Thus, Zn-deficiency-induced apoptosis in vivo is associated with increased caspase activity, (C) 2000 Academic Press.