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| Names | |
|---|---|
| Preferred IUPAC name Di(prop-2-en-1-yl)trisulfane | |
| Other names Allitridin | |
| Identifiers | |
3D model (JSmol) | |
| ChEBI | |
| ChemSpider | |
| ECHA InfoCard | 100.016.462 |
| EC Number |
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| UNII | |
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| Properties | |
| C6H10S3 | |
| Molar mass | 178.33 g·mol−1 |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Diallyl trisulfide (DATS), also known asAllitridin, is anorganosulfur compound with the formula S(SCH2CH=CH2)2. It is one of several compounds produced by hydrolysis ofallicin, includingdiallyl disulfide and diallyl tetrasulfide; DATS is one of the most potent.[1][clarification needed]
DATS has been shown to selectively kill cancerous cells in the prostate and breast,[2][3] leaving healthy cells unharmed. This effect is attributed to increased reactive oxygen species (ROS) within cancer cells, increased the number of cells that arrest in the G2 phase of mitosis, and promote an increase incaspase-3 activity.[4] These effects appear to contribute to theapoptosis of cancer cells and a decrease in cancer cellproliferation.
DATS can be metabolized byglutathione in red blood cells to formhydrogen sulfide (H2S).[5] This conversion occurs at a consistent rate over a prolonged period of time, rendering DATS a good source of H2S.[6] H2S is a cardioprotective agent that has antioxidant, anti-inflammatory, and anti-apoptotic effects.[6][7] A major topic of research is the impact of hydrogen sulfide on reducing myocardial ischemia-reperfusion injury. Reperfusion injury is a significant threat to myocardial function that arises with the reintroduction of blood flow to the heart following anischemic episode. Reperfusion triggers an inflammatory response and often results in oxidative damage. H2S decreases injury through many different effects such a decrease in oxidative stress, maintenance of mitochondrial function, and increased eNOS (endothelial nitric oxide synthase) activation.[6] eNOS is activated via phosphorylation by H2S through the activation of the PI3K/Akt pathway, which increases the formation and bioavailability of nitric oxide (NO).[6] This negatively impacts mitochondria functionality. The mitochondria has been known to protect the heart from ischemic-reperfusion injury through the opening of theATP-sensitive K+ channel.[5][8] This causes vasodilation and improveshemodynamics.[5]
DATS is a promising treatment forcardiac arrhythmias through its ability to change the opening of the human ether-à-go-go-related (hERG) channel. hERG is the pore-forming subunit of potassium channels that create delayed rectifier potassium ion currents in many cells, including cardiac myocytes.[9] The delayed rectifier potassium ion current is largely responsible for the repolarization of ventricular cardiac myocytes by permitting potassium efflux. DATS causes a decrease in the steady-state inactivation, alters deactivation, and impairs trafficking of the hERG channel from the endoplasmic reticulum to the plasma membrane of the cell.[10] This decreases the amount of functional potassium ion rectifier channels on the cell membrane and thus, slows depolarization.[10] However, hERG trafficking impairment has also been shown to cause arrhythmias due to the development oflong QT syndrome and should be considered in drug development.[10]
