Zinc induced apoptosis in HEP-2 cancer cells: The role of oxidative stress and mitochondria
Zinc induced apoptosis in HEP-2 cancer cells: The role of oxidative stress and mitochondria
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DOI：
10.1002/biof.5520230206
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发表时间：
2005-01-01
期刊：
影响因子：
6
通讯作者：
Cervinka, M
中科院分区：
文献类型：
--
作者：
Rudolf, E;Rudolf, K;Cervinka, M
在96小时暴露期间，研究了硫酸锌对癌Hep-2细胞系的凋亡诱导。在48小时的曝光，锌易位到线粒体和刺激生产的活性氧（ROS），影响细胞的GSH管理和诱导p53和线粒体膜电位的耗散适度激活。在锌暴露的细胞中，线粒体释放细胞色素c和AIF，其易位到细胞质或细胞核与细胞凋亡的激活相一致。使用抑制特定凋亡靶点的各种药理学抑制剂（抗氧化剂，如N-乙酰半胱氨酸和辅酶Q，半胱天冬酶抑制剂z-DEVD-fatase和z-VAD-fatase，环孢菌素A和bonkgrekic acid）证明，Zn直接和间接作用于线粒体，并且观察到的凋亡通过半胱天冬酶依赖性和半胱天冬酶非依赖性途径执行。
Induction of apoptosis by zinc sulfate was investigated during 96 h exposure on the cancer Hep-2 cell line. During 48 h of exposure, zinc translocated into mitochondria and stimulated production of reactive oxygen species (ROS), affected cellular GSH management and induced moderate activation of p53 and dissipation of mitochondrial membrane potential. In Zn-exposed cells, mitochondria released cytochrome c and AIF, whose translocation to the cytoplasm or the nucleus coincided with the activation of apoptosis. The use of various pharmacological inhibitors inhibiting particular apoptotic targets (antioxidants such as N-acetyl-cysteine and coenzyme Q, the caspase inhibitors z-DEVD-fmk and z-VAD-fmk, cyclosporin A and bonkgrekic acid) proved that Zn acts both directly and indirectly on mitochondria and observed apoptosis is executed by caspase-dependent and caspase-independent pathways.