cron-web.org

[A1CR]

The active ingredients of carcinogenic cigarette smoke
condensate[] appear
to involve oxidative processes. Previously, it was found
that, "cigarette
smoke-mediated proinflammatory events are regulated by the
redox status of
the cells", in (1). A more recent paper in the same
journal and by some of the same authors finds that SirT1 is
an HDAC (histone
deacetylase) that mediates the effects of cigarette smoke
condensate, and
this evidences for SirT1 "implicating a role of SIRT1 in
sustained
inflammation and aging of the lungs", as well as CR, which
appears to
involve a mechanism that reduces oxidation.

1. Yang SR, Chida AS, Bauter MR, Shafiq N, Seweryniak K,
Maggirwar SB,
Kilty I, Rahman I.
Cigarette smoke induces proinflammatory cytokine release by
activation of
NF-kappaB and posttranslational modifications of histone
deacetylase in
macrophages.
Am J Physiol Lung Cell Mol Physiol. 2006 Jul;291(1):L46-57.
Epub 2006 Feb
10.
PMID: 16473865

2. Yang SR, Wright J, Bauter M, Seweryniak K, Kode A, Rahman I.
Sirtuin regulates cigarette smoke induced pro-inflammatory
mediators release
via RelA/p65 NF-{kappa}B in macrophages in vitro and in rat
lungs in vivo.
Am J Physiol Lung Cell Mol Physiol. 2006 Oct 13; [Epub ahead
of print]
PMID: 17041012