Modulation of Histone Acetylation by Garlic Sulfur Compounds

ISSN: 1875-5992 (Online)
ISSN: 1871-5206 (Print)

Volume 16, 12 Issues, 2016

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Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

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  • 27th of 59 in Chemistry, Medicinal

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Michelle Prudhomme
Universite Blaise Pascal - C.N.R.S
Aubiere Cedex

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Modulation of Histone Acetylation by Garlic Sulfur Compounds

Anti-Cancer Agents in Medicinal Chemistry, 11(3): 254-259.

Author(s): Nathalie Druesne-Pecollo and Paule Latino-Martel.

Affiliation: Reseau NACRe/UREN, INRA, Batiment 230, 78352 Jouy en Josas cedex, France.


Preclinical studies have shown that fresh garlic extracts, aged garlic, garlic oil and specific organosulfur compounds generated by processing garlic could alter carcinogen metabolism, inhibit tumor cell growth through induction of cell cycle arrest or apoptosis, or angiogenesis. In particular, recent studies have suggested that anticarcinogenic effects of certain garlic compounds may implicate at least in part a modulation of histone acetylation, a process involved in the regulation of gene expression, resulting from the inhibition of histone deacetylase activity. The aim of this review is to describe the available data on sulfur compounds from garlic and histone acetylation and to discuss their potential for cancer prevention. Available data indicate that garlic compounds could inhibit histone deacetylase activity and induce histone hyperacetylation both in vitro as well as in vivo. Sparse studies provide evidence of involvement of histone acetylation in modulation of gene expression by diallyl disulfide and allyl mercaptan. These effects were observed at high concentrations. Further investigations are needed to determine if the HDAC inhibitory effects of garlic organosulfur compounds play a role in primary cancer prevention at doses achievable by human diet.


Garlic, sulfur compounds, diallyl disulfide, allyl mercaptan, histone acetylation, histone deacetylase activity, gene expression, cancer prevention, Tumoral Tissues, hyperacetylation, HDAC activity, CDKN1A gene, 3T3-L1 cells, HDACIs, [3H]thymidine.

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Article Details

Volume: 11
Issue Number: 3
First Page: 254
Last Page: 259
Page Count: 6
DOI: 10.2174/187152011795347540
Price: $58

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