L-Aspartic acid

133.10300

133.10

254-327-0

1439

DTXSID7022621

White, crystalline solid|Orthorhombic bisphenoidal leaflets or rods

29224995

100.62000

-2.8

Liquid

1.661 g/cm³ @ Temp: 12.5 °C

270-271 °C

264.1ºC at 760 mmHg

113.5ºC

1.531

H2O: 5 g/L (25 ºC)

Store at RT.

2.6X10-7 mm Hg at 25 deg C (est)

LD50 intraperitoneal in mouse: 6gm/kg

Specific optical rotation: +25.0 deg (c= 1.97 g in 100 ml 6 N hydrochloric acid) at 20 °C/D

Acidic/neutral

2.01(at 0 °C)

Henry's Law constant = 1.1X10-14 atm-cu m/mol at 25 °C (est)

2.01 (at 0 °C)|pK1 = 1.92 (COOH); pK2 =3.87 (COOH); pK3 = 9.87 (amine)

121.92 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|122 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine]|118.6 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|118.7 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|120.39 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|119.8 Ų [M-H]-

ASPARTIC ACID HAS RELATIVELY HIGH SOUR, RELATIVELY LOW MSG-LIKE TASTE INTENSITIES /ASPARTIC ACID/|DECOMPOSES AT 324 °C (RAPID HEATING)|Isoelectric point = 2.98|Forms supersaturated soln easily

Dust explosion possible if in powder or granular form, mixed with air. If dry, it can be charged electrostatically by swirling, pneumatic transport, pouring, etc.

NONH for all modes of transport

2

R36

S22-S24/25

CI9098500

Xi; Xn

Separated from strong oxidants.

Stable. Combustible. Incompatible with strong oxidising agents.

P264, P280, P305+P351+P338, P33, P313

H319

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

L-Aspartic 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.

Combustible. Finely dispersed particles form explosive mixtures in air.

Not Classified

In case of fire in the surroundings, use appropriate extinguishing media.

Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water. Personal protection: particulate filter respirator adapted to the airborne concentration of the substance.

Separated from strong oxidants.

Evaporation at 20 °C is negligible; a nuisance-causing concentration of airborne particles can, however, be reached quickly when dispersed, especially if powdered.

The substance is irritating to the eyes and respiratory tract.

NO open flames. Prevent build-up of electrostatic charges (e.g., by grounding). Closed system, dust explosion-proof electrical equipment and lighting. Prevent deposition of dust.

PREVENT DISPERSION OF DUST!

Use local exhaust or breathing protection.

Protective gloves.

Wear safety spectacles.

SOIL: Aspartic acid was not detectable in soil samples collected from 3 depths at a landfill in Spain containing urban wastes (detection limit not provided although measurements for other amino acids were provided in units of nmol/g)(1).|SEDIMENT: A Fanning Island (Central Pacific Ocean)lagoon carbonate mud sediment contained aspartic acid at concentrations of 10.68, 8.40, 4.14, 3.10, 2.60, 4.11 and 3.38 umol/g in grain size fractions of <2, 2-6, 6-10, 10-20, 20-40, 63-125, 125-250 microns, respectively(1).

Mild gastrointestinal side effects including diarrhea. LD50 (rat) > 5,000 mg/kg.

ASPARTIC ACID PREVENTED TO SOME EXTENT THE APPEARANCE OF SYMPTOMS OF PHYSICAL MORPHINE DEPENDENCE IN BALB/C MICE.|The effects of amino acids on the embryotoxicity and placental transfer of nickel chloride, day 10 rat embryos were cultured in rat serum medium containing nickel chloride or NiCl2-63 (0.34 or 0.68 uM NiCl with or without L-histidine (2 uM), L-aspartic acid, glycine (2 or 8 uM) or L-cysteine (2 uM). After 26 hr, conceptuses were assessed for survival, growth and development and malformations. The nickel-63 contents of embryos and yolk sacs and the extent of Nickel-63 binding to the proteins of the culture medium were also determined. Nickel chloride alone did not affect the embryonic development at 0.34 uM and caused growth retardation and brain and caudal abnormalities at 0.68 uM. Coincubation of L-histidine, L-cysteine, or L-aspartic acid 0.68 uM Ni reduced the growth retardation and the incidence and/or severity of brain defects caused by nickel chloride and decreased the concentrations of nickel-63 in the yolk sacs compared to 0.68 uM nickel-63 alone. In the presence of L-histidine, L-cysteine or L-aspartic acid there was a shift of nickel-63 binding from the high molecular weight proteins of the culture medium to the low molecular weight fraction.|The effect of oral D-aspartic acid and/or L-aspartic acid (aspartic acid) on the body weight of rats was studied. Rats given the D- or D- plus L-isomers showed a greater decrease in weight and in protein, triglyceride and glycogen than did rats given the L-isomer alone. The results were discussed with reference to amino acid antagonism of opioids.

Aspartic acid, as the DL mixture, is a naturally-occurring non-essential amino acid(1).

L-Aspartic acid's production and use as a roborant (1), a raw material in the synthesis of peptide drugs(2), and, as the DL-aspartic acid mixture, used in biological and clinical studies, preparation of culture media, an organic intermediate, an ingredient of aspartame, detergents, fungicides, germicides, and in metal complexation(3) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 39(SRC), determined from a water solubility of 5,360 mg/L at 25 °C(2) and a regression-derived equation(3), indicates that L-aspartic acid is expected to have very high mobility in soil(SRC). L-Aspartic acid has pKa values of 1.92, 3.87, and 9.87 at 25 °C(4) indicating that L-aspartic acid will exist as a zwitterion in the environment. Volatilization of L-aspartic acid from moist soil surfaces is not expected to be an important fate process(SRC) since ionic compounds do not volatilize. L-Aspartic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.6X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(5). Based on results from several screening tests, L-aspartic acid is expected to readily biodegrade under both aerobic (6-10) and anaerobic(11) conditions(SRC).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 39(SRC), determined from a water solubility of 5,360 mg/L at 25 °C(2) and a regression-derived equation(3), indicates that L-aspartic acid is not expected to adsorb to suspended solids and sediment(SRC). Measured pKa values of 1.92, 3.87, and 9.87 at 25 °C(4) indicate that L-aspartic acid will exist as a zwitterion in the environment. Volatilization from water surfaces is not expected because ionic compounds do not volatilize. According to a classification scheme(5), an estimated BCF of 0.7(SRC), from its water solubility(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low(SRC). The biodegradation of L-aspartic acid is expected to occur readily based on results from both screening and grab sample tests. Relative rates of total utilization of 2.7, 1.5, and 0.10%/hr were measured over a 4-hour period in three samples of seawater(6). In aerobic screening tests, 38.7 to 80.5% BODT was reached in 5 days using a sewage inoculum(7-9) while in an anaerobic screening test, 79% biodegradation was reported in 35 days(10).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), L-aspartic acid, which has an estimated vapor pressure of 2.6X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase L-aspartic 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 10 hours(SRC), calculated from its rate constant of 4.0x10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase L-aspartic acid may be removed from the air by wet or dry deposition(SRC). L-Aspartic acid does not contain chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(4).

The rate constant for the vapor-phase reaction of L-aspartic acid with photochemically-produced hydroxyl radicals has been estimated as 4.0X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 10 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). L-Aspartic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). L-Aspartic acid does not contain chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(2). Measured pKa values of 1.92 (COOH), 3.87 (COOH), and 9.87 (amine) at 25 °C(3) indicate that L-aspartic acid will exist as a zwitterion in the environment.|The chlorination of aspartic acid at 10 mg/L by sodium hypochlorite produced 2.7 ug/L dichloroacetonitrile following a 60-minute incubation(1).

An estimated BCF of 0.7 was calculated in fish for L-aspartic acid(SRC), using a water solubility of 5,360 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Koc of L-aspartic acid is estimated as 39(SRC), using a water solubility of 5,360 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that L-aspartic acid is expected to have very high mobility in soil. However, L-aspartic acid has pKa values of 1.92, 3.87, and 9.87(5), indicating that this compound will exist as a zwitterion in the environment. In H(Al) montmorillonite, aspartic acid showed an L-2 type adsorption isotherm with an initial preferential sorption when compared with the solvent or other solutes followed by a decrease in sorption as more solute was sorbed(4).

Measured pKa values of 1.92, 3.87, and 9.87 at 25 °C(1) indicate that L-aspartic acid will exist as a zwitterion in the environment. Volatilization from moist soil surfaces and water surfaces will not occur as ionic compounds do not volatilize. L-Aspartic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.6X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2).

SURFACE WATER: Water samples collected on June 3, 1986 from the lower Tama River, Japan, a highly eutrophic urban river, contained aspartic acid at concentrations of 0.66 to 1.09 umol/L(1).|SEAWATER: Concentrations of DL-aspartic acid were measured at 3 marine locations representing an estuarine, a coastal and an open sea environment during 1977-1978(1). DL-Aspartic acid concentrations ranged from 0.010 to 0.033 umol/L in water from the Scheldt estuary, from 0.019-0.031 umol/L in water collected from the Belgian coastal zone of the North Sea, and from 0.010 to 0.10 umol/L in water collected from the English Channel(1).|RAIN/SNOW/FOG: Aspartic acid was measured in 30 of 73 precipitation samples (range of <2 nM to 339 nM) collected from Charlottesville, VA, a small non-industrial town, from April, 1988 to April, 1989(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 9,033 workers (6,545 of these are female) are potentially exposed to L-aspartic acid in the US(1). Occupational exposure to L-aspartic acid may occur through inhalation of dust and dermal contact with this compound at workplaces where L-aspartic acid is produced or used(SRC). L-Aspartic acid is a non-essential amino acid which is naturally produced by both plants and animals. In addition, L-aspartic acid is ubiquitous in the diet of the general public through the ingestion of both plants and meats. Intake of L-aspartic acid may be increased by the additional use of nutritional supplements containing this compound by some individuals(SRC).

There is no support for the claim that aspartates are exercise performance enhancers, i.e. ergogenic aids.|Parenteral nutrition

MEDICATION (VET): TO REDUCE AMMONIA BLOOD LEVELS & SAID TO BE OF VALUE IN OVERCOMING FATIGUE. ... DOSAGE: GIVEN ORALLY OR AS FEED ADDITIVE AGAINST STRESS INDUCED HIGH BLOOD AMMONIA LEVELS IN POULTRY & AGAINST AMMONIA INTOXICATED RATS. /ASPARTIC ACID/|Parenteral nutrition|/EXPL/: L-aspartate is a glycogenic amino acid, and it can also promote energy production via its metabolism in the Krebs cycle. These latter activities were the rationale for the claim that supplemental aspartate has an anti-fatigue effect on skeletal muscle, a claim that was never confirmed. /L-aspartate/|There are claims that L-aspartate is a special type of mineral transporter for cations, such as magnesium, into cells. Magnesium aspartate has not been found to be more biologically effective when compared with other magnesium salts. There are also claims that L-aspartate has ergogenic effects, that it enhances performance in both prolonged exercise and short intensive exercise. It is hypothesized that L-aspartate, especially the potassium magnesium aspartate salt, spares stores of muscle glycogen and/or promotes a faster rate of glycogen resynthesis during exercise. It has also been hypothesized that L-aspartate can enhance short intensive exercise by serving as a substrate for energy production in the Krebs cycle and for stimulating the purine nucleotide cycle. An animal study using injected aspartate failed to find any evidence of a glycogen-sparing effect or any ergogenic effects whatsoever. A more recent double-blind human study of male weight trainers similarly found aspartate supplementation to have no effect, and another study of the effect of aspartate on short intensive exercise again found no effect. /L-aspartate/|For more Therapeutic Uses (Complete) data for (L)-ASPARTIC ACID (6 total), please visit the HSDB record page.

Mild gastrointestinal side effects including diarrhea have been reported. /L-aspartate/|Because of lack of long-term safety studies, L-aspartate salts should be avoided by children, pregnant women and lactating women. /L-Aspartate/|The effects of oral administration of potassium and magnesium aspartate (K + Mg Asp) on physiologic responses to 90 min of treadmill walking at approximately 62% VO2 max were evaluated in seven healthy males (VO2 max = 59.5 ml X kg-1 X min-1). A total of 7.2 g of K + Mg Asp were administered to each subject during a 24 h period prior to work and compared to control and placebo trials. For control, placebo, and K + Mg Asp trials, no significant differences were observed in resting or exercise values for ventilation (VE), oxygen uptake (VO2), carbon dioxide production (VCO2), respiratory exchange ratio (RO), heart rate (HR), or blood pressure (BP). In addition, there were no differences between the three trials for exercise-induced decreases in body weight and increases in rectal temperature, or for pre- and post-exercise alterations in serum lactic acid, creatine kinase, lactic dehydrogenase, and percentage change in plasma volume. The findings from this study indicate that oral ingestion of K+ Mg Asp prior to exercise had no effect on cardiorespiratory, hematologic, and metabolic responses to 90 min of work conducted at approximately 62% VO2 max. /Potassium magnesium aspartate/|This study examined the effects of aspartate supplementation (ASP) on plasma ammonia concentrations (NH4+) during and after a resistance training workout (RTW). Twelve male weight trainers were randomly administered ASP or vitamin C in a crossover, double blind protocol, each trial separated by 1 wk. ASP and vitamin C were given over a 2 hr period beginning 5 hr prior to the RTW. The RTW consisted of bench, incline, shoulder, and triceps presses, and biceps curls at 70% of one repetition maximum (1-RM). After the RTW a bench press test (BPT) to failure at 65% of 1-RM was used to assess performance. (NH4+) was determined preexercise, 20 and 40 min midworkout, immediately postexercise, and 15 min postexercise. Treatment-by-time ANOVAs, paired t tests, and contrast comparisons were used to identify mean differences. No significant differences were observed between treatments for (NH4+) or BPT. (NH4+) increased significantly from Pre to immediately postexercise for both the ASP and vitamin C trials. Acute ASP supplementation does not reduce (NH4+) during and after a high intensity RTW in weight trained subjects. /Potassium magnesium aspartate/

L-aspartate is considered a non-essential amino acid, meaning that, under normal physiological conditions, sufficient amounts of the amino acid are synthesized in the body to meet the body's requirements. L-aspartate is formed by the transamination of the Krebs cycle intermediate oxaloacetate. The amino acid serves as a precursor for synthesis of proteins, oligopeptides, purines, pyrimidines, nucleic acids and L-arginine. L-aspartate is a glycogenic amino acid, and it can also promote energy production via its metabolism in the Krebs cycle. These latter activities were the rationale for the claim that supplemental aspartate has an anti-fatigue effect on skeletal muscle, a claim that was never confirmed.

Absorbed from the small intestine by an active transport process|ASPARTIC ACID PLASMA CONCN WAS ELEVATED 30 MIN AFTER 1 G/KG L-ASPARTATE (ORAL OR IP) TO 15 DAY OLD & ADULT MICE. THEREAFTER, CONCN DECLINED EXPONENTIALLY WITH T/2 OF 0.2 HR IN BOTH. PLASMA CONCN NOT APPRECIABLY ALTERED BY 10 & 100 MG/KG L-ASPARTATE ORAL OR IP ADMIN.|Following ingestion, L-aspartate is absorbed from the small intestine by an active transport process. Following absorption, L-aspartate enters the portal circulation and from there is transported to the liver, where much of it is metabolized to protein, purines, pyrimidines and L-arginine, and is catabolized as well. L-aspartate is not metabolized in the liver; it enters the systemic circulation, which distributes it to various tissues of the body. The cations associated with L-aspartate independently interact with various substances in the body and participate in various physiological processes. /L-aspartate/|... Contents of D- and L-aspartic acids in rats at different stages of growth (from 1 day before birth to 90 days after birth) were determined. D-Aspartic acid was detected in all the brain tissue samples tested, but at different levels. In the cerebrum of rats 1 day before birth, D-aspartic acid was found to be at the highest concentration of 81 nmol/g wet tissue. The level of D-aspartic acid in rat brain falls rapidly after birth, while the L-aspartic acid level increases with age.|Enzymatic synthesis of 11C-(4)-L-aspartic acid was undertaken using commercially available wheat germ phosphoenolpyruvate carboxylase. Whole-body distribution of the radioactive compound in rats showed higher accumulation in the salivary gland, glandular stomach and the pancreas, as well as in the lungs. Within 60 minutes after intravenous injection of 11C-(4)-L-aspartic acid, about 60% is removed as 11CO2 by expiration, indicating that the carbon atom at the fourth position of the radioactive compound is easily subjected to decarboxylation.|The brain efflux index method has been used to clarify the mechanism of efflux transport of acidic amino acids such as L-aspartic acid (L-Asp), L-glutamic acid (L-Glu), and D-aspartic acid (D-Asp) across the blood-brain barrier (BBB). About 85% of L-[3H]Asp and 40% of L-(3H)Glu was eliminated from the ipsilateral cerebrum within, respectively, 10 and 20 min of microinjection into the brain. The efflux rate constant of L-(3H)Asp and L-(3H)Glu was 0.207 and 0.0346 min(-1), respectively. However, D-(3H)Asp was not eliminated from brain over a 20-min period. The efflux of L-(3H)Asp and L-(3H)Glu was inhibited in the presence of excess unlabeled L-Asp and L-Glu, whereas D-Asp did not inhibit either form of efflux transport. Aspartic acid efflux across the BBB appears to be stereospecific. Using a combination of TLC and the bioimaging analysis, attempts were made to detect the metabolites of L-(3H)Asp and L-(3H)Glu in the ipsilateral cerebrum and jugular vein plasma following a microinjection into parietal cortex, area 2. Significant amounts of intact L-(3H)Asp and L-(3H)Glu were found in all samples examined, including jugular vein plasma, providing direct evidence that at least a part of the L-Asp and L-Glu in the brain interstitial fluid is transported across the BBB in the intact form. To compare the transport of acidic amino acids using brain parenchymal cells, brain slice uptake studies were performed. Although the slice-to-medium ratio of D-(3H)Asp was the highest, followed by L-[3H]Glu and L-[3H]Asp, the initial uptake rate did not differ for both L-(3H)Asp and D-(3H)Asp, suggesting that the uptake of aspartic acid in brain parenchymal cells is not stereospecific. These results provide evidence that the BBB may act as an efflux pump for L-Asp and L-Glu to reduce the brain interstitial fluid concentration and act as a static wall for D-Asp.

FOR L-ASPARTIC ACID, OXALOACETIC ACID IS PRODUCT OF OXIDATIVE DEAMINATION OR TRANSAMINATION; ALPHA-ALANINE IS PRODUCT OF DECARBOXYLATION. /FROM TABLE/|METABOLIC PATHWAYS & PRODUCTS /IN ANIMAL BODY/: ASPARTIC ACID + CARBAMYLPHOSPHATE /PRODUCE/ PHOSPHORUS + CARBAMYLASPARTIC ACID GIVE PYRIMIDINES; ASPARTIC ACID /PRODUCES/ FUMARIC ACID + NH3; ASPARTIC ACID /PRODUCES/ ASPARTIC SEMIALDEHYDE /PRODUCES/ HOMOSERINE /PRODUCES/ (I) THREONINE, (II) METHIONINE, OR (III) LYSINE... /FROM TABLE/|METABOLIC PATHWAYS & PRODUCTS /IN ANIMAL BODY/: ASPARTIC ACID GIVES NITROGEN OF PURINE RING...ASPARTIC ACID + IMP GIVE ADENYLOSUCCINATE GIVES AMP + FUMARATE... /FROM TABLE/|Following ingestion, L-aspartate is absorbed from the small intestine by an active transport process. Following absorption, L-aspartate enters the portal circulation and from there is transported to the liver, where much of it is metabolized to protein, purines, pyrimidines and L-arginine, and is catabolized as well. D-aspartate is not metabolized in the liver; it enters the systemic circulation, which distributes it to various tissues of the body. The cations associated with L-aspartate independently interact with various substances in the body and participate in various physiological processes. /L-aspartate; D-aspartate/

There are also claims that L-aspartate has ergogenic effects, that it enhances performance in both prolonged exercise and short intensive exercise. It is hypothesized that L-aspartate, especially the potassium magnesium aspartate salt, spares stores of muscle glycogen and/or promotes a faster rate of glycogen resynthesis during exercise. It has also been hypothesized that L-aspartate can enhance short intensive exercise by serving as a substrate for energy production in the Krebs cycle and for stimulating the purine nucleotide cycle.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

(+-)-Aspartic Acid

The substance can be absorbed into the body by ingestion.

Cough. Sore throat.

Redness. Pain.

(VET) COMMERCIALLY AVAILABLE AS MIXT OF POTASSIUM & MAGNESIUM ASPARTATES= SPARTASE. /ASPARTIC ACID/|AVAILABLE COMMERCIALLY AS D(-)-, L(+)-, & DL-ASPARTIC ACID. /ASPARTIC ACID/|150 G ASPARTIC ACID WAS POLYMERIZED IN PRESENCE OF H3PO4 TO GIVE 150 G POLY(DEHYDROASPARTIC ACID) WHICH WAS TREATED WITH MORPHOLINE. POLYMER WAS INCORPORATED INTO AN ANIONIC SHAMPOO WITH 4% CONCN.|USP and FCC grades; 99% min grade

Oil and gas drilling, extraction, and support activities|L-Aspartic acid: ACTIVE|L-Aspartic acid, homopolymer: ACTIVE|PMN - indicates a commenced PMN (Pre-Manufacture Notices) substance.|Aspartic acid: ACTIVE|COMMONLY OCCURS IN THE L-FORM. ONE OF THE NONESSENTIAL AMINO ACIDS.|ASPARTIC ACID IS A POTENTIAL FLAVOR PRECURSOR ISOLATED FROM MEAT EXTRACTS /ASPARTIC ACID, FROM TABLE/|...ASPARTATE...FOUND IN VERY HIGH CONCN IN BRAIN.../HAS/ POWERFUL EXCITATORY EFFECTS ON NEURONS IN VIRTUALLY EVERY REGION OF THE CNS. ...EFFORTS TO SUPPORT...ASPARTATE AS EXCITATORY /TRANSMITTER/...IN MAMMALIAN CNS HAVE BEEN HAMPERED BY UNAVAILABILITY OF A CONVINCINGLY SELECTIVE RECEPTOR ANTAGONIST. /ASPARTATE/|POSTSYNAPTIC PHARMACOLOGY OF ASPARTATE: INCR NA+ & CATION CONDUCTANCES; DEPOLARIZES. /ASPARTATE/|For more General Manufacturing Information (Complete) data for (L)-ASPARTIC ACID (9 total), please visit the HSDB record page.

MANOMETRIC DETERMINATION OF L-ASPARTIC ACID, IN PROTEINS.|AMINO ACID ANALYZER, GLC.|AOAC method 960.47, Amino Acids in Vitamin Preparations; microbiological method using basal media /Amino acids/|The following methods have been developed for the analysis of free amino acids in blood, food, and feedstocks: (1) Protein hydrolysis, (2) Chromatographic methods that include high performance liquid chromatography (HPLC), gas chromatography (GC) and thin-layer chromatography (TLC), (3) Colorimetric and Fluorimetric Analysis, (4) Spectrometric Analysis, and (5) Enzymatic Determination and Microbial Assay /Amino acids/|For more Analytic Laboratory Methods (Complete) data for (L)-ASPARTIC ACID (19 total), please visit the HSDB record page.

Food additives -> Flavoring Agents|Human Drugs -> EU pediatric investigation plans|Flavoring Agents -> JECFA Flavorings Index|Cosmetics -> Antistatic

Flavoring Agents