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Science Forum Index » Life Extension Forum » Dicarbonyls Stimulate Cellular Protection Systems in...
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| Olafur Pall Olafsson... |
 Posted: Sun May 04, 2008 6:17 pm |
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Ann N Y Acad Sci. 2008 Apr;1126:113-7.
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Dicarbonyls Stimulate Cellular Protection Systems in Primary Rat
Hepatocytes and Show Anti-inflammatory Properties.
Buetler TM, Latado H, Baumeyer A, Delatour T.
Nestl¨¦ Research Center, Vers-chez-les-Blanc, 1000 Lausanne 26,
Switzerland. Timo.Buetler at (no spam) rdls.nestle.com.
Advanced glycation endproducts (AGEs) and their precursor
dicarbonyls are generally perceived as having adverse health effects.
They are also considered to be initiators and promoters of disease and
aging. However, proof for a causal relationship is lacking. On the
other hand, it is known that AGEs and melanoidins possess beneficial
properties, such as antioxidant and metal-chelating activities.
Furthermore, some AGEs may stimulate the cellular detoxification
system, generally known as the phase II drug metabolizing system. We
show here that several reactive dicarbonyl intermediates have the
capability to stimulate the cellular phase II detoxification systems
in both a reporter cell line and primary rat hepatocytes. In addition,
we demonstrate that dicarbonyls can attenuate the inflammatory
signaling induced by tumor necrosis factor-alpha in a reporter cell
system.
PMID: 18448803 [PubMed - in process]
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I and II drug metabolizing enzymes. [Curr Drug Metab. 2002]
* Advanced glycation endproducts and pro-inflammatory
cytokines in transgenic Tg2576 mice with amyloid plaque pathology. [J
Neurochem. 2003]
* Non-enzymatic model glycation reactions--a comprehensive
study of the reactivity of a modified arginine with aldehydic and
diketonic dicarbonyl compounds by electrospray mass spectrometry. [J
Mass Spectrom. 2006]
* Identification of alpha-dicarbonyl scavengers for cellular
protection against carbonyl stress. [Biochem Pharmacol. 2002]
* >> See all Related Articles...
Here is a quote from the discussion section of the full text:
"Our data show that dicarbonyls at low millimolar and sub-millimolar
concentrations can stimulate the expression of the phase II
detoxification system in both a reporter cell line and primary rat
hepatocytes. In addition, our results provide evidence that they can
also attenuate the pro-inflammatory response to TNF¦Á exposure in a
reporter cell line. These novel findings suggest that dicarbonyls can
have beneficial effects in cellular systems when used at low
concentrations. At higher concentrations, dicarbonyls showed some
toxicity, depending on the cell system used.
Although high dicarbonyl concentrations were needed to stimulate phase
II enzyme gene expression in hepatocytes, the concentration of
dicarbonyls that actually reached the cytoplasm to exert their action
is not known. Extracellularly added dicarbonyls could react with
proteins on the cell surface or membrane lipids, and it is likely that
only a fraction of the original concentration may have reached the
cytoplasm. Intracellular steady-state dicarbonyl levels were estimated
to be in the low micromolar range. Because the biologically relevant
dicarbonyls are most likely formed intracellularly from glucose
metabolism and breakdown, it appears realistic to suggest that these
dicarbonyls could induce protective responses to toxic insults,
especially under conditions of physiological stress. The concept that
toxicants at low concentrations could stimulate protection whereas
high concentrations are toxic is often referred to as hormesis.20" |
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