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Oxidative stress signalling in the apoptosis of Jurkat T‐lymphocytes by Raffaella Chiaramonte; Enrico Bartolini; Patrizia Riso; Elisabetta Calzavara; Daniela Erba; Giulio Testolin; Paola Comi; Gajanan V. Sherbet is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is Oxidative stress signalling in the apoptosis of Jurkat T‐lymphocytes about?

## Abstract The pathways of transduction of oxidative stress signals have been studied using the Jurkat T cell model. The oxidative stress was induced by exposure of the cells to 100 μM H~2~O~2~. DNA damage was detected within 15 min after commencement of treatment. DNA damage repair occurred within about 1 h in cells exposed to oxidative stress for 15 min. In continuous exposure to stress, DNA repair was slower and control levels of DNA integrity were not reached. DNA repair did not involve gene transcription. H~2~O~2~ at 100 μM caused cell death by necrosis as well as by apoptosis. Both these processes were induced by 15 min exposure to the stress stimulus. However, some important differences were found between necrosis and apoptosis. Necrosis was more rapid, began within an hour of treatment and continued to increase during the full duration of the experiment. But apoptosis was seen after 4 h from treatment and was conspicuous between 6 and 20 h after the start of treatment. The necrotic phase preceded apoptosis, although these did show an overlap. In the necrotic phase, __Bcl‐2, Caspase__ 8 genes were down regulated. The 6–20 h phase characterised by a marked increase in apopto

Who reads Oxidative stress signalling in the apoptosis of Jurkat T‐lymphocytes?

Author

Raffaella Chiaramonte; Enrico Bartolini; Patrizia Riso; Elisabetta Calzavara; Daniela Erba; Giulio Testolin; Paola Comi; Gajanan V. Sherbet

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0730-2312)

Published

2001

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)