L-Tyrosine

181.19

181.19

392441

200-460-4

42HK56048U

DTXSID1023730

C915

FINE SILKY NEEDLES|White crystals

29225000

83.6

-2.26

White to Pale-brown powder

1.46 g/cm³

344 °C

385.2±32.0 °C at 760 mmHg

176 °C

1.614

H2O: 0.45 g/L (25 ºC);1 M HCl: 25 mg/mL

Store at RT.

LD50 orally in Rabbit: > 5110 mg/kg

-11.65 º (c=5,DIL HCL/H2O 50/50)

5.66 (at isoelectric point)

2.2(at 25 °C)

2.2 (at 25 °C)|pK values= 2.20, 9.11 and 10.07 for the acid, base and phenol groups, respectively

145.7 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|143.97 Ų [M+Na]+ [CCS Type: DT, Method: stepped-field]|148.26 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|139 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine]|145.8 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|143.6 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|143.8 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|145.59 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|146.45 Ų [M+H]+ [CCS Type: DT, Method: stepped-field]|144.5 Ų [M-H]-

OPTICALLY ACTIVE|DECOMP @ 342-344 °C (CLOSED CAPILLARY, BATH PREHEATED TO 280 °C, RAPID HEATING|UV: 6-233 (Organic Electronic Spectral Data, Phillips et al, John Wiley & Sons, New York) /Tyrosine (dl)/

NONH for all modes of transport

3

36/37/38-40

26-36-37/39-22

YP2275600

Xi

Stable. Incompatible with strong oxidizing agents, strong reducing agents.

P261-P305 + P351 + P338

H315-H319-H335

Tyrosine used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.

P261; P305 + P351 + P338

|Warning|H315 (92.59%): Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 242 companies from 12 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./

L-Tyrosine has very low toxicity. There have been very few reports of toxicity. LD50 (oral, rat) > 5110 mg/kg.

NATURAL OCCURRENCE OF TYROSINE (G/100 G PROTEIN): GELATINS 0.7; CASEIN 6.3; GAMMA GLOBULIN 6.8; HEMOGLOBIN: HORSE HEMOGLOBIN 3.0; INSULIN 13.0; CLOSTRIDIUM BOTULINUM TOXIN 13.5 (G/16 G TOTAL NITROGEN): MILK: MIXED PROTEINS 6.0; SERUM ALBUMIN 5.5. /FROM TABLE/|Tyrosine is a non-essential amino acid involved in microbial, plant and animal metabolism(1).

Tyrosine may be released to the environment via effluents at sites where it is produced and used in biochemical research or as a growth factor or dietary supplement in nutrition(1).

TERRESTRIAL FATE: With pK values of 2.20, 9.11 and 10.07 for the acid, base and phenol groups, respectively(1), tyrosine will exist in soil as series of ions in varying proportions that are pH dependent(2). Ions are not expected to volatilize and the soil adsorption of organic molecules with both negative and positive charges is difficult to predict(2,SRC). Soil grab sample data, using radiolabeled tyrosine(3), and several aqueous aerobic biological screening studies, which utilized settled waste water, sewage, or activated sludge for inocula, have demonstrated that tyrosine is readily biodegradable(4-6). The tyrosine molecule contains the amine functional group which may be susceptible to hydrolysis(2), but does not contain a chromophore that absorbs UV light in the environmentally significant range (>290 nm)(4). Therefore, it is not susceptible to direct photolysis in sunlit soil surfaces(SRC).|AQUATIC FATE: With pK values of 2.20, 9.11 and 10.07 for the acid, base and phenol groups, respectively(1), tyrosine will exist in natural waters as a series of ions in varying proportions that are pH dependent(2). Ions are not expected to volatilize from water and the adsorption of organic molecules with both negative and positive charges is unpredictable(2,SRC). The potential for tyrosine to bioconcentrate in aquatic organisms is also low. Soil grab sample data, using radiolabeled tyrosine(3), and several aqueous aerobic biological screening studies, which utilized settled waste water, sewage, or activated sludge for inocula, have demonstrated that tyrosine is readily biodegradable(4-6).|AQUATIC FATE: The tyrosine molecule does not contain a chromophore that absorbs UV light in the environmentally significant range (>290 nm)(1) and should not be susceptible to direct photolysis in sunlit surface waters. Measured rate constants averaged 1.3X10+10 L/mole-sec(2) for the photochemical reaction of tyrosine with hydroxyl radicals in water at room temperatures and pH 4-7, which corresponds to a calculated half-life of 62 days assuming the hydroxyl radical concentration in full intensity sunlit natural water is 1.0X10-17 mole/L(3).|ATMOSPHERIC FATE: The rate constant for the vapor-phase reaction of tyrosine with photochemically produced hydroxyl radicals in air has been estimated to be 8.20X10-11 cu cm/molecule-sec at 25 °C(2,SRC). Based upon a average yearly atmospheric hydroxyl radical concentration of 5.0X10+5 molecules/cu cm in a typical atmosphere(2), the corresponding half-life for tyrosine would be about 5 hrs(SRC). However if released to the atmosphere, it will exist mainly in the particulate phase. Tyrosine is not expected to undergo direct photolysis in ambient air because its molecule does not contain a chromophore that absorbs UV light in the environmentally significant range (>29 nm)(1). Physical removal from air by dry and wet deposition (rainfall, dissolution in clouds) may be important removal mechanisms(SRC).

Experimental data pertaining to the hydrolysis or direct photolysis of tyrosine were not located in the available literature. The tyrosine molecule does not contain a chromophore that absorbs UV light in the environmentally significant range (>290 nm)(1). Therefore, it should not be susceptible to direct photolysis in sunlit environmental media. Measured rate constants for the photochemical reaction of tyrosine with hydroxyl radicals in water at room temperatures and pH 4-7 average 1.3X10+10 L/mole-sec(2), which corresponds to a calculated half-life of 62 days assuming the hydroxyl radical concentration in full intensity sunlit natural water is 1.0X10-17 mole/L(3). The rate constant for the vapor-phase reaction of tyrosine with photochemically produced hydroxyl radicals in air has been estimated to be 8.20X10-11 cu cm/molecule-sec at 25 °C(4,SRC). Based upon a average yearly atmospheric hydroxyl radical concentration of 5.0X10+5 molecules/cu cm in a typical atmosphere(4), the corresponding half-life for tyrosine would be about 5 hrs(SRC).

Tyrosine is a non-essential amino-acid found in both proteins and the free form in most living organisms(1). It is involved in microbial, plant and animal metabolism and metabolic processes tend to regulate amino acid concentrations within the cell(1). Therefore, it is not likely to bioconcentrate in aquatic organisms(SRC).

Tyrosine is a nonessential amino acid. With pK values of 2.20, 9.11 and 10.07 for the acid, base and phenol groups, respectively, tyrosine will exist in environmental media as series of ions in varying proportions that are pH dependent(1). The adsorption of organic molecules in soil with both negative and positive charges is difficult to predict(2,SRC).

With pK values of 2.20, 9.11 and 10.07 for the acid, base and phenol groups, respectively, tyrosine will exist in environmental media as series of ions in varying proportions that are pH dependent(1). Ions will not volatilize from water(2).

Tyrosine is used in foods as a growth factor or dietary supplement(1).

Occupational exposure may occur through dermal contact or inhalation of dusts at places where tyrosine is produced or used in biochemical research or as a growth factor or dietary supplement in nutrition(2). The National Occupational Exposure Survey (NOES as of 3/28/89) has estimated that 14,650 U.S. workers are potentially exposed to tyrosine in the workplace(1). The most common non-occupational exposures are likely to result from the ingestion of foods in which tyrosine was added(2).

Tyrosine is claimed to act as an effective antidepressant, however results are mixed. Tyrosine has also been claimed to reduce stress and combat narcolepsy and chronic fatigue, however these claims have been refuted by some studies.|Parenteral nutrition

Tyrosine is a nonessential amino acid synthesized in the body from phenylalanine. Tyrosine is critical for the production of the body's proteins, enzymes and muscle tissue. Tyrosine is a precursor to the neurotransmitters norepinephrine and dopamine. It can act as a mood elevator and an anti-depressant. It may improve memory and increase mental alertness. Tyrosine aids in the production of melanin and plays a critical role in the production of thyroxin (thyroid hormones). Tyrosine deficiencies are manifested by hypothyroidism, low blood pressure and low body temperature. Supplemental tyrosine has been used to reduce stress and combat narcolepsy and chronic fatigue.

L-tyrosine is absorbed from the small intestine by a sodium-dependent active transport process.|Semi-chronic exposure of ICR male Mice to Aflatoxin B1 in non-toxic doses results in elevated lung tryptophan levels without change in serotonin or 5-hydroxyindole-3-acetic acid levels. This change is organ specific in that tryptophan levels are not altered in spleen, duodenum, heart or central nervous system. Acute (48 hr) flunixin treatment decreases lung tryptophan levels and reverses the Aflatoxin B1 mediated increase in lung tryptophan levels. On the other hand, flunixin treatment decreases central nervous system tryptophan levels in control mice but not in Aflatoxin B1 treated mice. Aflatoxin B1 treated mice have an increase in splenic serotonin content. Acute (48 hr) treatment of mice with E. coli lipopolysaccharide also increases splenic serotonin, and Aflatoxin B1 treatment followed by lipopolysaccharide have a slightly additive effect on spleen serotonin content. Treatment of mice with lipopolysaccharide increases heart serotonin, an effect which is not altered in Aflatoxin B1 pretreated mice. Both lipopolysaccharide and Aflatoxin B1 per se increases lung tyrosine levels although the combination of treatments is not significantly different from the control value. Flunixin treatment increases lung tyrosine levels, an effect which is not altered by Aflatoxin B1 pretreatment. Acute treatment with either lipopolysaccharide or flunixin decreases the central nervous system tryptophan/tyrosine ratio; pretreatment with Aflatoxin B1 prevents those changes in the central nervous system tryptophan/tyrosine ratio. Central nervous system catecholamines are reduced in Aflatoxin B1 pretreated mice. However, central nervous system catecholamine changes in Aflatoxin B1 treated mice are normalized by vitamin E supplementation during the treatment period.|Male Wistar rats were divided in free choice conditions into heavy-drinkers consuming greater than 3.5 g/kg of ethanol daily, and light-drinkers consuming less than 2.0 g/kg/day. Subsequent 30 day intragastric administration of 25% ethanol (8-11 g/kg/day) caused an increase in permeability of the blood brain barrier to 14(C)-tyrosine, 14(C)-tryptophan and 14(C)-DOPA at all the stages of alcoholization. All the changes were more pronounced in light-drinkers than in heavy- drinker rats. Disulfiram, and to a lesser extent phenazepam and diazepam, when repeatedly injected (for 16-30 days) together with ethanol aggravated its effects.|Effects of mercury chloride (100 uM) para-chloromercuribenzene sulfonate (1 uM), and oxophenylarsine (250 uM) were determined on (a) the rate of sodium pump activity in intact winter flounder intestine; (b) activity of sodium potassium ATPase in tissue homogenates; and (c) sodium-dependent and sodium independent uptake of tyrosine in brush border membrane vesicles. All three agents decreased cell potassium, although effects on cell potassium lagged behind those for inhibition of the ATPase. At the concentrations used in the Ussing chamber (or at one-tenth concentration), all agents completely inhibited sodium potassium ATPase activity in enzyme assays performed with tissue homogenates. In contrast, only mercury chloride decreased sodium dependent uptake of tyrosine by brush border membrane vesicles. These results suggest that mercurial and arsenical effects on tyrosine absorption are due to inhibition of the sodium potassium ATPase thus decreasing the driving force for the cellular uptake by the sodium tyrosine cotransport system. Direct effects on sodium tyrosine cotransport may play a role in the inhibition observed with mercury chloride, but not for para-chloromercuribenzene sulfonate or oxophenylarsine.|Female Sprague-Dawley rats were treated acutely (12-hr) with aflatoxin B1 (100 ug/kg ip) or vehicle (10% acetone in 0.9% sodium chloride) and regional brain levels of tryptophan, serotonin and tyrosine were assayed. Brainstem but not cerebellar or cortical tyrosine levels were decreased in aflatoxin B1-treated rats. Brain tryptophan was increased in all 3 brain regions by acute aflatoxin B1 treatment, while serotonin levels were unaltered in the cerebellum and cortex and decreased in the brainstem. These experiments indicate that acute aflatoxin B1 treatment differentially alters brain amino acids and serotonin and that changes in brain tryptophan, the serotonin precursor, do not parallel changes in brain serotonin.|For more Absorption, Distribution and Excretion (Complete) data for L-TYROSINE (10 total), please visit the HSDB record page.

In the liver, L-tyrosine is involved in a number of biochemical reactions, including protein synthesis and oxidative catabolic reactions. L-tyrosine that is not metabolized in the liver is distributed via the systemic circulation to the various tissues of the body.|/METABOLIC PATHWAY FOR L-TYROSINE:/ /TYROSINE GIVES/ P-HYDROXYPHENYLPYRUVIC ACID GIVES CO2 + HOMOGENTISIC ACID GIVES MALEYLACETOACETIC ACID GIVES FUMARYLACETOACETIC ACID GIVES FUMARATE + ACETOACETATE; TYROSINE GIVES 3,4-DIHYDROXYPHENYLALANINE GIVES CO2 + 3,4-DIHYDROXYPHENYLETHYLAMINE GIVES NORADRENALIN GIVES ADRENALIN.|L-TYROSINE GIVES N-ACETYL-L-TYROSINE IN MAN; GIVES 3-CARBOXY-L-TYROSINE IN RESEDA; GIVES P-COUMARIC ACID IN SUGAR CANE, L-TYROSINE GIVES PARA-CRESOL IN PROTEUS; GIVES 3,4-DIHYDROXY-L-PHENYLALANINE IN HAMSTER; GIVES 3,4-DIHYDROXYSTILBENE-2-CARBOXYLIC ACID IN HYDRANGEA, L-TYROSINE GIVES 2,7-DIMETHYLNAPHTHOQUINONE IN CHIMAPHILA; GIVES L-DITYROSINE IN BEEF; GIVES PARA-HYDROXYMANDELONITRILE IN SORGHUM, L-TYROSINE GIVES PARA-HYDROXYPHENYLACETALDOXIME IN AUBRETIA; GIVES PARA-HYDROXYPHENYLPYRUVIC ACID IN RAT; GIVES 3-IODO-L-TYROSINE IN BEEF; L-TYROSINE GIVES LACHNANTHOSIDE IN LACHNANTHES; LOPHOCERINE IN LOPHOCERUS; MESEMBRINE IN SCELETIUM; NARWEDINE IN DAFFODIL, L-TYROSINE GIVES NOVOBIOCIN IN STREPTOMYCES; PHENOL IN RAT; BETA-TOCOPHEROL IN ANABAENA; TYLOPHORINE IN TYLOPHORA, L-TYROSINE GIVES TYRAMINE IN RAT; GIVES BETA-TYROSINE IN BACILLUS; GIVES L-TYROSINE HYDROXAMATE IN BEEF. L-TYROSINE GIVES L-TYROSINE-4-PHOSPHATE IN FLY; GIVES XANTHOCILLIN IN PENICILLIUM. /FROM TABLE/|Metabolism of tyrosine was impaired after chronic alcoholization of rats with 10% ethanol within 10 months. Within the first 3-4 months activation of tyrosine aminotransferase and a decrease in phenylalanine hydroxylase activity were found in liver tissue. Activity of tyrosine aminotransferase was not increased during the long term alcohol intoxication. At the same time, activity of tyrosine aminotransferase was decreased within 5-6 months simultaneously with activation of phenylalanine hydroxylase. An increase in the alcohol dehydrogenase activity was also observed in rat liver tissue during the initial period of intoxication. The enzymatic activity was decreased beginning from the 3-4 months of the alcoholization and maintained at the low level. Hyperthermia augmented these alterations observed in chronic alcoholization of rats.|Spontaneous behavior subsequent to acute oral administration of high doses of aspartame, phenylalanine, or tyrosine was analyzed using a computer pattern recognition system. Spraque Dawley male rats (250-300 g) were dosed orally with aspartame (500 or 100 mg/kg), phenylalanine (281 or 562 mg/kg), or tyrosine (309 or 618 mg/kg), and their behavior was analyzed 1 hr after dosing. The computer pattern recognition system recorded and classifed 13 different behavioral acts performed by the animals during the first 15-min exploration of a novel environment. These doses of aspartame, phenylalanine, and tyrosine did not induce any significant changes in spontaneous behavior. Unlike low doses of amphetamine and despite high plasma concentrations of phenylalanine and tyrosine, no behavioral alteration was detected by the computer pattern recognition system.|For more Metabolism/Metabolites (Complete) data for L-TYROSINE (7 total), please visit the HSDB record page.

Tyrosine is produced in cells by hydroxylating the essential amino acid phenylalanine. This relationship is much like that between cysteine and methionine. Half of the phenylalanine required goes into the production of tyrosine; if the diet is rich in tyrosine itself, the requirements for phenylalanine are reduced by about 50%. The mechanism of L-tyrosine's antidepressant activity can be accounted for by the precursor role of L-tyrosine in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain norepinephrine and dopamine levels are thought to be associated with antidepressant effects.

In human beings there are four or more systemic diseases involving excessive tyrosine (tyrosinosis or tyrosinemia), but apparently only one of these diseases affects the eyes. The Richner-Hanhart syndrome, first described in 1938 consists of bilateral pseudo-dendritic keratitis, hyperkeratotic lesions of the palms and soles, and usually some mental retardation. From the first month of life the patient may have photophobia and painful eyes with branching corneal lesions resembling dentritic figures, limited to the epithelium in some cases, but involving anterior stroma in others. The figures stain less with fluorescein than do real herpes simplex ulcers, and they are unresponsive to antiviral and antimicrobial treatments. Circumscribed round areas of keratosis develop on the palms and soles, and these are tender, and may make walking uncomfortable.|In human beings an abnormally high concentration of tyrosine in the blood, caused by an inborn defect in metabolism of dietary tyrosine, can be associated with development of a special type of keratitis at an early age. ... Most important, the keratitis in human beings can be dramatically relieved by changing to a diet with a specially low tyrosine content.

L Tyrosine

L-Tyrosine: ACTIVE|A WIDELY DISTRIBUTED AMINO ACID, CLASSIFIED AS NON-ESSENTIAL IN RESPECT TO THE GROWTH EFFECT IN RATS.|POLYPHENOL OXIDASES (TYROSINASE) OCCUR WIDELY IN PLANTS & MANY CAN OXIDIZE TYROSINE FORMING CMPD WHICH POLYMERIZE TO GREY-BLACK COLOR BODIES. FOODS SUCH AS MUSHROOM & POTATOES CONTAIN SUFFICIENT TYROSINE TO BE A SIGNIFICANT SOURCE OF COLOR PROBLEMS /IN FOOD INDUSTRY/.|TYROSINE IS PRESENT AT VARYING CONCN DURING VARIOUS PHASES OF BREAD PRODUCTION.

MANOMETRIC DETERMINATION.|DETERMINATION OF TYROSINE IN PHARMACEUTICAL AMINO ACID SOLUTION BY DIFFERENTIAL SPECTROPHOTOMETRY.|Identified using infrared absorption spectrum of a potassium bromide dispersion of it, previously dried, exhibits maxima only at the same wavelengths as that of a similar prepration of USP L-tyrosine RS.|Human head hairs from 18 individuals were analyzed by capillary column pyrolysis-gas chromatography. The pyrograms showed several components, three of which differed significantly among individuals. These major components were identified as benzene, toluene, and styrene by GC-MS. By capillary column pyrolysis-gas chromatography of 18 amino acids, it was found that differences among the individuals were due to the different amt of particular amino acids in the hair. Furthermore, the quantities of the components were found to change in 18 mo.|For more Analytic Laboratory Methods (Complete) data for L-TYROSINE (9 total), please visit the HSDB record page.

COLORIMETRIC DETERMINATION.

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