by Sánchez-Alcázar, José A, Schneider, Erasmus, Hernández-Muñoz, Inmaculada, Ruiz-Cabello, Jesus, Siles-Rivas, Eva, De la Torre, Paz, Bornstein, Belen, Brea, Gloria, Arenas, Joaquín, Garesse, Rafael, Solis-Herruzo, Jose A, Knox, Alan J and Navas, Plácido
Abstract:
In this study, we show that reactive oxygen species production induced by tumour necrosis factor alpha (TNF-alpha) in L929 cells was associated with a decrease in the steady-state mRNA levels of the mitochondrial transcript ATPase 6-8. Simultaneously, the transcript levels of two nuclear-encoded glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and phosphofructokinase, were increased. These changes were associated with decreased protein levels of the ATPase subunit a (encoded by the mitochondrial ATPase 6 gene) and cytochrome c oxidase subunit II, and increased protein levels of phosphofructokinase. Since TNF-alpha had no effect on the amount of mitochondrial DNA, the results suggested that TNF-alpha acted at the transcriptional and/or post-transcriptional level. Reactive oxygen species scavengers, such as butylated hydroxianisole and butylated hydroxytoluene, blocked the production of free radicals, prevented the down-regulation of ATPase 6-8 transcripts, preserved the protein levels of ATPase subunit a and cytochrome c oxidase subunit II, and attenuated the cytotoxic response to TNF-alpha, indicating a direct link between these two phenomena.
Reference:
Reactive oxygen species mediate the down-regulation of mitochondrial transcripts and proteins by tumour necrosis factor-alpha in L929 cells. (Sánchez-Alcázar, José A, Schneider, Erasmus, Hernández-Muñoz, Inmaculada, Ruiz-Cabello, Jesus, Siles-Rivas, Eva, De la Torre, Paz, Bornstein, Belen, Brea, Gloria, Arenas, Joaquín, Garesse, Rafael, Solis-Herruzo, Jose A, Knox, Alan J and Navas, Plácido), In Biochem J, Portland Press Limited, volume 370, 2003.
Bibtex Entry:
@article{SanchezAlcazar:2003kb,
author = {S{'a}nchez-Alc{'a}zar, Jos{'e} A and Schneider, Erasmus and Hern{'a}ndez-Mu{~n}oz, Inmaculada and Ruiz-Cabello, Jesus and Siles-Rivas, Eva and De la Torre, Paz and Bornstein, Belen and Brea, Gloria and Arenas, Joaqu{'i}n and Garesse, Rafael and Solis-Herruzo, Jose A and Knox, Alan J and Navas, Pl{'a}cido},
title = {{Reactive oxygen species mediate the down-regulation of mitochondrial transcripts and proteins by tumour necrosis factor-alpha in L929 cells.}},
journal = {Biochem J},
year = {2003},
volume = {370},
number = {Pt 2},
pages = {609--619},
month = mar,
publisher = {Portland Press Limited},
affiliation = {Laboratorio Andaluz de Biolog{'i}a, Universidad Pablo de Olavide, Carretera de Utrera Km 1, Sevilla 41013, Spain. jasanalc@dex.upo.es},
doi = {10.1042/BJ20021623},
pmid = {12470298},
pmcid = {PMC1223204},
language = {English},
rating = {0},
date-added = {2018-03-16T12:59:57GMT},
date-modified = {2020-07-09T13:27:52GMT},
abstract = {In this study, we show that reactive oxygen species production induced by tumour necrosis factor alpha (TNF-alpha) in L929 cells was associated with a decrease in the steady-state mRNA levels of the mitochondrial transcript ATPase 6-8. Simultaneously, the transcript levels of two nuclear-encoded glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and phosphofructokinase, were increased. These changes were associated with decreased protein levels of the ATPase subunit a (encoded by the mitochondrial ATPase 6 gene) and cytochrome c oxidase subunit II, and increased protein levels of phosphofructokinase. Since TNF-alpha had no effect on the amount of mitochondrial DNA, the results suggested that TNF-alpha acted at the transcriptional and/or post-transcriptional level. Reactive oxygen species scavengers, such as butylated hydroxianisole and butylated hydroxytoluene, blocked the production of free radicals, prevented the down-regulation of ATPase 6-8 transcripts, preserved the protein levels of ATPase subunit a and cytochrome c oxidase subunit II, and attenuated the cytotoxic response to TNF-alpha, indicating a direct link between these two phenomena.},
url = {http://biochemj.org/lookup/doi/10.1042/bj20021623},
uri = {url{papers3://publication/doi/10.1042/BJ20021623}}
}