L-Glutamine

146.14400

146.14

200-292-1

0RH81L854J

760081|759628

DTXSID1023100

C522

White crystalline powder|Fine opaque needles from water or dilute ethanol

A - Alimentary tract and metabolism

2932999099

106.41000

-3.1

white powder

1.321g/cm3

185.5 °C (decomp)

445.6ºC at 760mmHg

185ºC

1.564

H2O: 41.3 mg/mL

20ºC

1.9X10-8 mm Hg at 25 deg C (est)

LD50 orally in Rabbit: 7500 mg/kg

Henry's Law constant = 3.0X10-16 atm-cu m/mol at 25 °C (est)

2.17|pK1 = 2.17, pK2 = 9.13

133.7 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|133.45 Ų [M+H]+ [CCS Type: DT, Method: stepped-field]|138.11 Ų [M+Na]+ [CCS Type: DT, Method: stepped-field]|132.11 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|124 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine]|130.9 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|127.3 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|127.7 Ų [M-H]-

Hydroxyl radical reaction rate constant = 4.6X10-11 cu cm/molec-sec at 25 °C (est)

NONH for all modes of transport

2

R36

S24/25

MA2275100

Xi

Stability Moisture and light sensitive. Incompatible with moisture, strong oxidizing agents.

P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, P501

H315

SRP: 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.

Strong oxidizing agents

L-Glutamine 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.|The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including glutamine, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

Abcouwer SF; p. 287-296 in Encyclopedia of Dietary Supplements; Coates PM, Blackman MR et al, eds (2005): A review of Glutamine biochemistry and nutritional supplementation.

Not Classified

Not flammable or combustible.

Wear self contained breathing apparatus for fire fighting if necessary.|Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Keep in suitable, closed containers for disposal.|Do not let product enter drains.|Avoid breathing vapors, mist or gas.

Avoid breathing vapors, mist or gas.

Doses of L-glutamine up to 21 grams daily appear to be well tolerated. Reported adverse reactions are mainly gastrointestinal and not common. They include constipation and bloating. There is one older report of two hypomanic patients whose manic symptoms were exacerbated following the use of 2 to 4 grams daily of L-glutamine. The symptoms resolved when the L-glutamine was stopped. These patients were not rechallenged, nor are there any other reports of this nature. The most common adverse effects observed in clinical trials of Endari were constipation (21%), nausea (19%), headache (18%), abdominal pain (17%), cough (16%), extremity pain (13%), back pain (12%), and chest pain (12%).

In clinical trials of L-glutamine in patients with sickle cell disease, serum aminotransferase elevations were not mentioned, and there were no reports of clinically apparent liver injury. Patients with sickle cell disease frequently have jaundice, largely due to chronic hemolysis which raises serum indirect bilirubin levels. They also can have fluctuating liver test abnormalities due to complications of sickle cell disease, such as gall stone disease (from chronic hemolysis), viral hepatitis and iron overload (from blood transfusions), congestive liver disease (due to pulmonary hypertension), and veno-occlusive crises involving the liver which can be associated with serum aminotransferase elevations and hepatic dysfunction. In preregistration trials of L-glutamine, hepatic events were not reported and serious adverse events were no more common with the active drug than with placebo. L-glutamine is a normal constituent of virtually all tissues and is unlikely to have intrinsic toxicity, even in high doses.

Radiotherapy is often used to treat prostate tumors, but the normal bladder is usually adversely affected. Using an animal model of pelvic radiation, /the authors/ investigated whether glutamine nutritional supplementation can prevent radiation-induced damage to the bladder, especially in its more superficial layers. Male rats aged 3-4 months were divided into groups of 8 animals each: controls, which consisted intact animals; radiated-only rats, which were sacrificed 7 (R7) or 15 (R15) days after a radiation session (10Gy aimed at the pelvico-abdominal region); and radiated rats receiving l-glutamine supplementation (0.65g/kg body weight/day), which were sacrificed 7 (RG7) or 15 (RG15) days after the radiation session. Cells and blood vessels in the vesical lamina propria, as well as the urothelium, were then measured using histological methods. The effects of radiation were evaluated by comparing controls vs. either R7 or R15, while a protective effect of glutamine was assessed by comparing R7 vs. RG7 and R15 vs. RG15. The results showed that, in R7, epithelial thickness, epithelial cell density, and cell density in the lamina propria were not significantly affected. However, density of blood vessels in R7 was reduced by 48% (p<0.05) and this alteration was mostly prevented by glutamine (p<0.02). In R15, density of blood vessels in the lamina propria was not significantly modified. However, epithelial thickness was reduced by 25% (p<0.05) in R15, and this effect was prevented by glutamine (p<0.01). In R15, epithelial cell density was increased by 35% (p<0.02), but glutamine did not protect against this radiation-induced increase. Cell density in the lamina propria was likewise unaffected in R15. Density of mast cells in the lamina propria was markedly reduced in R7 and R15. The density was still reduced in RG7, but a higher density in RG15 suggested a glutamine-mediated recovery. Alpha-actin positive cells in the lamina propria formed a suburothelial layer and were identified as myofibroblasts. Thickness of this layer was increased in R7, but was similar to controls in RG7, while changes in R15 and RG15 were less evident. In conclusion, pelvic radiation leads to significant acute and post-acute alterations in the composition and structural features of the vesical lamina propria and epithelium. Most of these changes, however, can be prevented by glutamine nutritional supplementation. These results emphasize, therefore, the potential use of this aminoacid as a radioprotective drug.|Glutamine is a neutral amino acid that is used by rapidly dividing cells such as erythrocytes, lymphocytes, and fibroblasts. It is also the substrate of glutathione synthesis. In normal metabolic rates, glutamine is an amino acid synthesized endogenously, but in high metabolic conditions such as cancer, it must be taken exogenously. Animal studies strongly demonstrate that glutamine protects both the upper and lower gastrointestinal tract mucosa from the effects of chemotherapy, radiotherapy, or other causes of injury. In this study, ... the protective effect of glutamine on radiation-induced diarrhea /was investigated/.The patients were divided into glutamine-treated and placebo groups. In the glutamine-treated group, 15 g of oral glutamine was administered three times daily. The patients were evaluated for diarrhea grade according to the National Cancer Institute Common Toxicity Criteria version 3.0, need for loperamide use, need for supportive parenteral therapy, and treatment breaks due to diarrhea. There was no difference in overall diarrhea incidence when the two groups were compared. When diarrhea grade was evaluated, none of the patients in the glutamine-treated group had grade 3-4 diarrhea, but in the placebo group, grade 3-4 diarrhea was seen in 69% of the patients. In the placebo-treated group, patients requiring loperamide and parenteral supportive therapy were 39 and 92 %, respectively. There was no treatment break in glutamine-treated patients. Glutamine may have protective effect on radiation-induced severe diarrhea.

LD50 Mouse oral 700 mg/kg|LD50 Rat oral 7500 mg/kg

All plants that are involved in nitrogen metabolism require the presence of glutamine in the form of glutamine synthetase(1). Glutamine is a non-essential amino acid for human development and is the most abundant free amino acid in plasma and tissue(2). It can be isolated from sugar beet juice(2). Sources of glutamine include plant and animal proteins such as beef, pork and poultry, milk, yogurt, ricotta cheese, cottage cheese, raw spinach, raw parsley, and cabbage(3). Glutamine occurs in human milk(4).

Glutamine's production and use as a medicine, culture media, biochemical research agent and food additive(1) 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 10(SRC), determined from a structure estimation method(2), indicates that glutamine is expected to have very high mobility in soil(SRC). Glutamine has pKa values of 2.17 (the acid) and 9.13 (the amine)(3) indicating that this compound will exist as a zwitterion having both a cation and anion form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of glutamine from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.0X10-16 atm-cu m/mole(SRC), using a fragment constant estimation method(2). Glutamine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Utilizing the Japanese MITI test, 77% of the Theoretical BOD was reached in 4 weeks(5) suggesting that biodegradation could be an important environmental fate process in soil(SRC).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that glutamine is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 3.0X10-16 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). Glutamine has pKa values of 2.17 (the acid) and 9.13 (the amine)(4) indicating that this compound will exist as a zwitterion having both a cation and anion form in the environment that also suggests volatilization from water will not be an important fate process(SRC). According to a classification scheme(5), an estimated BCF of 3(SRC),from its log Kow of -3.15(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Glutamine is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). Glutamine does not contain chromophores that absorb at wavelengths >290 nm(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC). Utilizing the Japanese MITI test, 77% of the Theoretical BOD was reached in 4 weeks(7) suggesting that biodegradation could be an important environmental fate process in water(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), glutamine, which has an estimated vapor pressure of 1.9X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase glutamine 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 8.5 hours(SRC), calculated from its rate constant of 4.6X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Particulate-phase glutamine may be removed from the air by wet and dry deposition(SRC). Glutamine does not contain chromophores that absorb at wavelengths >290 nm(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of glutamine with photochemically-produced hydroxyl radicals has been estimated as 4.6X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 8.5 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the reaction of hydroxyl radicals in aqueous solutions at pH 6.0 is 5.4X10+8 L/mol-sec(2); this corresponds to an aquatic half-life of about 4 years at an aquatic concentration of 1X10-17 hydroxyl radicals per liter(3). With the exception of the amide function, glutamine does not contain functional groups that hydrolyze under environmental conditions(4), and the amide group of glutamine is expected to have a hydrolysis half-life on the order of years under environmental conditions (pH 5-9)(1). Glutamine does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated in fish for glutamine(SRC), using a log Kow of -3.15(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of glutamine can be estimated to be 10(SRC). According to a classification scheme(2), this estimated Koc value suggests that glutamine is expected to have very high mobility in soil. Glutamine has pKa values of 2.17 (the acid) and 9.13 (the amine)(3) indicating that this compound will exist as a zwitterion having both a cation and anion form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

The Henry's Law constant for glutamine is estimated as 3.0X10-16 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that glutamine is expected to be essentially nonvolatile from water surfaces(2). Glutamine has pKa values of 2.17 (the acid) and 9.13 (the amine)(3) indicating that this compound will exist as a zwitterion having both a cation and anion form in the environment that also suggests volatilization from water will not be an important fate process(SRC). Glutamine's Henry's Law constant indicates that volatilization from moist soil will not occur(SRC). Glutamine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-8 mm Hg(SRC), determined from a fragment constant method(1).

SEAWATER: Analysis of particulate matter collected in surface waters of the estuary of the Tama River (a highly eutrophic urban river in Japan) detected glutamine concentrations of 0.67 to 1.21 umol/L water(1).

Dietary sources of glutamine include plant and animal proteins such as beef, pork and poultry, milk, yogurt, ricotta cheese, cottage cheese, raw spinach, raw parsley, and cabbage(1). High-protein foods such as meat, fish, beans, and dairy products are sources of glutamine(2). Glutamine and glutamate comprise between 5 and 15% of the amino acid content of most foods and commercial and feedstuffs(3).

Free glutamine was detected in human milk samples at median concentrations of 4960-5000 umol/L milk(1). The concentration of glutamine in mother's milk was determined as 259 umol/cu dm(2). The glutamine concentration in the milk of 11 women from India ranged from 2.04 to 43.79 umol/100 mL with a median of 15.69 umol/100 mL(3).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 8,491 workers (5,700 of these were female) were potentially exposed to glutamine in the US(1). Occupational exposure to glutamine may occur through dermal contact with this compound at workplaces where glutamine is produced or used. The general population is exposed to glutamine via ingestion of food and food supplements containing this compound or other consumer products containing glutamine(SRC).

Glutamine is the most abundant free amino acid in human blood with a concentration of about 500-900 umol/L(1).

Used for nutritional supplementation, also for treating dietary shortage or imbalance. Used to reduce the acute complications of sickle cell disease in adult and pediatric patients 5 years of age and older.|FDA Label

L-glutamine is an essential amino acid and precursor of major intracellular antioxidant molecules that is used in high doses to prevent vaso-occlusive crises in patients with sickle cell disease. L-glutamine has not been associated with serum enzyme elevations during therapy or to instances of idiosyncratic acute liver injury.

Sickle Cell Disease Agents

EXPL THER Glutamine depletion has negative effects on the functional integrity of the gut and leads to immunosuppression. Very low birth weight (VLBW) infants are susceptible to glutamine depletion, as enteral nutrition is limited in the first weeks of life. Enteral glutamine supplementation may have a positive effect on feeding tolerance, infectious morbidity and short-term outcome. The aim of the study was to determine the effect of enteral glutamine supplementation on plasma amino acid concentrations, reflecting one aspect of safety of enteral glutamine supplementation in VLBW infants. In a double-blind placebo-controlled randomized controlled trial, VLBW infants (gestational age <32 weeks or birth weight <1500 g) received enteral glutamine supplementation (0.3 g/kg per day) or isonitrogenous placebo supplementation (alanine) between day 3 and day 30 of life. Supplementation was added to breast milk or to preterm formula. Plasma amino acid concentrations were measured at four time points: before the start of the study and at days 7, 14 and 30 of life.Baseline patient and nutritional characteristics were not different in glutamine (n = 52) and control (n = 50) groups. Plasma concentrations of most essential and non-essential amino acids increased throughout the study period. There was no effect of enteral glutamine supplementation. In particular, the increase of plasma glutamine and glutamate concentrations was not different between the treatment groups (P = 0.49 and P = 0.34 respectively, day 30).Enteral glutamine supplementation in VLBW infants does not alter plasma concentrations of glutamine, glutamate or other amino acids. Enteral supplementation in a dose of 0.3 g/kg per day seems safe in VLBW infants.|EXPL THER Critically ill patients have considerable oxidative stress. Glutamine and antioxidant supplementation may offer therapeutic benefit, although current data are conflicting.In this blinded 2-by-2 factorial trial, we randomly assigned 1223 critically ill adults in 40 intensive care units (ICUs) in Canada, the United States, and Europe who had multiorgan failure and were receiving mechanical ventilation to receive supplements of glutamine, antioxidants, both, or placebo. Supplements were started within 24 hours after admission to the ICU and were provided both intravenously and enterally. The primary outcome was 28-day mortality. Because of the interim-analysis plan, a P value of less than 0.044 at the final analysis was considered to indicate statistical significance. There was a trend toward increased mortality at 28 days among patients who received glutamine as compared with those who did not receive glutamine (32.4% vs. 27.2%; adjusted odds ratio, 1.28; 95% confidence interval [CI], 1.00 to 1.64; P=0.05). In-hospital mortality and mortality at 6 months were significantly higher among those who received glutamine than among those who did not. Glutamine had no effect on rates of organ failure or infectious complications. Antioxidants had no effect on 28-day mortality (30.8%, vs. 28.8% with no antioxidants; adjusted odds ratio, 1.09; 95% CI, 0.86 to 1.40; P=0.48) or any other secondary end point. There were no differences among the groups with respect to serious adverse events (P=0.83). Early provision of glutamine or antioxidants did not improve clinical outcomes, and glutamine was associated with an increase in mortality among critically ill patients with multiorgan failure.|NutreStore (L-glutamine powder for oral solution) is indicated for the treatment of Short Bowel Syndrome (SBS) in patients receiving specialized nutritional support when used in conjunction with a recombinant human growth hormone that is approved for this indication. /Included in US product label/

The safety and effectiveness of L-glutamine in pediatric patients have not been established.|It is not known whether L-glutamine is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when L-glutamine is administered to a nursing woman.|Glutamine is metabolized to glutamate and ammonia, which may increase in patients with hepatic dysfunction. Therefore, routine monitoring of renal and hepatic function is recommended in patients receiving intravenous parenteral nutrition (IPN) and NutreStore, particularly in those with renal or hepatic impairment.|FDA Pregnancy Risk Category: C /RISK CANNOT BE RULED OUT. Adequate, well controlled human studies are lacking, and animal studies have shown risk to the fetus or are lacking as well. There is a chance of fetal harm if the drug is given during pregnancy; but the potential benefits may outweigh the potential risk./|For more Drug Warnings (Complete) data for Glutamine (7 total), please visit the HSDB record page.

Like other amino acids, glutamine is biochemically important as a constituent of proteins. Glutamine is also crucial in nitrogen metabolism. Ammonia (formed by nitrogen fixation) is assimilated into organic compounds by converting glutamic acid to glutamine. The enzyme which accomplishes this is called glutamine synthetase. Glutamine can then be used as a nitrogen donor in the biosynthesis of many compounds, including other amino acids, purines, and pyrimidines. L-glutamine improves nicotinamide adenine dinucleotide (NAD) redox potential.

Absorption is efficient and occurs by an active transport mechanism. Tmax is 30 minutes after a single dose. Absorption kinetics following multiple doses has not yet been determined.|Primarily eliminated by metabolism. While L-glutamine is filtered though the glomerulus, nearly all is reabsorbed by renal tubules.|Volume of distribution is 200 mL/kg after intravenous bolus dose.|After an intravenous bolus dose in three subjects, the volume of distribution was estimated to be approximately 200 mL/kg.|Following single dose oral administration of glutamine at 0.1 g/kg to six subjects, mean peak blood glutamine concentration was 1028uM (or 150 mcg/mL) occurring approximately 30 minutes after administration. The pharmacokinetics following multiple oral doses have not been adequately characterized.|Metabolism is the major route of elimination for glutamine. Although glutamine is eliminated by glomerular filtration, it is almost completely reabsorbed by the renal tubules.

Exogenous L-glutamine likely follows the same metabolic pathways as endogenous L-glutamine which is involved in the formation of glutamate, proteins, nucleotides, and amino acid sugars.|Glutamine plays an important role in nitrogen homeostasis and intestinal substrate supply. It has been suggested that glutamine is a precursor for arginine through an intestinal-renal pathway involving inter-organ transport of citrulline. The importance of intestinal glutamine metabolism for endogenous arginine synthesis in humans, however, has remained unaddressed. The aim of this study was to investigate the intestinal conversion of glutamine to citrulline and the effect of the liver on splanchnic citrulline metabolism in humans. Eight patients undergoing upper gastrointestinal surgery received a primed continuous intravenous infusion of [2-(15)N]glutamine and [ureido-(13)C-(2)H(2)]citrulline. Arterial, portal venous and hepatic venous blood were sampled and portal and hepatic blood flows were measured. Organ specific amino acid uptake (disposal), production and net balance, as well as whole body rates of plasma appearance were calculated according to established methods. The intestines consumed glutamine at a rate that was dependent on glutamine supply. Approximately 13% of glutamine taken up by the intestines was converted to citrulline. Quantitatively glutamine was the only important precursor for intestinal citrulline release. Both glutamine and citrulline were consumed and produced by the liver, but net hepatic flux of both amino acids was not significantly different from zero. Plasma glutamine was the precursor of 80% of plasma citrulline and plasma citrulline in turn was the precursor of 10% of plasma arginine. In conclusion, glutamine is an important precursor for the synthesis of arginine after intestinal conversion to citrulline in humans.|Endogenous glutamine participates in various metabolic activities, including the formation of glutamate, and synthesis of proteins, nucleotides, and amino sugars. Exogenous glutamine is anticipated to undergo similar metabolism.

The half life of elimination is 1 h.|After an IV bolus dose in three subjects, the terminal half-life of glutamine was approximately 1 hour.

Supplemental L-glutamine's possible immunomodulatory role may be accounted for in a number of ways. L-glutamine appears to play a major role in protecting the integrity of the gastrointestinal tract and, in particular, the large intestine. During catabolic states, the integrity of the intestinal mucosa may be compromised with consequent increased intestinal permeability and translocation of Gram-negative bacteria from the large intestine into the body. The demand for L-glutamine by the intestine, as well as by cells such as lymphocytes, appears to be much greater than that supplied by skeletal muscle, the major storage tissue for L-glutamine. L-glutamine is the preferred respiratory fuel for enterocytes, colonocytes and lymphocytes. Therefore, supplying supplemental L-glutamine under these conditions may do a number of things. For one, it may reverse the catabolic state by sparing skeletal muscle L-glutamine. It also may inhibit translocation of Gram-negative bacteria from the large intestine. L-glutamine helps maintain secretory IgA, which functions primarily by preventing the attachment of bacteria to mucosal cells. L-glutamine appears to be required to support the proliferation of mitogen-stimulated lymphocytes, as well as the production of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma). It is also required for the maintenance of lymphokine-activated killer cells (LAK). L-glutamine can enhance phagocytosis by neutrophils and monocytes. It can lead to an increased synthesis of glutathione in the intestine, which may also play a role in maintaining the integrity of the intestinal mucosa by ameliorating oxidative stress. The exact mechanism of the possible immunomodulatory action of supplemental L-glutamine, however, remains unclear. It is conceivable that the major effect of L-glutamine occurs at the level of the intestine. Perhaps enteral L-glutamine acts directly on intestine-associated lymphoid tissue and stimulates overall immune function by that mechanism, without passing beyond the splanchnic bed. The exact mechanism of L-glutamine's effect on NAD redox potential is unknown but is thought to involve increased amounts of reduced glutathione made available by glutamine supplementation. This improvement in redox potential reduces the amount of oxidative damage which sickle red blood cells are more susceptible to. The reduction in cellular damage is thought to reduce chronic hemolysis and vaso-occlusive events.|L-glutamine has important functions in regulation of gastrointestinal cell growth, function, and regeneration. Under normal conditions, glutamine concentration is maintained in the body by dietary intake and synthesis from endogenous glutamate. Data from clinical studies indicate that the role of and nutritional requirements for glutamine during catabolic illness, trauma, and infection may differ significantly from the role of and nutritional requirements for glutamine in healthy individuals. Glutamine concentrations decrease and tissue glutamine metabolism increases during many catabolic disease states, and thus glutamine is often considered a "conditionally essential" amino acid.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/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/

/HUMAN EXPOSURE STUDIES/ We investigated the effect of glutamine supplementation on plasma glutamine (Gln), glutamate (Glu), and whole-blood glutathione (GSH) concentrations in human volunteers. Subjects first adapted to a standard diet with known intakes of protein, total GSH, cysteine, methionine, and total Glu (Glu values include Glu and Gln) for 3 d. Plasma Gln, Glu, and whole-blood GSH levels were then measured at 4-hr intervals over 24 hr. Supplemental oral Gln (0.3 g x kg(-1) x d(-1)) was ingested for 10 d and then 24-hr plasma levels of Gln, Glu, and whole-blood GSH were measured.The plasma concentrations of Glu (116%; P = 0.006) and Gln (20%; P = 0.046) were significantly higher, whereas concentrations of GSH were significantly lower (37%; P = 0.00091) after oral Gln supplementation. Oral Gln increases Glu and Gln levels in plasma of healthy subjects but does not increase GSH red cell (whole-blood) levels. Thus, GSH biosynthesis and preservation of GHS stores in red blood cells may involve rate-limiting substrates other than Gln.|/HUMAN EXPOSURE STUDIES/ To evaluate the safety of nutraceutical oral administration of L-glutamine (L-Gln) in middle-aged and elderly individuals. In this randomized, crossover, double-blind clinical study, 30 residents of a long-term-care institution, selected according to a modified SENIEUR protocol (Working Party of the EURAGE Concerted Action Programme on Ageing of the European Community), were studied. Fourteen subjects received orally 0.5 g/kg/d of L-Gln and 16 received calcium caseinate for 14 d, followed by a 5-d washout. Supplements were switched for the second 14-d trial. Laboratory tests for hepatic and renal functions and ammonemia were performed and the estimated glomerular filtration rate (eGFR) was calculated. Of the 30 subjects, 16 were men, mean age was 69+/-8.8 y, average weight was 61.8+/-14.2 kg, and mean serum albumin was 4.0+/-0.3 g/dL. Neither adverse clinical effects nor clinically significant laboratory changes were noted during L-Gln supplementation. There was no difference in ammonemia between the groups. There were statistically but not clinically significant increases in plasma urea nitrogen and creatinine concentrations. There was no significant decrease in eGFR during calcium caseinate supplementation (-2.9%). The eGFR decreased significantly after L-Gln supplementation (-13.3%) but well below the 25% limit for biologic significance. Increases in serum urea nitrogen and creatinine and decrease in eGFR are probably due to difficulties by older kidneys in metabolizing the supplemented protein sources. Although not clinically significant, those alterations impose a rigorous control on the evaluation parameters of renal function during oral L-Gln supplementation, with doses of 0.5 g/kg/d in middle-aged and elderly individuals.|/HUMAN EXPOSURE STUDIES/ seven male subjects participated in three trials, in each of which they received one of three different drinks by systematic rotation: 18.5 % (wt/vol) glucose polymer solution (containing glucose, maltose, maltotriose, tetrasaccharide, pentasaccharide and "higher sugars"), a solution containing 8 g glutamine, or 18.5 % glucose polymers containing 8 g glutamine. Tests were undertaken one month apart. On each test day, subjects followed a validated standard exercise protocol designed to deplete of glycogen both type I and type II muscle fibres. A muscle biopsy was taken from the quadriceps femoris muscle within 15 min of the end of exercise. Within 20 min, a 2 h constant [1-(13)C]glucose intravenous infusion started at a rate of 8.5 mg/kg/hr for the first 30 min after a 9 mg/kg bolus of [1-(13)C]glucose. Subjects then consumed the test drinks (330 mL) within 2 min of the start of the infusion. Second and third quadriceps femoris muscle biopsies were taken after 1 and 2 hr of recovery. No significant differences with respect to the average rate of net muscle glycogen storage during the 2 hr of recovery after exercise were observed between the test drinks.|/HUMAN EXPOSURE STUDIES/ eight trained subjects were studied during 3 hr of recovery while consuming one of four drinks in random order. Drinks were ingested in three 500 mL boluses. Each bolus of the control drink contained 0.8 g/kg body weight of glucose. The other drinks contained the same amount of glucose and either 0.3 g/kg body weight of glutamine, or a wheat hydrolysate (26 % glutamine), or a whey hydrolysate (6.6 % glutamine). On each test day (7 days apart), subjects followed a validated standard exercise protocol for glycogen depletion. A biopsy was taken from the quadriceps muscle 15 min after the end of exercise, and the first bolus was taken immediately thereafter. The other boluses followed after 1 and 2 hr of recovery. A second muscle biopsy was taken after 3 hr of recovery. The rate of glycogen re-synthesis in skeletal muscle was not significantly different between the four test drinks.|For more Human Toxicity Excerpts (Complete) data for Glutamine (9 total), please visit the HSDB record page.

D Glutamine

PowerSleep /contains/ 250 mg L-glutamine /and other amino acids with vitamins, minerals and herbs/|Neu-Recovery-SA /contains/ 50 mg L-glutamine /and other amino acids with vitamins and minerals/|Neu-Recovery-DA /contains/ 25 mg L-glutaine /and other amino acids with vitamins and minerals/|NeuroSlim /contains/ 15 mg L-glutamine /and other amino acids with vitamins and minerals/|NutreStore (L-glutamine powder for oral solution) for oral administration is formulated as a white crystalline powder in a paper-foil-plastic laminate packet. Each packet of NutreStore contains 5 g of L-glutamine.

Food, beverage, and tobacco product manufacturing|L-Glutamine: ACTIVE

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