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Review
. 2011 Nov;49(11):805-16.

Molecular Mechanisms and Targets of Cancer Chemoprevention by Garlic-Derived Bioactive Compound Diallyl Trisulfide

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Free PMC article
Review

Molecular Mechanisms and Targets of Cancer Chemoprevention by Garlic-Derived Bioactive Compound Diallyl Trisulfide

Marie Lue Antony et al. Indian J Exp Biol. .
Free PMC article

Abstract

Health benefits of garlic and other Allium vegetables (e.g., onions), such as lipid lowering and anticancer effects, are credited to metabolic byproducts, including diallyl trisulfide (DATS). Evidence for anticancer effects of garlic derives from both population-based case-control studies, and clinical and laboratory investigations using purified garlic constituents such as DATS. Studies have shown that DATS can offer protection against chemically-induced neoplasia as well as oncogene-driven spontaneous cancer development in experimental rodents. Mechanisms underlying cancer chemopreventive effects of DATS are not completely understood, but known pharmacological responses to this natural product include alteration in carcinogen-metabolizing enzymes, cell cycle arrest, induction of apoptotic cell death, suppression of oncogenic signal transduction pathways, and inhibition of neoangiogenesis. This article reviews mechanisms and targets of cancer chemoprevention by DATS.

Figures

Figure 1
Figure 1
Biochemical synthesis and chemical structure of diallyl trisulfide.
Figure 2
Figure 2
Molecular mechanisms of DATS-induced cell cycle arrest in human prostate cancer cells-. The DATS treatment causes degradation of ferritin to cause an increase in levels of labile iron leading to ROS generation. The DATS-induced ROS generation results in down-regulation of Cdc25C, which is attenuated in the presence of antioxidants such as N-acetylcysteine and superoxide dismutase and catalase mimetic EUK134. The DATS treatment down-regulates Cdk1 expression in prostate cancer cells, but the mechanism of this effect is not yet clear. Mitotic arrest resulting from DATS exposure, characterized by accumulation of cyclin B1 and securin, is caused by checkpoint kinase 1-dependent inactivation of anaphase-promoting complex/cyclosome.

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