What makes BLACK GARLIC so effective???

Wonder why BLACK GARLIC is so effective even though it is THE ONLY ingredient that is being used in its production process?

It is because it contains S-ALLYL cysteine..its a scientific term, but hopefully with just very few of articles below, you can understand and perhaps surf more for SAC!!!

S-Allyl cysteine (SAC) is an organic compound that is a natural constituent of fresh garlic. It is a derivative of the amino acid cysteine in which an allyl group has been added to the sulfur atom.

Allyl cysteine has the capacity as a cholesterol lowering agent and as a chemopreventive.

S-allyl cysteine reduces oxidant load in cells involved in the atherogenic process.

Ho SE, Ide N, Lau BH.

Department of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, CA 92350, USA.

Abstract

Oxidation of low-density lipoprotein (LDL) and activation of the pleiotropic transcription factor nuclear factor kappa B (NF-kappaB), are often the chemical and molecular alterations associated with the development of the atherosclerotic lesion. We have reported previously on the antioxidant properties of a garlic compound, S-allyl cysteine (SAC), and its ability to inhibit damage caused by oxidative stress in bovine endothelial cells. In this study, the antioxidant effects of SAC were further determined, using several in vitro assay systems. First, we determined the effect of SAC on Cu2+-induced oxidation of LDL. Varying concentrations of SAC were co-incubated with a standardized Cu2+/LDL solution, and LDL-oxidation was then ascertained by determining the formation of thiobarbituric acid reactive substances (TBARS). SAC inhibited LDL-oxidation at an optimum concentration of 1 mM. In another experiment, we determined the effects of SAC on oxidized-LDL (ox-LDL) activation of J774 murine macrophages and human umbilical vein endothelial cells (HUVEC). Cells were grown on 96-well plates, preincubated with SAC at 37 degrees C and 5% CO2 for 24 h, washed, and exposed to ox-LDL for 24 h. Levels of hydrogen peroxide (H2O2) were determined by a fluorometric assay. In both cell lines, SAC exhibited dose-dependent inhibition of H2O2 formation. We also studied the effects of SAC on NF-kappaB activation in HUVEC using tumor necrosis factor-a (TNF-alpha) or H2O2 as stimulators. Cells were grown in 75 cm2 flasks at 37 degrees C and 5% CO2 and were preincubated with SAC 24 h before stimulation with TNF-alpha or H2O2. Nuclear extracts were then prepared and NF-kappaB activation was determined using an electrophoretic mobility shift assay with a 32P-labeled probe. SAC exhibited dose-dependent inhibition of NF-kappaB activation. Our data suggest that SAC may act via antioxidant mechanisms to inhibit the atherogenic process.

S-allylcysteine attenuates oxidative stress in endothelial cells.

Ide N, Lau BH.

Department of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, California 92350, USA.

Abstract

Oxidation of low-density lipoprotein (LDL) has been recognized as playing an important role in the initiation and progression of atherosclerosis. We recently reported that S-allylcysteine (SAC), one of the major compounds in the aged garlic extract (AGE), inhibited LDL oxidation and minimized oxidized LDL-induced cell injury. In this study, the antioxidant effects of SAC were further determined using several in vitro assay systems. Pulmonary artery endothelial cells (PAECs) were preincubated with SAC at 37 degrees C and 5% CO2 for 24 hr, washed, and then exposed to 0.1 mg/ml oxidized LDL for 24 hr. Lactate dehydrogenase (LDH) release, as an index of membrane injury, and intracellular glutathione (GSH) level were determined. Oxidized LDL caused an increase of LDH release and depletion of GSH. Pretreatment with SAC prevented these changes. Peroxides were measured directly in 24-well plates using a fluorometric assay. SAC dose-dependently inhibited oxidized LDL-induced release of peroxides in PAEC. In a cell-free system, SAC was shown to scavenge hydrogen peroxide. Our data demonstrate that SAC can protect endothelial cells from oxidized LDL-induced injury by removing peroxides and preventing the intracellular GSH depletion and suggest that this compound may be useful for the prevention of atherosclerosis.