Mitochondria-targeted antioxidants do not prevent tumour necrosis factor-induced necrosis of L929 cells |
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Authors: | Jarvis Reagan M Göttert Jana Murphy Michael P Ledgerwood Elizabeth C |
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Affiliation: | a Department of Biochemistry, University of Otago, Dunedin, New Zealandb MRC Dunn, Human Nutrition Unit, Cambridge, UK |
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Abstract: | Mitochondrial production of reactive oxygen species (ROS) is widely reported as a central effector during TNF-induced necrosis. The effect of a family of mitochondria-targeted antioxidants on TNF-induced necrosis of L929 cells was studied. While the commonly used lipid-soluble antioxidant BHA effectively protected cells from TNF-induced necrosis, the mitochondria-targeted antioxidants MitoQ3, MitoQ5, MitoQ10 and MitoPBN had no effect on TNF-induced necrosis. Since BHA also acts as an uncoupler of mitochondrial membrane potential, two additional uncouplers were tested. FCCP and CCCP both provided dose-dependent inhibition of TNF-induced necrosis. In conclusion, the generation of mitochondrial ROS may not be necessary for TNF-induced necrosis. Instead, these results suggest alternative mitochondrial functions, such as a respiration-dependent process, are critical for necrotic death. |
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Keywords: | Tumour necrosis factor reactive oxygen species mitochondria antioxidants L929 cells necrosis |
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