DL-o-Tyrosine
(Synonyms: DL-O-络氨酸,NSC 72345; Ortho-tyrosine; o-DL-Tyrosine; o-Tyrosine) 目录号 : GC49081A phenylalanine hydroxylation product
Cas No.:2370-61-8
Sample solution is provided at 25 µL, 10mM.
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DL-o-Tyrosine is a hydroxylation product of phenylalanine.1 It is formed from phenylalanine by hydroxyl radicals generated during radiolysis and can be further hydroxylated to form 2,3-dihydroxyphenylalanine (2,3-DOPA). DL-o-Tyrosine has been used as a marker of irradiation processing in poultry meat.2
1.?egota, H., Ko?odziejczyk, K., KrÓl, M., et al.o-Tyrosine hydroxylation by OH
Cas No. | 2370-61-8 | SDF | |
别名 | DL-O-络氨酸,NSC 72345; Ortho-tyrosine; o-DL-Tyrosine; o-Tyrosine | ||
Canonical SMILES | O=C(C(CC1=C(O)C=CC=C1)N)O | ||
分子式 | C9H11NO3 | 分子量 | 181.2 |
溶解度 | H2O : 5 mg/mL (27.60 mM; ultrasonic and warming and heat to 60°C); DMSO : 2 mg/mL (11.04 mM; Need ultrasonic) | 储存条件 | -20°C |
General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
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Shipping Condition | 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。 |
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1 mg | 5 mg | 10 mg | |
1 mM | 5.5188 mL | 27.5938 mL | 55.1876 mL |
5 mM | 1.1038 mL | 5.5188 mL | 11.0375 mL |
10 mM | 0.5519 mL | 2.7594 mL | 5.5188 mL |
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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% DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度: mg/ml;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
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Oxidation and oxygenation of L-amino acids catalyzed by a L-phenylalanine oxidase (deaminating and decarboxylating) from Pseudomonas sp. P-501
J Biochem 1984 Aug;96(2):421-7.PMID:6501250DOI:10.1093/oxfordjournals.jbchem.a134853.
A number of L-amino acids and derivatives were tested as substrates for the purified Pseudomonas L-phenylalanine oxidase. The reaction products of these amino acids were analyzed by high performance liquid chromatography and the kinetic properties of the reactions were partially characterized. In addition to L-phenylalanine, L-tyrosine, DL-o-Tyrosine, DL-m-tyrosine, p-fluoro-DL-phenylalanine and beta-2-thienyl-DL-alanine served as substrates for both oxidation and oxygenation catalyzed by the enzyme. On the other hand, L-methionine and L-norleucine were enzymically converted to the corresponding alpha-keto acids with the consumption of oxygen and with the formation of ammonia and hydrogen peroxide in stoichiometric amounts. Kinetic studies showed that the Km values for oxidation and oxygenation of L-phenylalanine by the enzyme were 2.04 mM and 1.96 mM for oxygen, and 13.3 microM and 11.1 microM for L-phenylalanine, respectively. omega-Phenyl fatty acids such as phenylacetic acid, 3-phenylpropionic acid and 4-phenylbutyric acid were competitive inhibitors of the enzyme towards L-phenylalanine. Both oxidation and oxygenation of L-phenylalanine by the enzyme were also inhibited by phenylacetic acid competitively.
Mechanisms underlying the effects of 5-hydroxytryptamine and 5-hydroxytryptophan in pancreatic islets. A proposed role for L-aromatic amino acid decarboxylase
Endocrinology 1983 Apr;112(4):1524-9.PMID:6339207DOI:10.1210/endo-112-4-1524.
Microdissected pancreatic islets of noninbred ob/ob mice were used in studies of 5-hydroxytryptamine (5-HT) and 5-hydroxytryptophan (5-HTP) effects on insulin release. The potentiating effect of 4 mM L-5-HTP on glucose-induced insulin release was inhibited by the decarboxylase inhibitors benserazide (100 microM), alpha-monofluoromethyldopa (10 or 100 microM), carbidopa (50 or 500 microM), and NSD 1015 (5 or 50 microM). Activation of L-aromatic amino acid decarboxylase by DL-m-tyrosine (4 mM) or DL-o-Tyrosine (4 mM) potentiated glucose-induced insulin release, whereas L-dopa (4 mM) inhibited it. Glucose oxidation was unaffected by L-5-HTP but slightly stimulated by 5-HT. Glucose-induced efflux of 33Pi was reduced by 5-HT but not affected by 5-HTP. These results are compatible with the ideas that 5-HT inhibits glucose-induced insulin release by affecting early steps in the beta-cell stimulus-secretion coupling and that 5-HTP-potentiation of insulin release is probably mediated by the decarboxylase activity but is independent of the 5-HT formed.