L-글루타민산

Cosmetic ingredients (Glutamic Acid) -> CIR (Cosmetic Ingredient Review)

Hair conditioning; Humectant; Antistatic

Between 3,0 and 3,5 (saturated solution)

Aqueous solutions have pH values of approximately 2

log Kow = -3.69 at pH 7.0

-3.69

Umami sour taste

Acidic (glutamate-like) taste

Sparingly soluble in water; practically insoluble in ethanol or ether

In water, 8570 mg/L at 25 °C

Insoluble in methanol, ethanol, ether, acetone, cols glacial acetic acid and common neutral solvents.

8.57 mg/mL

Slight soluble in water and ether

This chemical does not meet GHS hazard criteria for 95.4% (293 of 307) of all reports.

Not Classified

Aggregated GHS information provided per 307 reports by companies from 5 notifications to the ECHA C&L Inventory.

Danger

H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

P260, P264, P264+P265, P280, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P321, P363, P405, and P501 (click each P-code to see the statement)

Chemical: L-Glutamic acid

Regulation (EC) No 1333/2008 (amended)

L-Glutamic acid is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of L-Glutamic acid are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 31-03-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/12560

L-Glutamic acid: Does not have an individual approval but may be used under an appropriate group standard

Glutamic acid: Does not have an individual approval but may be used under an appropriate group standard

Causes mild eye irritation in rabbits (classified by the EC as not irritating); Not a skin sensitizer in guinea pigs; [IUCLID] Safe when used as a flavoring agent in food; [JECFA] May cause irritation; [Sigma-Aldrich MSDS] See DL-Glutamic acid.

L-Glutamic acid is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity of the substance added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) any substance intended for use in or on food is of appropriate food grade and is prepared and handled as a food ingredient.

This substance is generally recognized as safe when used as a salt substitute in accordance with good manufacturing practice.

This substance is generally recognized as safe when used as a salt substitute in accordance with good manufacturing practice. /Glutamic acid hydrochloride/

Residues of L-glutamic acid are exempted from the requirement of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops only. Use: Plant nutrient. Limit: Seed treatment use only.

L-glutamic acid is exempt from the requirement of a tolerance on all food commodities when used in accordance with good agricultural practices.

Wear self contained breathing apparatus for fire fighting if necessary. /L-Glutamic acid hydrochloride/

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. /L-Glutamic acid hydrochloride/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal. /L-Glutamic acid hydrochloride/

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: Dispose of as unused product. /L-Glutamic acid hydrochloride/

Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday. /L-Glutamic acid hydrochloride/

Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. Normal measures for preventive fire protection. /L-Glutamic acid hydrochloride/

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands. /L-Glutamic acid hydrochloride/

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Residues of l-glutamic acid are exempted from the requirement of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops only. Use: Plant nutrient. Limit: Seed treatment use only.

L-glutamic acid is exempt from the requirement of a tolerance on all food commodities when used in accordance with good agricultural practices.

Skin protection: Handle with gloves. /L-Glutamic acid hydrochloride/

Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU). /L-Glutamic acid hydrochloride/

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). /L-Glutamic acid hydrochloride/

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace. /L-Glutamic acid hydrochloride/

The purpose of this study was to evaluate the extent to which orally administered glutamic acid hydrochloride decreased mean gastric pH in both fasting and simulated hypochlorhydric states. Patients with elevated gastric pH resulting from physiologic or pharmacologic decreases in acid secretion may experience a decrease in drug absorption when receiving pH-dependent drugs or dosage formulations. Although various doses of oral glutamic acid (GA) have been used to lower gastric pH and enhance drug absorption, the in vivo effect of a specific dose and regimen on the magnitude and duration of gastric pH is unknown. This study was conducted in six young, healthy, male volunteers using the Heidelberg capsule technique to measure gastric pH. In Phase I, all subjects received two 680 mg (340 mg capsules x 2) doses of GA given ten minutes apart. In Phase II, 300 mg (150 mg tablet x 2) of oral ranitidine hydrochloride was administered in order to simulate hypochlorhydria. This was followed by the administration of two oral 680 mg doses of GA given ten minutes apart. Gastric pH was monitored continuously pre- and post-GA administration in both phases. Our results indicate that the administration of two oral 680 mg doses of GA given ten minutes apart does not significantly lower fasting gastric pH in healthy young males. However, when subjects were pretreated with 300 mg of oral ranitidine, the administration of two oral 680 mg doses of GA given ten minutes apart resulted in a decrease of mean gastric pH from 5.83+/-0.86 to 1.67+/-0.81. Gastric pH remained less than 3.0 for an average of 39.0+/-11.7 minutes following the second GA dose. The administration of two oral 680 mg doses of GA given ten minutes apart can significantly lower the magnitude of gastric pH in a simulated hypochlorhydric model. It is likely that this dosing strategy will provide an adequate period of low gastric pH in most hypochlorhydric patients receiving oral drugs such as ketoconazole which require a low gastric pH for maximal dissolution and absorption. /Glutamic acid hydrochloride/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 13(SRC), determined from a structure estimation method(2), indicates that glutamic acid is expected to have very high mobility in soil(SRC). Glutamic acid is a zwitterionic amino acid with pKa values of 2.19, 4.25 and 9.67(3) indicating that this compound will exist almost entirely in ionic form (anion, cation or both) in the environment and cations generally adsorb (anions generally do not adsorb) more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of glutamic acid from moist soil surfaces is not expected to be an important fate process since it will exist almost entirely in ionic form in moist soil(SRC). Glutamic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an extrapolated vapor pressure of 1.7X10-8 mm Hg at 25 °C(5). Glutamic acid has been determined to be readily biodegradable by two standardized biodegradation tests (OECD 301E and OECD 301B)(6,7). Using OECD Guideline 301E (Ready biodegradability: Modified OECD Screening Test), glutamic acid achieved 90% degradation in 4 days and 97% degradation in 28 days(6). Other studies have observed rapid biodegradation of glutamic acid(8-10).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 13(SRC), determined from a structure estimation method(2), indicates that glutamic acid is not expected to adsorb to suspended solids and sediment(SRC). Glutamic acid is a zwitterionic amino acid with pKa values of 2.19, 4.25 and 9.67(3) which indicates glutamic acid will exist almost entirely in ionic form (anion, cation or both) at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from its log Kow of -3.69(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Glutamic acid has been determined to be readily biodegradable by two standardized biodegradation tests (OECD 301E and OECD 301B)(6,7). Using OECD Guideline 301E (Ready biodegradability: Modified OECD Screening Test), glutamic acid achieved 90% degradation in 4 days and 97% degradation in 28 days(6). Other studies have observed rapid biodegradation of glutamic acid(8-10). Glutamic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(11).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), glutamic acid, which has an extrapolated vapor pressure of 1.7X10-8 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase glutamic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 9.4 hours(SRC), calculated from its rate constant of 4.1X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase glutamic acid may be removed from the air by wet and dry deposition(SRC). Aliphatic amino acids exhibit no absorption in the UV region above 220 nm(4), therefore glutamic acid is not expected to be susceptible to direct photolysis by sunlight(SRC).

Natural glutamic acid concentrations in some foods(1).[Table#1354]

Top 25 of the 5,024 foods with glutamic acid detections(1).[Table#1355]

Previous short observational studies on the free amino acid (FAA) content of human milk have shown that glutamine and glutamic acid increase in the first 4 to 6 weeks of life. Changes in human milk content of free amino acids (FAAs) was determined at colostrum, 1 month, and 3 months of lactation in 16 healthy lactating women after delivery of full-term infants. Milk was collected at the end of each feeding (hindmilk) during 24 hours. Glutamic acid and taurine were the most abundant FAAs at colostrum. Although taurine remained stable throughout lactation, glutamic acid (the prevalent FAA) and glutamine increased approximately 2.5 and 20 times, respectively, with progressing lactation representing more than 50% of total FAA at 3 months. The content of essential FAA was also stable, so the change in total FAA content was almost entirely due to the changes in glutamic acid and glutamine. Breast-fed infants are supplied with progressively increasing amounts of glutamine and glutamic acid throughout lactation. The increasing intake of glutamic acid and glutamine could benefit breast-fed infants with molecules that are likely to protect the enteral mucosa and act as neurotransmitters and as a source of nitrogen.

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

IDENTIFICATION AND USE: Glutamic acid is a white crystalline powder. It is used as a flavoring agent, salt substitute, and as a medication. HUMAN EXPOSURE AND TOXICITY: Ingestion of monosodium glutamate (MSG) solutions have been demonstrated to cause transient clinical symptoms resembling those of "Chinese Restaurant Syndrome" and there is evidence that some individuals may respond to relatively small doses. In epidemiology studies, a high intake of glutamic acid, in terms of a percentage of total protein, was significantly associated with a decreased risk of mortality from total stroke in women after controlling for covariates. Breast-fed infants are supplied with progressively increasing amounts of glutamine and glutamic acid throughout lactation. The increasing intake of glutamic acid and glutamine could benefit breast-fed infants with molecules that are likely to protect the enteral mucosa and act as neurotransmitters and as a source of nitrogen. ANIMAL STUDIES: Long-term oral administration of MSG into the diet to various animal species has revealed no adverse effects, while data showing neuropathological lesions in neonatal animals resulting from subcutaneous or forced oral dosing of MSG has thus far been confirmed only in rodents. The administration of protein or carbohydrate products concurrently with MSG has been shown to lower plasma glutamate levels, and in two recent studies, to reduce the incidence of hypothalamic lesions in mice. In pregnant monkeys, glutamate does not appear to readily cross the placental barrier. Glutamic acid was among 80 compounds examined for toxicity. Fresh fertile eggs of single-comb white leghorn chickens were given injections at 0 hr and at 96 hr. Highest tested was 20 mg/egg. No teratogenic response found. In vitro in PC12 cells addition of glutamate (1-10 mmol/L) led to a dose-dependent cell damage (70% of cell lysis at 10 mmol/L as estimated by lactate dehydrogenase release). This effect which was not due to an inhibition of cell proliferation was only obvious after 8-10 hr of incubation and required the continuous presence of glutamate for at least 4-6 hr, to become apparent.

Glutamate activates both ionotropic and metabotropic glutamate receptors. The ionotropic ones being non-NMDA (AMPA and kainate) and NMDA receptors. Free glutamic acid cannot cross the blood-brain barrier in appreciable quantities; instead it is converted into L-glutamine, which the brain uses for fuel and protein synthesis. It is conjectured that glutamate is involved in cognitive functions like learning and memory in the brain, though excessive amounts may cause neuronal damage associated in diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. Also, the drug phencyclidine (more commonly known as PCP) antagonizes glutamate at the NMDA receptor, causing behavior reminiscent of schizophrenia. Glutamate in action is extremely difficult to study due to its transient nature.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of glutamic acid can be estimated to be 13(SRC). According to a classification scheme(2), this estimated Koc value suggests that glutamic acid is expected to have very high mobility in soil. Glutamic acid is a zwitterionic amino acid with pKa values of 2.19, 4.25 and 9.67(3) indicating that this compound will exist almost entirely in ionic form (anion, cation or both) in the environment and cations generally adsorb (anions generally do not adsorb) more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

Glutamic acid is a non-essential amino acid that occurs in plants and animals(1,2) and is formed via protein metabolism(2). Specific soil microorganisms generate and excrete glutamic acid(3). Glutamic acid has been quantified in numerous plant species(4).

/HUMAN EXPOSURE STUDIES/ To determine the extent to which oral glutamic acid hydrochloride (Acidulin) decreases mean gastric pH in fasting persons with and without simulated hypochlorhydria, 6 men (ages 20-28 yr) were randomly assigned to one of 2 drug regimens followed by the other regimen after a one wk washout period; in regimen 1, the subjects received two 680 mg doses of glutamic acid hydrochloride given 10 min apart; regimen 2 was the same, except that 300 mg of oral ranitidine hydrochloride (Zantac) was administered 1-2 hr before the first dose of glutamic acid hydrochloride to simulate hypochlorhydria. For regimen 1, the gastric pH before glutamic acid hydrochloride was given was not significantly different from that after administration. In regimen 2, the median gastric pH increased to 4.0 within 2 hr after ranitidine treatment. Median gastric pH after the second dose of glutamic acid was significantly lower than before the first dose. The time to minimum pH was 2-15 min, and pH remained 3.0 for a mean of 45 min. It was concluded that glutamic acid hydrochloride alone did not decrease gastric pH, but it significantly reduced pH in subjects with simulated hypochlorhydria produced by orally administered ranitidine. /Glutamic acid hydrochloride/

/EPIDEMIOLOGY STUDIES/ Dietary intakes of glutamic acid and glycine have been reported to be associated with blood pressure. However, the link between intakes of these amino acids and stroke has not been studied. We aimed to examine the association between glutamic acid and glycine intakes and the risk of mortality from stroke in a population-based cohort study in Japan. The analyses included 29,079 residents (13,355 men and 15,724 women) of Takayama City, Japan, who were aged 35-101 y and enrolled in 1992. Their body mass index ranged from 9.9 to 57.4 kg/sq m. Their diets were assessed by a validated food frequency questionnaire. Deaths from stroke were ascertained over 16 y. During follow-up, 677 deaths from stroke (328 men and 349 women) were identified. A high intake of glutamic acid in terms of a percentage of total protein was significantly associated with a decreased risk of mortality from total stroke in women after controlling for covariates; the HR (95% CI) for the highest vs. lowest quartile was 0.72 (0.53, 0.98; P-trend: 0.03). Glycine intake was significantly associated with an increased risk of mortality from total and ischemic stroke in men without history of hypertension at baseline; the HRs (95% CIs) for the highest vs. lowest tertile were 1.60 (0.97, 2.51; P-trend: 0.03) and 1.88 (1.01, 3.52; P-trend: 0.02), respectively. There was no association between animal or vegetable protein intake and mortality from total and any subtype of stroke. The data suggest that glutamic acid and glycine intakes may be associated with risk of stroke mortality.

/OTHER TOXICITY INFORMATION/ From comparisons of plasma glutamate levels, healthy term and premature infants have already developed the capability to metabolize glutamates. Ingestion of monosodium glutamate (MSG) solutions has been demonstrated to cause transient clinical symptoms resembling those of "Chinese Restaurant Syndrome" and there is evidence that some individuals may respond to relatively small doses. Similar symptoms can be evoked by certain other food substances. ...According to industry sources, MSG is not added to infant and junior foods. Because, however, a proportion of the consuming public may be sensitive acute responders, even though the unpleasant symptoms are transient, ...there should be some constraint placed on the addition of MSG to processed foods. ...There is no evidence in the available information on L-glutamic acid, L-glutamic acid hydrochloride, monosodium L-glutamate, monoammonium L-glutamate, and monopotassium L-glutamate that demonstrates, or suggests reasonable grounds to suspects, a hazard to the public when they are used at levels that are now current and in the manner now practices. However, it is not possible to determine, without additional data, whether a significant increase in consumption would constitute a dietary hazard. /Monosodium glutamate/

Glutamic acid's production and use as an intermediate to manufacture monosodium glutamate (a food additive), pesticides (glufosinate), medicinals and polyglutamic acid esters(1) and use as a nutritional supplement(2) may result in its release to the environment through various waste streams(SRC). Its use as a seed treatment in agriculture(3) will result in its direct relase to the environment(SRC).

AEROBIC: Using OECD Guideline 301E (Ready biodegradability: Modified OECD Screening Test) and a non-adapted activated sludge inoculum, glutamic acid achieved 90% degradation in 4 days and 97% degradation in 28 days which classified the compound as readily biodegradable(1). Using OECD Guideline 301B (Ready Biodegradability: CO2 Evolution Test) and a non-adapted activated sludge inoculum, glutamic acid (sodium salt) at 37.5 mg/L achieved 78-87% CO2 evolution over a 28-day incubation period which classified the compound as readily biodegradable(2). Glutamic acid, present at 6 ppm, reached 45.5-47.8% of its theoretical BOD in 5 days in a seawater biodegradation study(3). Glutamic acid reached 60% of its theoretical BOD in 100 hours in an electrolytic respirometer study(4).

ANAEROBIC: Glutamic acid was completely biodegraded after 7 days of incubation using an anaerobic test protocol(1).

L-Glutamic acid is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity of the substance added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) any substance intended for use in or on food is of appropriate food grade and is prepared and handled as a food ingredient.

This substance is generally recognized as safe when used as a salt substitute in accordance with good manufacturing practice.

This substance is generally recognized as safe when used as a salt substitute in accordance with good manufacturing practice. /Glutamic acid hydrochloride/

Residues of L-glutamic acid are exempted from the requirement of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops only. Use: Plant nutrient. Limit: Seed treatment use only.

L-glutamic acid is exempt from the requirement of a tolerance on all food commodities when used in accordance with good agricultural practices.

Cortical excitability reflects a balance between excitation and inhibition. Glutamate is the main excitatory and GABA the main inhibitory neurotransmitter in the mammalian cortex. Changes in glutamate and GABA metabolism may play important roles in the control of cortical excitability. Glutamate is the metabolic precursor of GABA, which can be recycled through the tricarboxylic acid cycle to synthesize glutamate. GABA synthesis is unique among neurotransmitters, having two separate isoforms of the rate-controlling enzyme, glutamic acid decarboxylase. The need for two separate genes on two chromosomes to control GABA synthesis is unexplained. Two metabolites of GABA are present in uniquely high concentrations in the human brain. Homocarnosine and pyrrolidinone have a major impact on GABA metabolism in the human brain. Both of these GABA metabolites have anticonvulsant properties and can have a major impact on cortical excitability. /Glutamate/

The significant role the amino acid glutamate assumes in a number of fundamental metabolic pathways is becoming better understood. As a central junction for interchange of amino nitrogen, glutamate facilitates both amino acid synthesis and degradation. In the liver, glutamate is the terminus for release of ammonia from amino acids, and the intrahepatic concentration of glutamate modulates the rate of ammonia detoxification into urea. In pancreatic beta-cells, oxidation of glutamate mediates amino acid-stimulated insulin secretion. In the central nervous system, glutamate serves as an excitatory neurotransmittor. Glutamate is also the precursor of the inhibitory neurotransmittor GABA, as well as glutamine, a potential mediator of hyperammonemic neurotoxicity. The recent identification of a novel form of congenital hyperinsulinism associated with asymptomatic hyperammonemia assigns glutamate oxidation by glutamate dehydrogenase a more important role than previously recognized in beta-cell insulin secretion and hepatic and CNS ammonia detoxification. Disruptions of glutamate metabolism have been implicated in other clinical disorders, such as pyridoxine-dependent seizures, confirming the importance of intact glutamate metabolism. This article will review glutamate metabolism and clinical disorders associated with disrupted glutamate metabolism. /Glutamate/

Glutamate activates both ionotropic and metabotropic glutamate receptors. The ionotropic ones being non-NMDA (AMPA and kainate) and NMDA receptors. Free glutamic acid cannot cross the blood-brain barrier in appreciable quantities; instead it is converted into L-glutamine, which the brain uses for fuel and protein synthesis. It is conjectured that glutamate is involved in cognitive functions like learning and memory in the brain, though excessive amounts may cause neuronal damage associated in diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. Also, the drug phencyclidine (more commonly known as PCP) antagonizes glutamate at the NMDA receptor, causing behavior reminiscent of schizophrenia. Glutamate in action is extremely difficult to study due to its transient nature.

Hepatic

Cortical excitability reflects a balance between excitation and inhibition. Glutamate is the main excitatory and GABA the main inhibitory neurotransmitter in the mammalian cortex. Changes in glutamate and GABA metabolism may play important roles in the control of cortical excitability. Glutamate is the metabolic precursor of GABA, which can be recycled through the tricarboxylic acid cycle to synthesize glutamate. GABA synthesis is unique among neurotransmitters, having two separate isoforms of the rate-controlling enzyme, glutamic acid decarboxylase. The need for two separate genes on two chromosomes to control GABA synthesis is unexplained. Two metabolites of GABA are present in uniquely high concentrations in the human brain. Homocarnosine and pyrrolidinone have a major impact on GABA metabolism in the human brain. Both of these GABA metabolites have anticonvulsant properties and can have a major impact on cortical excitability. /Glutamate, GABA/

The measurement of the intestinal metabolism of the nitrogen moiety of glutamic acid has been investigated by oral ingestion of l-[(15)N]glutamic acid and sampling of arterialized blood. Measurements have been made in six normal adults weighing an average of 72.8 kg ingesting 100 mg of l-[(15)N]glutamic acid after an overnight fast. Measurement of the enrichment of arterial glutamic acid, glutamine and alanine was by gas chromatography-mass spectrometry. Isotopic enrichment of the amino acids was followed for 150 min after the ingestion of the amino acid. Arterialized venous blood amino acid concentrations, measured by HPLC, demonstrated no significant changes during the course of the experiment. From the observed appearance of label in arterialized glutamic acid, alanine and glutamine, little luminal glutamic acid reaches the extracellular pool. The majority of the administered nitrogen label appears in the arterial alanine and glutamine components.

Hepatic

Absorbed from the lumen of the small intestine into the enterocytes.Absorption is efficient and occurs by an active transport mechanism.

/MILK/ Previous short observational studies on the free amino acid (FAA) content of human milk have shown that glutamine and glutamic acid increase in the first 4 to 6 weeks of life. Changes in human milk content of free amino acids (FAAs) was determined at colostrum, 1 month, and 3 months of lactation in 16 healthy lactating women after delivery of full-term infants. Milk was collected at the end of each feeding (hindmilk) during 24 hours. Glutamic acid and taurine were the most abundant FAAs at colostrum. Although taurine remained stable throughout lactation, glutamic acid (the prevalent FAA) and glutamine increased approximately 2.5 and 20 times, respectively, with progressing lactation representing more than 50% of total FAA at 3 months. The content of essential FAA was also stable, so the change in total FAA content was almost entirely due to the changes in glutamic acid and glutamine. Breast-fed infants are supplied with progressively increasing amounts of glutamine and glutamic acid throughout lactation. The increasing intake of glutamic acid and glutamine could benefit breast-fed infants with molecules that are likely to protect the enteral mucosa and act as neurotransmitters and as a source of nitrogen.

In this report, (13)N -labeled L-glutamine and L-glutamic acid was synthesized by an enzymatic method ... . Organ distribution studies and whole body scans in mongrel dogs demonstrated low myocardial uptake of glutamine and glutamic acid and that the liver demonstrated a greater uptake of glutamine than glutamic acid or ammonia.

The measurement of the intestinal metabolism of the nitrogen moiety of glutamic acid has been investigated by oral ingestion of l-[(15)N]glutamic acid and sampling of arterialized blood. Measurements have been made in six normal adults weighing an average of 72.8 kg ingesting 100 mg of l-[(15)N]glutamic acid after an overnight fast. Measurement of the enrichment of arterial glutamic acid, glutamine and alanine was by gas chromatography-mass spectrometry. Isotopic enrichment of the amino acids was followed for 150 min after the ingestion of the amino acid. Arterialized venous blood amino acid concentrations, measured by HPLC, demonstrated no significant changes during the course of the experiment. From the observed appearance of label in arterialized glutamic acid, alanine and glutamine, little luminal glutamic acid reaches the extracellular pool. The majority of the administered nitrogen label appears in the arterial alanine and glutamine components.

CIR ingredient: Glutamic Acid

Glutamic acid is a non-essential amino acid and an excitatory neurotransmitter; Used as a nutritional supplement; [Merck Index] Active product registrations in the US for use as a crop growth enhancer (increases yield, size and/or quality, etc.); [NPIRS] Used as a flavoring agent, nutritional supplement, and pH control agent for foods; [FDA] Permitted for use as an inert ingredient in non-food pesticide products; [EPA]

For L-glutamic acid (USEPA/OPP Pesticide Code: 374350) ACTIVE products with label matches. /SRP: Registered for use in the USA but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

Gastric medicines; infusion solutions/diagnostic aids; raw material (peptide drugs).

Nutritional supplement. Hydrochloride as gastric acidifier.

MEDICATION (VET)

2023: 264,555 lb

(1972) PROBABLY GREATER THAN 4.54X10+5 GRAMS

(1975) PROBABLY GREATER THAN 4.54X10+5 GRAMS

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: L-Glutamic acid. National Production Volume: Withheld.

By hydrolysis of gluten (wheat, corn or other vegetable sources); by fermentation from glucose-containing raw materials; the racemic acid may be resolved into the d- and l-isomer by fractional crystallization; from 2-cyclopentenylamine; by microbial conversion of alpha-ketoglutaric acid; or by an alternative method, using Bacillus megatherium-cereus; from fumaric acid, using Bacillus pumilus; from starch.

The first industrial production process was an extraction method in which vegetable proteins were treated with hydrochloric acid to disrupt peptide bonds. L-Glutamic acid hydrochloride was then isolated from this material and purified as MSG. Initial production of MSG was limited because of the technical drawbacks of this method. Better methods did not emerge until the 1950s. One of these was direct chemical synthesis, which was used from 1962 to 1973. In this procedure, acrylonitrile was the starting material, and optical resolution of DL-glutamic acid was achieved by preferential crystallization. In 1956 a direct fermentation method to produce glutamate was introduced. The advantages of the fermentation method (eg, reduction of production costs and environmental load) were large enough to cause all glutamate manufacturers to shift to fermentation. Today, total world production of MSG by fermentation is estimated to be 2 million tons/y (2 billion kg/y). However, future production growth will likely require further innovation.

Microbial fermentation medium + Corneybacterium glutamicum bacteria (fermentation/separation)

Hydrolysis of vegetable protein (e.g., beet sugar waste, wheat gluten), organic synthesis based on acrylonitrile. It comprises 40% of the gliadin in wheat gluten.

Available commercially as the naturally-occurring L(+)-enantiomer in the form of the free base or hydrochloride salt. /L-Glutamic acid/

Auxigro WP Plant Metabolic Primer (Emerald Bioagriculture Corporation): Active ingredient: Gamma-aminobutyric acid 29.2%; L-Glutamic acid 29.2%.

Grade: FCC /Food Chemical Codex/ (L-form)

Food additives

Food Additives -> FLAVOUR_ENHANCER; SALT_SUBSTITUTE -> JECFA Functional Classes

Flavoring Agents -> JECFA Flavorings Index

Cosmetics -> Hair conditioning; Humectant; Antistatic

All Other Basic Inorganic Chemical Manufacturing

L-Glutamic acid: ACTIVE

Glutamic acid: ACTIVE

In 1907 Kikunae Ikeda, a professor at the Tokyo Imperial University, began his research to identify the umami component in kelp. Within a year, he had succeeded in isolating, purifying, and identifying the principal component of umami and quickly obtained a production patent. In 1909 Saburosuke Suzuki, an entrepreneur, and Ikeda began the industrial production of monosodium L-glutamate (MSG). The first industrial production process was an extraction method in which vegetable proteins were treated with hydrochloric acid to disrupt peptide bonds. L-Glutamic acid hydrochloride was then isolated from this material and purified as MSG. Initial production of MSG was limited because of the technical drawbacks of this method. Better methods did not emerge until the 1950s. One of these was direct chemical synthesis, which was used from 1962 to 1973. In this procedure, acrylonitrile was the starting material, and optical resolution of DL-glutamic acid was achieved by preferential crystallization. In 1956 a direct fermentation method to produce glutamate was introduced. The advantages of the fermentation method (eg, reduction of production costs and environmental load) were large enough to cause all glutamate manufacturers to shift to fermentation. Today, total world production of MSG by fermentation is estimated to be 2 million tons/y (2 billion kg/y). However, future production growth will likely require further innovation.