Gliotoxin induces apoptosis in cultured macrophages via production of reactive oxygen species and cytochrome c release without mitochondrial depolarization
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摘要The cytotoxicity and its underlying mechanisms induced by gliotoxin (GT), an immunosuppressive agent, in macrophages are poorly understood. We report here that GT induced a rapid apoptosis (DNA fragmentation and hypodiploid nuclei obtained within 4hrs of treatment) in murine macrophages PU5-1.8 in a dose-dependent and cell cycle-independent manner. The GT-induced apoptosis was suppressed by z-Asp, z-VAD-fmk and antioxidants suggesting that production of reactive oxygen species (ROS) and activation of caspases were important in this process. Also, release of cytochrome c from mitochondria was found to be an early event (within I hr) after addition of GT (250 ng/ml) and its presence in the cytosol was sufficient to elicit apoptosis. Interestingly, the release of cytochrome c was not accompanied by a reduction in the mitochondrial membrane potential (psi (m)) as determined by several psi (m)-sensitive fluorescent indicators. Taken together, our results indicate that GT is a potent apoptotic agent in PU5-1.8 cells and the loss of psi (m) is not a universal early marker for apoptosis.
著者Suen YK, Fung KP, Lee CY, Kong SK
期刊名稱Free Radical Research
出版年份2001
月份1
日期1
卷號35
期次1
出版社HARWOOD ACAD PUBL GMBH
頁次1 - 10
國際標準期刊號1071-5762
語言英式英語
關鍵詞apoptosis; cytochrome c; gliotoxin; macrophage; mitochondrial potential; ROS
Web of Science 學科類別Biochemistry & Molecular Biology; BIOCHEMISTRY & MOLECULAR BIOLOGY

上次更新時間 2020-31-07 於 02:41