Involvement of reactive oxygen species-independent mitochondrial pathway in gossypol-induced apoptosis

被引：48

作者：

Hou, DX ^{[1
]}

Uto, T ^{[1
]}

Tong, XH ^{[1
]}

Takeshita, T ^{[1
]}

Tanigawa, S ^{[1
]}

Imamura, I ^{[1
]}

Ose, T ^{[1
]}

Fuji, M ^{[1
]}

机构：

[1] Kagoshima Univ, Fac Agr, Dept Biochem Sci & Technol, Kagoshima 8900065, Japan

来源：

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 2004年 / 428卷 / 02期

关键词：

gossypol; apoptosis; HL-60; cell; caspase; mitochondria; cytochrome C; reactive oxygen species;

D O I：

10.1016/j.abb.2004.06.007

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Gossypol is a component present in cottonseeds and has been demonstrated to be an effective contraceptive drug in preventing spermatogenesis in mammalian species. In the present, we reported that gossypol could induce apoptosis in human promyelocytic leukemia cells (HL-60), as characterized by DNA fragmentation, poly(ADP) ribose polymerase (PARP) cleavage. The efficacious induction of apoptosis was observed at 50 muM for 6 h. Further molecular analysis showed that gossypol induced the truncation of Bid protein, the loss of mitochondrial membrane potential (DeltaPsi(m)), cytochrome c release from mitochondria into cytosol, and activation of caspase-3, -8, and -9. However, gossypol did not increase the level of reactive oxygen species (ROS), and antioxidants including N-acetyl cysteine (NAC) and catalase could not block gossypol-induced apoptosis in the HL-60 cells. These data suggest that gossypol induces apoptosis in HL-60 cells through ROS-independent mitochondrial dysfunction pathway. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：179 / 187

页数：9

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