Nitroxide TEMPOL impairs mitochondrial function and induces apoptosis in HL60 cells
✍ Scribed by Elena Monti; Rosanna Supino; Mariapia Colleoni; Barbara Costa; Raffaella Ravizza; Marzia B. Gariboldi
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 156 KB
- Volume
- 82
- Category
- Article
- ISSN
- 0730-2312
- DOI
- 10.1002/jcb.1160
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The piperidine nitroxide TEMPOL induces apoptosis in a number of tumor cell lines through free radical‐dependent mechanisms. As mitochondria play a major role in apoptosis as both source and target for free radicals, the present study focuses on mitochondrial effects of TEMPOL in a human promyelocytic leukemic cell line (HL‐60). On 24‐h exposure to TEMPOL, the following alterations were observed: 1) decrease in both the intracellular and mitochondrial glutathione pools; 2) impairment of oxidative phosphorylation; and 3) decrease in mitochondrial membrane potential. In addition, TEMPOL was found to specifically target complex I of the respiratory chain, with minor effects on complexes II and IV, suggesting that mitochondrial effects might play a role in TEMPOL‐induced oxidative stress and apoptosis, and that TEMPOL might sensitize tumor cells to the pro‐apoptotic effects of cytotoxic agents. J. Cell. Biochem. 82: 271–276, 2001. © 2001 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
## Abstract Thymoquinone (TQ), the major biologically active component isolated from a traditional medicinal herb, __Nigella sativa__ Linn, is a potential chemopreventive and chemotherapeutic compound. Despite the promising antineoplastic activities of TQ, the molecular mechanism of its pharmacolog
## Abstract As an extension of our recently published work (Mlejnek and Kuglík [2000] J. Cell. Biochem. 77:6–17), the role of caspases in N^6^‐benzylaminopurine riboside (BAPR)‐induced apotosis in HL‐60 cells was evaluated in this study. Here, BAPR‐induced apoptosis was accompanied by activation of