Exact Mass: 135.0354

Exact Mass Matches: 135.0354

Found 165 metabolites which its exact mass value is equals to given mass value 135.0354, within given mass tolerance error 0.01 dalton. Try search metabolite list with more accurate mass tolerance error 0.001 dalton.

S-Methylcysteine

S-Methyl-L-cysteine, substrate for methionine sulfoxide reductase A

C4H9NO2S (135.0354)

S-methylcysteine is a cysteine derivative that is L-cysteine in which the hydrogen attached to the sulfur is replaced by a methyl group. It has a role as a human urinary metabolite and a plant metabolite. It is a tautomer of a S-methylcysteine zwitterion. S-Methyl-L-cysteine is a natural product that acts as a substrate in the catalytic antioxidant system mediated by methionine sulfoxide reductase A (MSRA), with antioxidative, neuroprotective, and anti-obesity activities.

Homocysteine

(2S)-2-amino-4-sulfanylbutanoic acid

C4H9NO2S (135.0354)

A high level of blood serum homocysteine is a powerful risk factor for cardiovascular disease. Unfortunately, one study which attempted to decrease the risk by lowering homocysteine was not fruitful. This study was conducted on nearly 5000 Norwegian heart attack survivors who already had severe, late-stage heart disease. No study has yet been conducted in a preventive capacity on subjects who are in a relatively good state of health.; Elevated levels of homocysteine have been linked to increased fractures in elderly persons. The high level of homocysteine will auto-oxidize and react with reactive oxygen intermediates and damage endothelial cells and has a higher risk to form a thrombus. Homocysteine does not affect bone density. Instead, it appears that homocysteine affects collagen by interfering with the cross-linking between the collagen fibers and the tissues they reinforce. Whereas the HOPE-2 trial showed a reduction in stroke incidence, in those with stroke there is a high rate of hip fractures in the affected side. A trial with 2 homocysteine-lowering vitamins (folate and B12) in people with prior stroke, there was an 80\\\\\\% reduction in fractures, mainly hip, after 2 years. Interestingly, also here, bone density (and the number of falls) were identical in the vitamin and the placebo groups.; Homocysteine is a sulfur-containing amino acid that arises during methionine metabolism. Although its concentration in plasma is only about 10 micromolar (uM), even moderate hyperhomocysteinemia is associated with increased incidence of cardiovascular disease and Alzheimers disease. Elevations in plasma homocysteine are commonly found as a result of vitamin deficiencies, polymorphisms of enzymes of methionine metabolism, and renal disease. Pyridoxal, folic acid, riboflavin, and Vitamin B(12) are all required for methionine metabolism, and deficiency of each of these vitamins result in elevated plasma homocysteine. A polymorphism of methylenetetrahydrofolate reductase (C677T), which is quite common in most populations with a homozygosity rate of 10-15 \\\\\\%, is associated with moderate hyperhomocysteinemia, especially in the context of marginal folate intake. Plasma homocysteine is inversely related to plasma creatinine in patients with renal disease. This is due to an impairment in homocysteine removal in renal disease. The role of these factors, and of modifiable lifestyle factors, in affecting methionine metabolism and in determining plasma homocysteine levels is discussed. Homocysteine is an independent cardiovascular disease (CVD) risk factor modifiable by nutrition and possibly exercise. Homocysteine was first identified as an important biological compound in 1932 and linked with human disease in 1962 when elevated urinary homocysteine levels were found in children with mental retardation. This condition, called homocysteinuria, was later associated with premature occlusive CVD, even in children. These observations led to research investigating the relationship of elevated homocysteine levels and CVD in a wide variety of populations including middle age and elderly men and women with and without traditional risk factors for CVD. (PMID 17136938, 15630149); Homocysteine is an amino acid with the formula HSCH2CH2CH(NH2)CO2H. It is a homologue of the amino acid cysteine, differing by an additional methylene (-CH2-) group. It is biosynthesized from methionine by the removal of its terminal C? methyl group. Homocysteine can be recycled into methionine or converted into cysteine with the aid of B-vitamins.; Studies reported in 2006 have shown that giving vitamins [folic acid, B6 and B12] to reduce homocysteine levels may not quickly offer benefit, however a significant 25\\\\\\% reduction in stroke was found in the HOPE-2 study even in patients mostly with existing serious arterial decline although the overall death rate was not significantly changed by the intervention in the trial. Clearly, reducing homocysteine does not quickly repair existing... Homocysteine (CAS: 454-29-5) is a sulfur-containing amino acid that arises during methionine metabolism. Although its concentration in plasma is only about 10 micromolar (uM), even moderate hyperhomocysteinemia is associated with an increased incidence of cardiovascular disease and Alzheimers disease. Elevations in plasma homocysteine are commonly found as a result of vitamin deficiencies, polymorphisms of enzymes of methionine metabolism, and renal disease. It has been identified as a uremic toxin according to the European Uremic Toxin Working Group (PMID: 22626821). Pyridoxal, folic acid, riboflavin, and vitamin B(12) are all required for methionine metabolism, and deficiency of each of these vitamins result in elevated plasma homocysteine. A polymorphism of methylenetetrahydrofolate reductase (C677T), which is quite common in most populations with a homozygosity rate of 10-15 \\\\\\%, is associated with moderate hyperhomocysteinemia, especially in the context of marginal folate intake. Plasma homocysteine is inversely related to plasma creatinine in patients with renal disease. This is due to an impairment in homocysteine removal in renal disease. The role of these factors, and of modifiable lifestyle factors, in affecting methionine metabolism and in determining plasma homocysteine levels is discussed. Homocysteine is an independent cardiovascular disease (CVD) risk factor modifiable by nutrition and possibly exercise. Homocysteine was first identified as an important biological compound in 1932 and linked with human disease in 1962 when elevated urinary homocysteine levels were found in children with mental retardation. This condition, called homocystinuria, was later associated with premature occlusive CVD, even in children. These observations led to research investigating the relationship of elevated homocysteine levels and CVD in a wide variety of populations including middle age and elderly men and women with and without traditional risk factors for CVD (PMID: 17136938 , 15630149). Moreover, homocysteine is found to be associated with cystathionine beta-synthase deficiency, cystathioninuria, methylenetetrahydrofolate reductase deficiency, and sulfite oxidase deficiency, which are inborn errors of metabolism. [Spectral] L-Homocysteine (exact mass = 135.0354) and L-Valine (exact mass = 117.07898) were not completely separated on HPLC under the present analytical conditions as described in AC$XXX. Additionally some of the peaks in this data contains dimers and other unidentified ions. Homocysteine is biosynthesized naturally via a multi-step process.[9] First, methionine receives an adenosine group from ATP, a reaction catalyzed by S-adenosyl-methionine synthetase, to give S-adenosyl methionine (SAM-e). SAM-e then transfers the methyl group to an acceptor molecule, (e.g., norepinephrine as an acceptor during epinephrine synthesis, DNA methyltransferase as an intermediate acceptor in the process of DNA methylation). The adenosine is then hydrolyzed to yield L-homocysteine. L-Homocysteine has two primary fates: conversion via tetrahydrofolate (THF) back into L-methionine or conversion to L-cysteine.[10] Biosynthesis of cysteine Mammals biosynthesize the amino acid cysteine via homocysteine. Cystathionine β-synthase catalyses the condensation of homocysteine and serine to give cystathionine. This reaction uses pyridoxine (vitamin B6) as a cofactor. Cystathionine γ-lyase then converts this double amino acid to cysteine, ammonia, and α-ketobutyrate. Bacteria and plants rely on a different pathway to produce cysteine, relying on O-acetylserine.[11] Methionine salvage Homocysteine can be recycled into methionine. This process uses N5-methyl tetrahydrofolate as the methyl donor and cobalamin (vitamin B12)-related enzymes. More detail on these enzymes can be found in the article for methionine synthase. Other reactions of biochemical significance Homocysteine can cyclize to give homocysteine thiolactone, a five-membered heterocycle. Because of this "self-looping" reaction, homocysteine-containing peptides tend to cleave themselves by reactions generating oxidative stress.[12] Homocysteine also acts as an allosteric antagonist at Dopamine D2 receptors.[13] It has been proposed that both homocysteine and its thiolactone may have played a significant role in the appearance of life on the early Earth.[14] L-Homocysteine. CAS Common Chemistry. CAS, a division of the American Chemical Society, n.d. https://commonchemistry.cas.org/detail?cas_rn=454-28-4 (retrieved 2024-06-29) (CAS RN: 6027-13-0). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0). DL-Homocysteine is a weak neurotoxin, and can affect the production of kynurenic acid in the brain. DL-Homocysteine is a weak neurotoxin, and can affect the production of kynurenic acid in the brain. L-Homocysteine, a homocysteine metabolite, is a homocysteine that has L configuration. L-Homocysteine induces upregulation of cathepsin V that mediates vascular endothelial inflammation in hyperhomocysteinaemia[1][2].

DL-Homocysteine

2-Amino-4-mercaptobutyric acid

C4H9NO2S (135.0354)

DL-Homocysteine is a weak neurotoxin, and can affect the production of kynurenic acid in the brain. DL-Homocysteine is a weak neurotoxin, and can affect the production of kynurenic acid in the brain.

2-Benzoxazolol

InChI=1/C7H5NO2/c9-7-8-5-3-1-2-4-6(5)10-7/h1-4H,(H,8,9

C7H5NO2 (135.032)

2-benzoxazolinone is a member of the class of benzoxazoles that is 2,3-dihydro-1,3-benzoxazole carrying an oxo group at position 2. It has a role as an allelochemical and a phytoalexin. 2-Benzoxazolinone is a natural product found in Scoparia dulcis, Acanthus ilicifolius, and other organisms with data available. A member of the class of benzoxazoles that is 2,3-dihydro-1,3-benzoxazole carrying an oxo group at position 2. 2-Benzoxazolol is found in cereals and cereal products. 2-Benzoxazolol is found in rye seedlings. Found in rye seedlings 2-Benzoxazolinone is an anti-leishmanial agent with an LC50 of 40 μg/mL against L. donovani[1]. A building block in chemical synthesis. 1,3-Benzoxazol-2(3H)-one derivatives have antimicrobial activity against a selection of Gram-positive, Gram-negative bacteria and yeasts[3]. Derivatives as anti-quorum sensing agent[4]. 2-Benzoxazolinone is an anti-leishmanial agent with an LC50 of 40 μg/mL against L. donovani[1]. A building block in chemical synthesis. 1,3-Benzoxazol-2(3H)-one derivatives have antimicrobial activity against a selection of Gram-positive, Gram-negative bacteria and yeasts[3]. Derivatives as anti-quorum sensing agent[4].

S-methylcysteine

S-methylcysteine, hydrochloride, (L-Cys)-isomer

C4H9NO2S (135.0354)

Methylcysteine is one of the identified number of bioactive substances in garlic that are water soluble (PMID 16484549). It has been suggested that the use of these organosulfur agents derived from garlic could protect partially oxidized and glycated LDL or plasma against further oxidative and glycative deterioration, which might benefit patients with diabetic-related vascular diseases (PMID 15161248). It may also exert some chemopreventive effects on chemical carcinogenesis. However, it should be borne in mind that may also demonstrate promotion potential, depending on the organ examined (PMID 9591199). Methylcystein is a biomarker for the consumption of dried and cooked beans. S-n-methylcysteine, also known as (2r)-2-amino-3-(methylsulfanyl)propanoic acid or 3-(methylthio)-L-alanine, is a member of the class of compounds known as L-cysteine-s-conjugates. L-cysteine-s-conjugates are compounds containing L-cysteine where the thio-group is conjugated. S-n-methylcysteine is soluble (in water) and a moderately acidic compound (based on its pKa). S-n-methylcysteine can be found in soft-necked garlic, which makes S-n-methylcysteine a potential biomarker for the consumption of this food product. S-n-methylcysteine can be found primarily in blood and urine. S-Methyl-L-cysteine is a natural product that acts as a substrate in the catalytic antioxidant system mediated by methionine sulfoxide reductase A (MSRA), with antioxidative, neuroprotective, and anti-obesity activities.

1-Hydroxybenzotriazole

1-Hydroxybenzotriazole, ammonium salt