S-Methyl-L-cysteine
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S-Methyl-L-cysteine

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S-Methyl-L-cysteine, a theurapeutic for neurodegenerative diseases, is a substrate in the catalytic antioxidant system mediated by methionine sulfoxide reductase A (MSRA), with antioxidative, neuroprotective, and anti-obesity activities.

Category
Others
Catalog number
BAT-008144
CAS number
1187-84-4
Molecular Formula
C4H9NO2S
Molecular Weight
135.18
S-Methyl-L-cysteine
IUPAC Name
(2R)-2-amino-3-methylsulfanylpropanoic acid
Synonyms
S-Methyl-L-cysteine; NSC 15387; NSC15387; NSC-15387; (2R)-2-amino-3-methylsulfanylpropanoic acid; S-11C-methyl-L-cysteine; S-methylcysteine; S-methylcysteine, (DL-Cys)-isomer; S-methylcysteine, (L-Cys)-isomer; S-methylcysteine, hydrochloride, (L-Cys)-isomer
Appearance
White to Off-White Solid
Purity
98%
Density
1.26g/cm3
Melting Point
~240 °C (dec.)
Boiling Point
300.3°C at 760mmHg
Storage
Store at-20 °C
Solubility
Soluble in Aqueous Base, Water
InChI
1S/C4H9NO2S/c1-8-2-3(5)4(6)7/h3H,2,5H2,1H3,(H,6,7)/t3-/m0/s1
InChI Key
IDIDJDIHTAOVLG-VKHMYHEASA-N
Canonical SMILES
CSCC(C(=O)O)N
1.Accelerated oligosaccharide absorption and altered serum metabolites during oral glucose tolerance test in young Japanese with impaired glucose tolerance.
Miki T;Lee EY;Eguchi A;Sakurai K;Sawabe Y;Yoshida T;Saito K;Yokoh H;Ishikawa K;Yokote K;Kuzuya T;Miki E;Mori C;Nomura F J Diabetes Investig. 2017 Aug 2. doi: 10.1111/jdi.12719. [Epub ahead of print]
AIMS/INTRODUCTION: ;Impaired glucose tolerance (IGT) is a subtype of prediabetes, a condition having high risk for development to diabetes mellitus, but its pathophysiology is not fully understood. In the present study, we examined metabolic changes in IGT by using two types (D-glucose [Glc] and partial hydrolysate of starch [PHS]) of oral glucose tolerance tests (OGTTs), with emphasis on serum incretins and metabolites.;MATERIALS AND METHODS: ;We carried out the two types of OGTT (Glc/OGTT and PHS/OGTT) in 99 young Japanese individuals who had tested either positive (GU;+; ; n = 48) or negative (GU;-; ; n = 51) for glycosuria. After OGTT, they were sub-grouped into five categories: normal glucose tolerance (NGT) in the GU;-; group (GU;-; /NGT; n = 49), NGT in the GU;+; group (GU;+; /NGT; n = 28), IGT (n = 12), diabetes mellitus (n = 1) and renal glycosuria (n = 9). Serum incretin and metabolites of GU;-; /NGT and IGT were then measured.;RESULTS: ;When the serum insulin level at each time-point during PHS/OGTT was expressed as its ratio relative to Glc/OGTT, it was increased time-dependently in GU;-; /NGT, but not in IGT. Such an increase in the ratio was also detected of serum incretin levels in GU;-; /NGT, but not in IGT, suggesting a lack of deceleration of oligosaccharide absorption in IGT.
2.Isotope effects in the enzymatic oxidation of tryptamine to 3-indolyl-acetaldehyde.
Dragulska S;Winnicka E;Kańska M Isotopes Environ Health Stud. 2014 Jun;50(2):269-76. doi: 10.1080/10256016.2013.839558. Epub 2014 Jan 20.
The reaction mechanisms of the enzymatic deamination of tryptamine catalysed by the enzyme monoamine oxidase (MAO, EC 1.4.3.4) were investigated using the kinetic isotope effect and solvent isotope effect methods. The numerical values of these deuterium effects in the (1S) and (1R) positions of tryptamine were determined using the non-competitive spectrophotometry. The deuterium-labelled isotopologue [(1S)-(2)H]tryptamine was obtained in two steps by enzymatic coupling of indole with S-methyl-l-cysteine in a deuterated medium followed by enzymatic decarboxylation of the resulting [2-(2)H]-l-tryptophan. [(1R)-(2)H]tryptamine was obtained by enzymatic decarboxylation of l-tryptophan in the fully deuterated medium.
3.s-Methyl cysteine enhanced survival of nerve growth factor differentiated PC12 cells under hypoxic conditions.
Liu CL;Hsia TC;Yin MC Food Funct. 2014 Jun;5(6):1125-33. doi: 10.1039/c3fo60689a. Epub 2014 Apr 8.
A nerve growth factor-differentiated PC12 cell line was used to investigate the protective effects of s-methyl cysteine (SMC) at 1, 2, 4, and 8 μM under oxygen-glucose deprivation (OGD) conditions. OGD decreased the cell viability. However, SMC pre-treatments at 2, 4 and 8 μM improved the cell viability, decreased cleaved caspase-3 and Bax expression, and reserved Bcl-2 expression. Furthermore, SMC maintained the mitochondrial membrane potential, lowered the intracellular Ca(2+) concentration and DNA fragmentation, and decreased the activity and expression of caspase-3 and caspase-8. OGD increased the reactive oxygen species (ROS) and 3-nitrotyrosine production, decreased glutathione peroxide (GPX) and glutathione reductase (GR) activities and the expression, enhanced nitric oxide synthase (NOS) activity and inducible NOS (iNOS) expression. SMC pre-treatments at 2, 4 and 8 μM lowered the ROS and 3-nitrotyrosine formation, maintained GPX and GR activities and expression, and decreased NOS activity and iNOS expression. OGD up-regulated hypoxia-inducible factor (HIF)-1α, nuclear transcription factor kappa (NF-κ) B p50, NF-κB p65 and p-p38 expression. SMC pre-treatments at 1-8 μM lowered HIF-1α expression and decreased p38 phosphorylation.
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