دورية أكاديمية

Tumor necrosis factor-α increases ATP content in metabolically inhibited L929 cells preceding cell death

التفاصيل البيبلوغرافية
العنوان: Tumor necrosis factor-α increases ATP content in metabolically inhibited L929 cells preceding cell death
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
الوصف
تدمد:00219258
1083351X
DOI:10.1074/jbc.272.48.30167