α-Amino-β-methylaminopropionic acid

118.13

118.13

75.4

log Kow = -4.00 (est)

165-167 °C @ Solvent: Water, Ethanol

In water, 1.0X10+6 mg/L /miscible/ at 25 °C (est)

2-8°C

3.9X10-9 mm Hg at 25 °C (est)

Henry's Law constant = 3.4X10-13 atm-cu m/mol at 25 °C (est)

pKa1 = 1.16; pKa 2 = 6.47; pKa3 = 10.47 (est)

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. 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 soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Norden (The Nordic Council, Nordic Council of Ministers); Analysis, Occurrence, and Toxicity of beta-Methylaminoalanine (BMAA). A risk for the consumer? (2007).[Available from, as of May 4, 2012: http://www.slv.se/upload/dokument/rapporter/kemiska/Analysis,_occurrence,_and_toxicity_of_ß-methylaminoalanine_(BMAA).pdf]

Personnel protection: Wear appropriate chemical protective gloves, boots, and goggles.

If material on fire or involved in fire: Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use "alcohol" foam, dry chemical or carbon dioxide. Use water spray to knock-down vapors.

Environmental considerations: Land spill: Dig a pit, pond, lagoon holding area to contain liquid or solid material. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash or cement powder.|Environmental considerations: Water spill: Neutralize with agricultural lime (CaO), crushed limestone (CaCO3), or sodium bicarbonate (NaHCO3). If dissolved, in region of 10 ppm or greater concentration, apply activated carbon at ten times the spilled amount. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.|Environmental considerations: Air spill: Apply water spray or mist to knock down vapors. Vapors knockdown water is corrosive or toxic should be diked for containment.

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Use water spray to knock-down vapors. Neutralize spilled material with crushed limestone, soda ash, or lime.|Personnel protection: Avoid breathing vapors. Keep upwind. Avoid bodily contact with the material. Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water. If contact with the material anticipated, wear appropriate chemical protective clothing.

Determination of the environmental factors involved in neurodegenerative diseases has been elusive. Methylmercury and beta-N-methylamino-L-alanine (BMAA) have both been implicated in this role. Exposure of primary cortical cultures to these compounds independently induced concentration-dependent neurotoxicity. Importantly, concentrations of BMAA (10-100 uM) that caused no toxicity alone potentiated methylmercury (3 uM) toxicity. In addition, concentrations of BMAA and methylmercury that had no effect by themselves on the main cellular antioxidant glutathione together decreased glutathione levels. Furthermore, the combined toxicity of methylmercury and BMAA was attenuated by the cell permeant form of glutathione, glutathione monoethyl ester. The results indicate a synergistic toxic effect of the environmental neurotoxins BMAA and methylmercury, and that the interaction is at the level of glutathione depletion. /beta-N-methylamino-L-alanine/

3-(Methylamino)-(L)-alanine was shown to be produced by members of the genera Microcystis, Anabaena, Planktothrix, Hapalosiphon, Anabaenopsis and Nostoc and may be produced by any cyanobacterial symbionts or free-living cyanobacteria(1).|3-(Methylamino)-(L)-alanine is found in seeds of Cycas circinalis /Queen Sago/.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.8(SRC), determined from a structure estimation method(2), indicates that 3-(methylamino)-(DL)-alanine is expected to have very high mobility in soil(SRC). Estimated pKa values of 3-(methylamino)-(DL)-alanine are 1.16, 6.47 and 10.47(3), indicating that this compound will partially exist in cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of 3-(methylamino)-(DL)-alanine from moist soil surfaces is not expected to be an important fate process(SRC) given its pKa values(3) and estimated Henry's Law constant of 3.4X10-13 atm-cu m/mole(SRC), using a fragment constant estimation method(5). 3-(Methylamino)-(DL)-alanine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.9X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(6).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.8(SRC), determined from a structure estimation method(2), indicates that 3-(methylamino)-(DL)-alanine is not expected to adsorb to suspended solids and sediment(SRC). Volatilization of neutral 3-(methylamino)-(DL)-alanine from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 3.4X10-13 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Estimated pKa values of 1.16, 6.47 and 10.47(5) indicate that 3-(methylamino)-(DL)-alanine will exist partially in the cation form at pH values of 5 to 9 and, therefore, volatilization from water surfaces of the ion is not expected to be an important fate process(SRC). According to a classification scheme(6), an estimated BCF of 3(SRC), from an estimated log Kow of -4.0(7) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is low(SRC). However studies have demonstrated a 10,000 fold biomagnification of free 3-(methylamino)-(DL)-alanine and a 50 fold biomagnification of total 3-(methylamino)-(DL)-alanine(9).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 3-(methylamino)-(DL)-alanine, which has an estimated vapor pressure of 3.9X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase 3-(methylamino)-(DL)-alanine may be removed from the air by wet or dry deposition(SRC). 3-(Methylamino)-(DL)-alanine 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).

3-(Methylamino)-(DL)-alanine does not contain chromophores that absorb at wavelengths >290 nm(1) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

3-(Methylamino)-(DL)-alanine is soluble in water and has a low Kow, therefore it would not be expected to biomagnify up the food chain(1). An estimated BCF of 3 was calculated in fish for 3-(methylamino)-(DL)-alanine(SRC), using an estimated log Kow of -4.0(2) and a regression-derived equation(3). According to a classification scheme(4), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC). However studies have demonstrated a 10,000 fold biomagnification of free 3-(methylamino)-(DL)-alanine and a 50 fold biomagnification of total 3-(methylamino)-(DL)-alanine(1).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 3-(methylamino)-(DL)-alanine can be estimated to be 1.8(SRC). According to a classification scheme(2), this estimated Koc value suggests that 3-(methylamino)-(DL)-alanine is expected to have very high mobility in soil. Estimated pKa values of 1.16, 6.47 and 10.47(3) indicates that 3-(methylamino)-(DL)-alanine will exist partially in cation 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 3-(methylamino)-(DL)-alanine is estimated as 3.4X10-13 atm-cu m/mole(SRC) using a fragment constant estimation method(1). Estimated pKa values of 1.16, 6.47 and 10.47(2) indicate that 3-(methylamino)-(DL)-alanine will exist partially in the cation form at pH values of 5 to 9(SRC). This Henry's Law constant and estimated pKa values indicate that 3-(methylamino)-(DL)-alanine is expected to be essentially nonvolatile from moist soil and water surfaces(3). 3-(Methylamino)-(DL)-alanine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.9X10-9 Hg(SRC), determined from a fragment constant method(4).

Monitoring data indicate that the general population may be exposed to 3-(methylamino)-(DL)-aniline via ingestion of food containing 3-(methylamino)-(DL)-aniline, specifically seafood. (SRC)

3-(Methylamino)-(DL)-aniline was detected in the brain tissues of eight of nine Canadian Alzheimer's patients, but not detected in the brain tissues of 14 other Canadians who died of causes unrelated to neurodegeneration(1). 3-(Methylamino)-(DL)-aniline was found in the brain tissues of Chamorros who died of amyotropic lateral sclerosis or parkinsonism-dementia complex, but not in patients who died of causes unrelated to neurodegenerative disease(1).

Drugs that bind to and activate excitatory amino acid receptors. (See all compounds classified as Excitatory Amino Acid Agonists.)

2-Amino-3-(methylamino)-propanoic acid (BMAA) is a neurotoxic, excitatory amino acid which has been linked through cycad use and consumption with the onset of a variant of amyotrophic lateral sclerosis occurring with high incidence in the western Pacific region. ... To evaluate its kinetics and uptake, BMAA (25-400 mg/kg) was administered to rats, either acutely or chronically, and then plasma and brain concentrations were determined at various times thereafter by combined gas chromatography mass spectrometry. After single dose i.v. injection, BMAA was cleared from plasma in a rapid distribution phase (Vd approximately 16 liters/kg) followed by a slower elimination phase (half life approximately 1 day). Brain uptake was limited by a low blood-brain barrier permeability-surface area product of 2 to 5 x 10(-5) mL/sed/g. Brain BMAA levels peaked within 8 hr after injection, and then declined with a t1/2 similar to that of plasma. After two weeks of continuous infusion (100 mg/kg/day), steady-state brain concentrations equalled 10 to 30 ug/g, and only moderately exceeded those in plasma. The results suggest that BMAA may reach potentially toxic levels in brain (i.e., greater than 250 uM) after large doses (greater than 100 mg/kg). However, such doses are orders of magnitude greater than those available from dietary or medicinal use of cycads.|beta-N-Methylamino-L-alanine (BMAA) is a neurotoxic plant amino acid that has been implicated in the pathogenesis of the high incidence amyotrophic lateral sclerosis and related parkinsonism dementia of the western Pacific. Previous studies have demonstrated that BMAA is taken up into brain following intravenous or oral administration. To examine the kinetics and mechanism of brain transfer, BMAA influx across the blood-brain barrier was measured in rats using an in situ brain perfusion technique. BMAA influx was found to be saturable with a maximal transfer rate (Vmax) of 1.6 +/- 0.3 x 10(-3) umol/s/g and a half-saturation constant (Km) of 2.9 +/- 0.7 mM based on total perfusate BMAA concentration. Uptake was sodium independent and inhibitable by excess L-leucine, but not by L-lysine, L-glutamate, or methylaminoisobutyric acid, indicative of transfer by the cerebrovascular large neutral amino acid carrier. L-BMAA competitively reduced brain influx of L-[14C]leucine, as expected for cross-inhibition. The results demonstrate that BMAA is taken up into brain by the large neutral amino acid carrier of the blood-brain barrier and suggest that uptake may be sensitive to the same factors that affect neutral amino acid transport, such as diet, metabolism, disease, and age. /beta-N-Methylamino-L-alanine/

The non-protein amino acid, beta-N-methylaminoalanine (BMAA), is neurotoxic and has been implicated in the amyotrophic lateral sclerosis-Parkinsonism-dementia (ALS-PD) complex of Guam. This concept remains controversial, in part because of the lack of a convincing animal model. The neuropharmacology of BMAA is well established, but little is known of its metabolism. ... BMAA changed the distribution of taurine, glycine and serine between rat brain slices and their incubation medium; the glutamate/glutamine cycle between neurones and glia was also compromised. In model experiments BMAA reacted non-enzymatically with pyridoxal-5'-phosphate, releasing methylamine. Rat liver and kidney homogenates, but not brain homogenates, also formed methylamine and 2,3-diaminopropanoic acid when incubated with BMAA. These results provide evidence that several biochemical mechanisms are involved in the neurotoxicity of BMAA. The novel discovery that methylamine is formed from BMAA in rat liver and kidney preparations may be significant since chronic administration of methylamine to rats causes oxidative stress. The extent to which this reaction occurs in different animal species might be a decisive factor in selecting an animal model. /beta-N-methylamino-L-alanine/

... 2-Amino-3-(methylamino)-propanoic acid (BMAA) (25-400 mg/kg) was administered to rats, either acutely or chronically, ... . After single dose iv injection elimination half life /was/ approximately 1 day.

beta-N-methylamino-l-alanine (BMAA), a neurotoxic amino acid produced by cyanobacteria, has been suggested to be involved in the etiology of a neurodegenerative disease complex which includes Parkinson-dementia complex (PDC). In PDC, neuromelanin-containing neurons in substantia nigra are degenerated. Many PDC patients also have an uncommon pigmentary retinopathy. The aim of this study was to investigate the distribution of (3)H-BMAA in mice and frogs, with emphasis on pigment-containing tissues. Using autoradiography, a distinct retention of (3)H-BMAA was observed in melanin-containing tissues such as the eye and neuromelanin-containing neurons in frog brain. Analysis of the binding of (3)H-BMAA to Sepia melanin in vitro demonstrated two apparent binding sites. In vitro-studies with synthetic melanin revealed a stronger interaction of (3)H-BMAA with melanin during synthesis than the binding to preformed melanin. Long-term exposure to BMAA may lead to bioaccumulation in melanin- and neuromelanin-containing cells causing high intracellular levels, and potentially changed melanin characteristics via incorporation of BMAA into the melanin polymer. Interaction of BMAA with melanin may be a possible link between PDC and pigmentary retinopathy. /beta-N-methylamino-l-alanine/|... Various in vivo studies on rats, mice, chicks and monkeys have shown that /alpha-amino-beta-methylaminopropionic acid (BMAA)/ can cause neurodegenerative symptoms such as ataxia and convulsions. Zebrafish research has also shown disruption to neural development after BMAA exposure. In vitro studies on mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca(2+) influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. ...|Beta-N-methylamino-L-alanine (BMAA) is a nonprotein amino acid that may be involved in neurodegenerative diseases. It is produced by a large variety of cyanobacteria and is found at high levels in the brains of Alzheimer's disease and amyotrophic lateral sclerosis patients. Although BMAA is clearly a neurotoxin, previous studies using cortical cultures indicated that millimolar concentrations were required to cause toxicity. ... The toxicity of BMAA /was tested/ in septal cultures containing cholinergic neurons and mesencephalic cultures containing dopaminergic neurons. We found that cholinergic, but not dopaminergic, neurons were selectively vulnerable to BMAA toxicity, with toxicity occurring at 30 uM. The toxicity of BMAA to total septal neurons involved activation of N-methyl D-aspartate receptors, whereas the death of cholinergic neurons was mediated by AMPA/kainate receptors. /Beta-N-methylamino-L-alanine/|... Although the role of N-methylamino-L-alanine (BMAA) in human neurodegenerative disease is still highly debated, it appears to injure cultured neurons via mechanisms involving overactivation of neuroexcitatory glutamate receptors. However, BMAA lacks the side-chain acidic group of glutamate and other excitatory amino acids, and in its place has an amino group. In past studies we found that toxic and excitatory effects of BMAA on cultured neurons were dependent upon the presence of bicarbonate in the medium, and suggested that formation of a carbamate adduct of the side-chain amino group might produce structures capable of activating glutamate receptors. Also, while BMAA is a weal agonist at NMDA-type glutamate receptors, we found low levels of BMAA to selectively damage vulnerable sub-populations of neurons, including motor neurons, via activation of AMPA/kainate receptors. ... /N-methylamino-L-alanine/|For more Mechanism of Action (Complete) data for 3-(METHYLAMINO)-(DL)-ALANINE (10 total), please visit the HSDB record page.

/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/

/SURVEILLANCE/ The investigators/ tested the brain tissues of the Chamorro people of Guam who died of amyotrophic lateral sclerosis/Parkinsonism dimentia complex (ALS/PDC) for the neurotoxin beta-methylamino-l-alanine (BMAA). /The investigators/ used validated high-pressure liquid chromatography and liquid chromatography-mass spectrometry analyses to test well-characterized archival tissues of the superior frontal gyrus from eight Chamorros from Guam and a comparison group of 15 Canadians. BMAA was found as a free amino acid in 83% of Chamorro ALS/PDC patients (3-10 ug/g) as a protein-associated amino acid in 100% of the Chamorro individuals (149-1190 ug/g). Both forms of BMAA were also found at comparable levels in two Canadians who died of progressive neurodegenerative disease. ... /Beta-methylamino-l-alanine/|/SURVEILLANCE/ The aim of this study was to screen for and quantify the neurotoxic amino acid beta-N-methylamino-L-alanine (BMAA) in a cohort of autopsy specimens taken from Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and non-neurological controls. BMAA is produced by cyanobacteria found in a variety of freshwater, marine, and terrestrial habitats. The possibility of geographically broad human exposure to BMAA had been suggested by the discovery of BMAA in brain tissues of Chamorro patients with ALS/Parkinsonism dementia complex from Guam and more recently in AD patients from North America. These observations warranted an independent study of possible BMAA exposures outside of the Guam ecosystem. Postmortem brain specimens were taken from neuropathologically confirmed cases of 13 ALS, 12 AD, 8 HD patients, and 12 age-matched non-neurological controls. BMAA was quantified using a validated fluorescent HPLC method previously used to detect BMAA in patients from Guam. Tandem mass spectrometric (MS) analysis was carried out to confirm the identification of BMAA in neurological specimens. BMAA /was detected and quantified/ in neuroproteins from postmortem brain tissue of patients from the United States who died with sporadic AD and ALS but not HD. Incidental detections observed in two out of the 24 regions were analyzed from the controls. The concentrations of BMAA were below what had been reported previously in Chamarro ALS/ Parkinsonism dementia complex patients, but demonstrated a two-fold range across disease and regional brain area comparisons. The presence of BMAA in these patients was confirmed by triple quadrupole liquid chromatography/mass spectrometry/mass spectrometry. The occurrence of BMAA in North American ALS and AD patients suggests the possibility of a gene/environment interaction, with BMAA triggering neurodegeneration in vulnerable individuals. /beta-N-methylamino-L-alanine/|/SURVEILLANCE/ Cyanobacteria produce many neurotoxins including beta-methylamino-L-alanine (BMAA) that has been liked to amyotrophic lateral sclerosis (ALS) and neurodegenerative disease. A number of ALS cases have been diagnosed among residents of Enfield, NH, a town encompassing a lake with a history of cyanobacteria algal blooms. To investigate an association between toxic cyanobacterial blooms in New Hampshire and development of ALS, we reviewed records from our institution and other community databases to obtain demographic information on patients diagnosed with ALS within New England. ... Nine ALS patients who lived near Lake Mascoma in Enfield, NH, an incidence of sporadic ALS that is 10 to 25 times the expected incidence of 2/100,000/year /were identified/. /The investigators/ suggest that the high incidence of ALS in this potential cluster could be directly related to chronic exposure to cyanobacterial neurotoxins such as BMAA. Possible routes of toxin exposure include inhalation of aerosolized toxins, consuming fish, or ingestion of lake water. ... /beta-methylamino-L-alanine/|/OTHER TOXICITY INFORMATION/ As root symbionts of cycad trees, cyanobacteria of the genus Nostoc produce beta-methylamino-l-alanine (BMAA), a neurotoxic nonprotein amino acid. The biomagnification of BMAA through the Guam ecosystem fits a classic triangle of increasing concentrations of toxic compounds up the food chain. However, because BMAA is polar and nonlipophilic, a mechanism for its biomagnification through increasing trophic levels has been unclear. /The investigators/ report that BMAA occurs not only as a free amino acid in the Guam ecosystem but also can be released from a bound form by acid hydrolysis. After first removing free amino acids from tissue samples of various trophic levels (cyanobacteria, root symbioses, cycad seeds, cycad flour, flying foxes eaten by the Chamorro people, and brain tissues of Chamorros who died from amyotrophic lateral sclerosis/Parkinsonism dementia complex), we then hydrolyzed the remaining fraction and found BMAA concentrations increased 10- to 240-fold. This bound form of BMAA may function as an endogenous neurotoxic reservoir, accumulating and being transported between trophic levels and subsequently being released during digestion and protein metabolism. Within brain tissues, the endogenous neurotoxic reservoir can slowly release free BMAA, thereby causing incipient and recurrent neurological damage over years or even decades, which may explain the observed long latency period for neurological disease onset among the Chamorro people. The presence of BMAA in brain tissues from Canadian patients who died of Alzheimer's disease suggests that exposure to cyanobacterial neurotoxins occurs outside of Guam. /beta-methylamino-l-alanine/|For more Human Toxicity Excerpts (Complete) data for 3-(METHYLAMINO)-(DL)-ALANINE (7 total), please visit the HSDB record page.

2-amino-3(methylamino)propionic acid

3-(Methylamino)-(DL)-alanine was shown to be produced by members of the genera Microcystis, Anabaena, Planktothrix, Hapalosiphon, Anabaenopsis and Nostoc and may be produced by any cyanobacterial symbionts or free-living cyanobacteria.|3-(Methylamino)-(l)-alanine is found in seeds of Cycas circinalis /Queen Sago/.

The cyanobacterial neurotoxin, beta-N-methylamino-l-alanine (BMAA), has been suggested as an important environmental factor for neurodegenerative disease such as amyotrophic lateral sclerosis- Parkinsonism dementia complex (ALS/PDC) in Guam. BMAA was detected within the majority of cyanobacterial isolates surveyed in both free and symbiotic cyanobacteria, living in freshwater as well as marine environments. In this study, we report two methods using liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS/MS) each coupled with a different type of hydrophilic interaction liquid chromatography (HILIC) column to detect BMAA. A third method using AQC-derivatized BMAA was also used for comparison. Axenic cultures of Microcystis aeruginosa and Nostoc sp. isolated from Chinese freshwater were analyzed for both free and protein-bound BMAA at the exponential growth stage. Cultures of two strains of M. aeruginosa collected at four growth stages were also analyzed for the presence of BMAA. BMAA was detected in the Nostoc sp. at very low concentrations (<0.07pmoles on column) only when precolumn AQC derivatization was used. No BMAA was detected in the Chinese derived axenic cultures of Microcystis; detection limits for the LC-ESI-MS and LC-ESI-MS/MS without precolumn derivatization were 10ng and 2pg BMAA on column, respectively. We suggest that cyanobacteria grown under some culture conditions may be relatively free of BMAA. /beta-N-methylamino-l-alanine/|Two different assays have been developed and used in order to investigate the optimal conditions for derivatization and detection of acid beta-N-methyl-amino-L-alanine (BMAA) in a cyanobacterial sample. BMAA was extracted from cyanobacterial cultures both from the cytosolic ("free") fraction and in the precipitated ("protein") fraction using a newly developed extraction scheme and the sample matrix was standardized according to protein concentration to ensure the highest possible derivative yield. A rapid and sensitive HPLC method for fluorescence detection of the non-protein amino acid BMAA in cyanobacteria, utilizing the Waters AccQ-Tag chemistry and Chromolith Performance RP-18e columns was developed. Using this new method and utilizing a different buffer system and column than that recommended by Waters, we decreased the time between injections by 75%. The limit of quantification was determined to be 12 nmol and limit of detection as 120 fmol. The linear range was in the range of 8.5 nmol-84 pmol. Accuracy and precision were well within FDA guidelines for bioanalysis. /beta-N-methyl-amino-L-alanine/|A capillary electrophoretic method for the determination of the amino acid beta-N-methylamino-l-alanine (BMAA) was achieved using a fused-silica capillary column (50 cm x 75 um I.D.) filled with 5 mM sodium tetraborate solution (pH 9), with an applied voltage of 25 kV, at 25 °C. The method was then applied in quantifying BMAA in eighteen strains of lyophilized estuarine cyanobacteria, following amino acid extraction using 0.1 M trichloroacetic acid and 6 M hydrochloric acid, sequentially. /beta-N-methylamino-l-alanine/|Nonprotein amino acids from nine species of cycad seeds were analyzed as N-ethoxycarbonyl ethyl ester (ECEE) derivatives by positive chemical-ionization gas chromatography-mass spectrometry. Based on the retention times and mass spectrometry analyses, 12 nonprotein amino acids were identified in these seeds. In addition to the excitatory and putative neurotoxin beta-N-methylamino-L-alanine (BMAA), the known neurotoxin beta-N-oxalylamino-L-alanine (BOAA) was detected from the seeds of Macrozamia moorei and M. communis, and delta-N-oxalyl-ornithine was obtained from the Cycas revoluta seeds. A novel nonprotein amino acid named cycasindene, previously reported from C. revoluta, was also found in the seeds of members of the C. angulata and C. rumphii complex. Eight additional known nonprotein amino acids were also identified. This is the first report of the neurotoxin BOAA from cycad seeds. /beta-N-methylamino-L-alanine/|For more Analytic Laboratory Methods (Complete) data for 3-(METHYLAMINO)-(DL)-ALANINE (7 total), please visit the HSDB record page.

L-Beta-methylamino-alanine (BMAA) has been proposed as a worldwide contributor to neurodegenerative diseases, including Parkinson dementia complex (PDC) of Guam and Alzheimer's disease (AD). Recent conflicting reports of the presence of this amino acid in human brain from patients affected by these diseases have made it necessary to develop methods that provide unambiguous detection in complex samples. Comprehensive two-dimensional gas chromatography coupled with time-of-flight-mass-spectrometry analysis (GCxGC-TOFMS) followed by a targeted Parallel Factor Analysis (PARAFAC) deconvolution method has been used recently in metabolomic investigations to separate, identify, and quantify components of complex biological specimens. We have extended and applied this methodology to the toxicological problem of detecting BMAA in extracts of brain tissue. Our results show that BMAA can be isolated from closely eluting compounds and detected in trace amounts in extracts of brain tissue spiked with low levels of this analyte, ranging from 2.5ppb to 50ppb, with a limit of detection (LOD) of 0.7ppb. This new method was sufficiently sensitive to detect BMAA in cerebral extracts of mice fed BMAA. This optimized approach was then applied to analyze tissue from humans; however, no BMAA was detected in the brain extracts from controls or patients with PDC or AD. Our results demonstrate the application of multidimensional chromatography-mass spectrometry methods and computational deconvolution analysis to the problem of detecting trace amounts of a potential toxin in brain extracts from mice and humans. /L-Beta-methylamino-alanine/