Abstract：
:An increasing body of data has been demonstrating that mammalian cells have elaborate networks of molecular signalling in counteracting heat shock and in developing adaptation to oxidative stress to avoid cell death. However, the precise mechanisms linking heat shock, oxidative stress and cell survival/cell death mechanisms are not yet clearly understood. The purpose of this study was thus to study the time course of hyperthermia-induced oxidative stress and cellular signalling through the activation of heat shock factor 1 (HSF1) and heat shock protein 70 (HSP70), using freshly isolated mouse hepatocytes. The results accomplished in this work demonstrated that mild continuous hyperthermia (41 degrees ) leads to oxidative stress and loss of cellular viability in a time-dependent manner, with significant effects already observed at the first hour of incubation. These toxic effects developed concomitantly with activation of HSF1 and emerged before the formation of HSP70 levels. Thus, although cell signalling was triggered through the transcriptional activation of HSP70 via HSF1, this putative protective process did not modify the trend of hepatotoxic effects mediated by this type of hyperthermic challenging.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Santos-Marques MJ,Carvalho F,Sousa C,Remião F,Vitorino R,Amado F,Ferreira R,Duarte JA,de Lourdes Bastos Mdoi
10.1016/j.tox.2006.04.028subject
Has Abstractpub_date
2006-07-25 00:00:00pages
210-8issue
3eissn
0300-483Xissn
1879-3185pii
S0300-483X(06)00234-4journal_volume
224pub_type
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