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Dietary Sulfur – Diallyl sulfide (DAS), diallyl disulfide (DADS), and diallyl trisulfide (DATS) and Skin cancer

Monday, January 21, 2013 17:41

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Home of Kyle J. Norton for The Better of Living & Living Health Sulfur represents approximately 1/4% of our total body weight and occurs principally in the body as a constituent of the cysteine and methionine. It plays an important role in protein synthesis and enzyme reaction functions and is found abundantly in broccoli, cauliflower, cabbage, kale, kohlrabi, etc.
Organosulfides
Organosulfur compounds present in natural food are generally considered as beneficial for health because of their antioxidant and anticarcinogenic properties. This has led to their excessive and long-term consumption. However, there is also evidence that these compounds demonstrate toxicity and adverse health effects suggesting their potential dual biological roles. Thus, they can act as double-edged biological swords(a).
Diallyl disulfide and Trisulfide are organosulfur compounds derived from garlic and a few other genus Allium, such as onions, garlic, chives, and leeks, etc.
Diallyl sulfide (DAS), diallyl disulfide (DADS), and diallyl trisulfide (DATS) and Skin cancer
Diallyl sulfide (DAS), diallyl disulfide (DADS), and diallyl trisulfide (DATS), extracted from crushed garlic by steam-distillation, have been reported to provide the anticancer activity in several cancer types. According to the study by the National Taiwan University, found that DATS revealed better growth inhibition of A375 and BCC cells than DADS and DAS did. DATS increased intracellular reactive oxygen species (ROS) generation, induced cytosolic Ca(2+) mobilization, and decreased mitochondrial membrane potential (DeltaPsim). Western blot results showed the concordance for the expression of molecules involved in G(2)/M arrest and apoptosis observed by cell cycle and cell viability analysis. Moreover, we detected the activation of p53 pathway in response to the oxidative DNA damage. DATS also displayed selective target of growth inhibition between skin cancer cells and normal keratinocyte HaCaT cells(15).