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Effect of formaldehyde on cell proliferation and death
Author(s) -
Szende Béla,
Tyihák Ernő
Publication year - 2010
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100532
Subject(s) - methylamine , apoptosis , cell growth , programmed cell death , chemistry , endogeny , methylation , arginine , resveratrol , cell , methionine , hydroxymethyl , biochemistry , demethylation , cell cycle , formaldehyde , cell division , lysine , dna , dna methylation , stereochemistry , amino acid , gene expression , gene
Formaldehyde (HCHO) may reach living organisms as an exogenous agent or produced within cells. The so‐called formaldehydogenic compounds like S‐adenosyl‐ l ‐methionine, N‐hydroxymethyl‐ l ‐arginine, 1′‐methyl ascorbigen, methanol, E‐N‐trimethyl lysine and methylamine are special exogenous sources of HCHO. Endogenous HCHO can be formed from hydroxymethyl groups during enzymatic methylation and demethylation processes. HCHO, as a highly reactive compound, is considered to be involved in the induction of apoptosis, consequently in the pathogenesis of atherosclerosis and neurodegenerative processes. The biological action of HCHO is dose‐dependent. In vitro studies on tumour cell and endothelial cell cultures showed that HCHO in the concentration of 10.0 mM caused necrotic cell death, 1.0 mM resulted in enhanced apoptosis and reduced mitotic activity, while 0.5 and 0.1 mM enhanced cell proliferation and reduced apoptotic activity. Among formaldehydogenic compounds N‐hydroxymethyl‐ l ‐arginine, 1′‐methyl ascorbigen and the HCHO donor resveratrol may be considered as potential inhibitors of cell proliferation. Endogenous HCHO in plants apparently play a role in regulation of apoptosis and cell proliferation. The genotoxic and carcinogentic effects of HCHO is due to production of DNA—protein cross‐links. Low doses of HCHO, reducing apoptotic activity may also accumulate cells with such cross‐links. Experimental data point to the possible therapeutic use of methylated lysine residues and methylated arginine residues in the case of neoplasms.