دورية أكاديمية
Tumor necrosis factor-α increases ATP content in metabolically inhibited L929 cells preceding cell death
العنوان: | Tumor necrosis factor-α increases ATP content in metabolically inhibited L929 cells preceding cell death |
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المؤلفون: | Sánchez-Alcázar, José Antonio, Ruiz-Cabello, Jesús, Hernández-Muñoz, Inmaculada, Sánchez Pobre, Pilar, Torre, Paz de la, Siles, Eva, García, Inmaculada, Kaplan, Ofer, Muñoz-Yagüe, María T., Solís-Herruzo, José A. |
المساهمون: | Dirección General de Investigación Científica y Técnica, DGICT (España), Instituto de Salud Carlos III, Fundación Salud 2000 |
بيانات النشر: | American Society for Biochemistry and Molecular Biology |
سنة النشر: | 1997 |
المجموعة: | Digital.CSIC (Consejo Superior de Investigaciones Científicas / Spanish National Research Council) |
الوصف: | The effects of tumor necrosis factor-alpha (TNF) on ATP levels were studied in metabolically inhibited L929 cells. Treatment of these cells with TNF in the presence of actinomycin D or cycloheximide induces cyclic changes in the intracellular ATP content preceding cell death. After 3 h of incubation, the intracellular ATP content increased by 48 +/- 6% (p < 0.001), but at 4 h, it decreased to the control level. Two hours later, it increased again by 23 +/- 5% over the control level (p < 0.001). Coinciding with cell death, ATP content decreased progressively until almost complete depletion. These changes in ATP content were associated with parallel alterations in the respiratory coupling and with increased generation of reactive oxygen species. The mechanism by which TNF/actinomycin D or TNF/cycloheximide increased cellular ATP seemed to be dependent on the mitochondrial ATP synthesis and related to the cytotoxic effect of TNF, since blockade of mitochondrial electron transport prevented the increase in cellular ATP, the formation of reactive oxygen species, and the apoptotic cell death caused by TNF. We suggest that the TNF/actinomycin D- or TNF/cycloheximide-induced changes in intracellular ATP levels may be involved in the cytotoxic effect of TNF in metabolically inhibited L929 cells. ; This study was supported in part by “Fondo de Investigaciones Sanitarias” Grant 95/609, by “Dirección General de Investigación Cientı́fica y Técnica” Grants PB94/001 and PB92/316, and by Fundación “Salud 2000,” Spain. ; Peer reviewed |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
تدمد: | 0021-9258 1083-351X |
العلاقة: | Publisher's version; https://doi.org/10.1074/jbc.272.48.30167Test; No; Journal of Biological Chemistry 272(48): 30167-30177 (1997); http://hdl.handle.net/10261/198116Test; http://dx.doi.org/10.13039/501100004587Test; http://dx.doi.org/10.13039/501100007043Test; http://dx.doi.org/10.13039/501100008737Test; 9374498 |
DOI: | 10.1074/jbc.272.48.30167 |
DOI: | 10.13039/501100004587 |
DOI: | 10.13039/501100007043 |
DOI: | 10.13039/501100008737 |
الإتاحة: | https://doi.org/10.1074/jbc.272.48.30167Test https://doi.org/10.13039/501100004587Test https://doi.org/10.13039/501100007043Test https://doi.org/10.13039/501100008737Test http://hdl.handle.net/10261/198116Test |
حقوق: | open |
رقم الانضمام: | edsbas.213ADBA6 |
قاعدة البيانات: | BASE |
تدمد: | 00219258 1083351X |
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DOI: | 10.1074/jbc.272.48.30167 |