National Toxicology Program

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. ¹

Names (NTP)

• Allylamine
• 2-PROPEN-1-AMINE (9CI)

Human Toxicity Excerpts

• ... AT 14 PPM IT CAUSED INTOLERABLE IRRITATION OF EYES AND RESP TRACT. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 69]**PEER REVIEWED**
  
• ... EXPERIMENTERS EXPERIENCED TRANSIENT IRRITATION OF THE MUCUS MEMBRANES OF NOSE, EYES, AND MOUTH, WITH LACRIMATION, CORYZA, AND SNEEZING AFTER ACCIDENTAL EXPOSURE TO AN UNSPECIFIED CONCN OF THE VAPOR OF ALLYLAMINE. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3157]**PEER REVIEWED**
  
• CAUTION: STRONG IRRITANT. CAN CAUSE EXCITEMENT, CONVULSIONS, DEATH. [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989., p. 49]**PEER REVIEWED**
  
• IN GENERAL THE ALLYL AMINES IRRITATED THE NOSE AND THROAT AT LOWER CONCN THAN WERE IRRITANT TO THE EYES. /ALLYL AMINES/ [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 69]**PEER REVIEWED**
  
• A potent irritant, allylamine is intolerable at 14 ppm, with recognizable odor and chest and mucous membrane discomfort at 2.5 ppm. [Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 707]**PEER REVIEWED**
  

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Non-Human Toxicity Excerpts

• ... TESTED BY DROPPING ON RABBIT EYES ... MONOALLYL AMINE WAS EXTREMELY IRRITATING. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 69]**PEER REVIEWED**
  
• TOXICITY OF /MONOALLYLAMINE/ FOR RATS: REPEATED INHALATION, 7 HR X 50; CHANGES IN LIVER & KIDNEY WT @ 5 PPM; REDUCED GROWTH @ 10 PPM & DEATHS @ 40 PPM. /FROM TABLE/ ... BOTH MONO- & DIALLYLAMINES WERE SEVERELY IRRITATING TO SKIN... ACUTE EXPOSURES TO THE VAPORS PRODUCED SYMPTOMS & FINDINGS OF RESPIRATORY TRACT IRRITATION. PATHOLOGICAL CHANGES...FOLLOWING REPEATED INHALATION INCL CHEMICAL PNEUMONIAS &...LIVER & KIDNEY DAMAGE. MOST PROMINENT PATHOLOGICAL EFFECT...WAS MYOCARDITIS... [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3157]**PEER REVIEWED**
  
• IN RATS, 0.05 CC OF ALLYLAMINE...PRODUCED SEVERE NECROSIS & DEATH WHEN APPLIED TO 1 SQ CM AREA OF SHAVED ABDOMINAL SKIN. [Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 2057]**PEER REVIEWED**
  
• ...ALL BUT 1 OR 2 OF 30 MICE EXPOSED TO CONCN OF 1.27 MILLIMOLES/L OF ALLYLAMINE...DIED DURING COURSE OF 10 MIN INHALATION. ... SYMPTOMS WERE IRRITATION, FLUSHING OF EARS, IRREGULAR RESPIRATION, CYANOSIS, CONVULSIONS, COMA, & DEATH. [Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 2057]**PEER REVIEWED**
  
• ... RATS, RABBITS, AND DOGS WERE EXPOSED FOR 8 HR/DAY, 5 DAYS/WK /FOR 1 YR/ TO 5 OR 20 PPM. NO ADVERSE EFFECTS ON GROWTH, BEHAVIORAL REACTIONS, OR ABNORMAL BLOOD OR URINE CHANGES WERE OBSERVED. DEATHS FROM PNEUMONIA OCCURRED IN 3 OF 6 RABBITS EXPOSED TO 20 PPM. LUNG CHANGES CONSISTENT WITH CHRONIC IRRITATION WERE FOUND AT BOTH EXPOSURE LEVELS. HOWEVER, NO MYOCARDIAL DAMAGE WAS FOUND IN RABBITS OR DOGS AND ONLY A FEW RATS SHOWED SLIGHT CHANGES, WHICH WERE NOT CONSIDERED DIFFERENT FROM THOSE EXPECTED IN UNEXPOSED RATS. PERIODIC LIVER AND KIDNEY FUNCTION TESTS, TRANSAMINASE DETERMINATIONS, AND ELECTROCARDIOGRAPHIC EXAMINATIONS OF DOGS DID NOT REVEAL ANY ABNORMALITIES. CONGESTIVE CHANGES IN THE LIVER AND KIDNEYS WERE NOTED IN DOGS AT BOTH EXPOSURE LEVELS. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3158]**PEER REVIEWED**
  
• MYOCARDIAL FIBROSIS WITH CARDIAC HYPERTROPHY WAS PRODUCED IN LONG-EVANS RATS AFTER CONSUMING ALLYLAMINE HYDROCHLORIDE FOR PERIODS OF 4-8 MONTHS. FOCAL EDEMA & NECROSIS OF SMOOTH MUSCLE CELLS IN MEDIA OF CORONARY ARTERIES WERE ALSO OBSERVED. [LALICH JJ, PAIK WCW; EXP MOL PATHOL 21 (1): 29 (1974)]**PEER REVIEWED**
  
• ABSORPTION SPECTRA SHOWED THAT ALLYLAMINE FORMED A COMPLEX WITH PYRIDOXAL PHOSPHATE IN SOLN AT PH 5.2, 7.4 & 8.0. AT 1X10-2 MOLAR, ALLYLAMINE INHIBITED ACTIVITY OF SERUM GLUTAMIC-OXALACETIC TRANSAMINASE BY 22.5%, & AT 1X10-4 MOLAR IT INHIBITED SERUM GLUTAMIC-PYRUVIC TRANSAMINASE BY 13.2%. IT INHIBITED ACTIVITY OF SERUM ENZYMES IN VITRO AT SAME CONCN AS ISONICOTINIC ACID HYDRAZIDE. IV INJECTION OF 60 MG/KG INTO RATS DECREASED ACTIVITIES OF HEPATIC GLUTAMIC-OXALACETIC TRANSAMINASE & GLUTAMIC-PYRUVIC TRANSAMINASE BY ABOUT 50%, WHEN THESE LEVELS WERE DETERMINED ABOUT 5 MIN AFTER INJECTION. [KUZUYA F ET AL; J NUTR 93 (3): 280 (1967)]**PEER REVIEWED**
  
• ULTRASTRUCTURAL STUDIES WERE MADE OF EARLY CHANGES INDUCED IN LEFT VENTRICULAR MYOCARDIUM BY ALLYLAMINE GIVEN TO RATS IN DRINKING WATER (10.7 MMOLAR FOR 1-7 DAYS) OR BY GAVAGE (100 MG/KG/DAY FOR 1-2 DAYS). RATS ON WATER PROTOCOL DEVELOPED MYOCARDIAL ALTERATIONS EVIDENT BY LIGHT MICROSCOPY WITHIN 2 DAYS; GAVAGE ADMIN PRODUCED LESIONS AFTER 24 HR. EARLIEST ALTERATIONS CONSISTED OF INTERSTITIAL EDEMA & ACTIVATION OF INTERSITITAL CELLS POSSESSING OBLONG SHAPE, ABUNDANT ROUGH ENDOPLASMIC RETICULUM, OCCASIONAL LYSOSOMES, PROMINENT GOLGI APPARATUS, FEW MITOCHONDRIA, & LARGE IRREGULAR NUCLEI (OFTEN WITH TYPICAL ANITSCHKOW MORPHOLOGY). MITOSIS OF INTERSTITIAL CELLS WERE FREQUENT & ALSO OBSERVED IN ENDOTHELIAL CELLS. MYOCARDIAL NECROSIS WAS CHARACTERIZED BY FOCAL MYOFIBRILLAR DEGENERATION WITH LIPID DROPLET ACCUM & Z-LINE DISTORTION & DISSOLUTION, PROMINENT IN AREAS OF INTERCELLULAR JUNCTIONS. MITOCHONDRIA OF SEVERELY ALTERED CELLS WERE SWOLLEN & CONTAINED DENSE INCLUSIONS. LARGE AREAS OF NECROTIC MYOCARDIUM SHOWED EXTRAVASATED RED BLOOD CELLS & MINIMAL INTRA- & EXTRACELLULAR DEPOSITION OF FIBRIN. [BOOR PJ, FERRANS VJ; LAB INVEST 47 (1): 76 (1982)]**PEER REVIEWED**
  
• Allylamine was evaluated for mutagenicity in the Salmonella/microsome preincubation assay using the standard protocol approved by the National Toxicology Program. Allylamine was tested at doses of 0, 1, 3, 10, 33, 100, 333, 1000, and 3333 ug/plate in four Salmonella typhimurium strains (TA98, TA100, TA1535, and TA1537) in the presence and absence of Aroclor-induced rat or hamster liver S9. Allylamine was negative in these tests and the highest ineffective dose level tested in any Salmonella tester strain was 3333 ug/plate. [Zeiger E et al; Environ Mutagen 9:1-110 (1987)]**PEER REVIEWED**
  
• Allylamine produces dose dependent myocardial and vascular lesions in male rats when supplied in the drinking water at concentrations ranging between 0.005 to 0.1% for 21-104 days. Rats given allylamine for 3 weeks developed severe myocardial fibrosis which were between grossly evident as white tissue in the myocardium and marked thinning and aneurysmal dilation of the apical right and ventricular walls. The amine significantly reduced monoamine oxidase activities of the brain and liver towards almost all substrates. The monoamine oxidase activity of the heart, however, increased in rats ingesting allylamine, after an initial decrease in cardiac monoamine oxidase activity during the first day of treatment. [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 7]**PEER REVIEWED**
  
• Allylamine produced direct toxic mechanism when given orally to rats for a few weeks, it produced vascular smooth muscle hyperplasia that resulted in coronary artery and aortic lesions mimicking the atherosclerotic process. [Amdur, M.O., J. Doull, C.D. Klaasen (eds). Casarett and Doull's Toxicology. 4th ed. New York, NY: Pergamon Press, 1991., p. 450]**PEER REVIEWED**
  
• FORMATION OF ACROLEIN MAY BE BASIS OF CARDIOTOXIC ACTION. [NELSON TJ, BOOR PJ; BIOCHEM PHARMACOL 31 (4): 509 (1982)]**PEER REVIEWED**
  
• Allylamine causes vascular lesions in aorta and medium-sized arteries. The amine is metabolized to acrolein both in vivo and in vitro. Acrolein acts as a strong peroxidizing agent and the deamination of allylamine is accompanied by production of hydrogen peroxide. To investigate the relative roles of oxidative stress and lipid peroxidation in allylamine intoxication, the authors conducted an acute in vivo time-course study following administration of allylamine (150 mg/kg) to rats by gavage. At 1, 3, and 5 hr after allylamine treatment, subcellular fractions of aorta, epicardium and endocardium were assayed for enzymes of the oxidant defense system and thiol (-SH) status capacity for lipid peroxidation, and .OH radical generation. ... In vivo treatment with allylamine causes preferential damage to aortic mitochondria. A marked depletion of total and free -SH content was found in aorta epicardium and endocardium with a striking increase in the formation of thiobarbiturate-reactive substance by aortic mitochondria at all time points. A significant increase in the capacity to generate .OH was found in aorta (with lesser increases in epicardium and endocardium) after allylamine treatment. Levels of defense system enzymes were not consistently altered, however. In a totally in vitro experiment, liposomes incubated with acrolein (0.2-2 mM) showed a proportional increase in lipid peroxidation of liposomal membrane. A likely basis of allylamine's cardiovascular toxicity is acrolein-induced lipid peroxidation especially in mitochondria. [Awasthi S, Boor PJ;J Vasc Res; 31 (1): 33-41 (1994)]**PEER REVIEWED**
  
• The profile of endogenous protein phosphorylation mediated by protein kinase C (PKC) was examined in cell fractions prepared from subcultured aortic smooth muscle cells (SMCs) isolated from rats treated with 70 mg/kg allylamine (AAM) or tap water for 20 days. Increased phosphorylation of endogenous proteins was observed under unstimulated conditions in the particulate but not cytosolic, fraction of cells from allylamine-treated animals (ie allylamine cells). Although the same phosphorylation bands were observed in the particulate or cytosolic fraction of control and allylamine cells following phorbol ester stimulation of the enzyme, enhancedprotein kinase C-mediated phosphorylation was observed in 60th fractions of allylamine cells. Measurements of exogenous histone Type III-S phosphorylation by protein kinase C followlng in vitro exposure of native smooth muscle cells to 100 uM allylamine for up to 60 min revealed that allylamine selectively increased histone phosphorylation in the cytosolic fraction of SMCs. AAM treatment enhances protein kinase C-mediated protein phosphorylation in rat aortic smooth muscle cells. [Ramos KS, Ou X; Toxicol Lett; 73 (2): 123-33 (1994)]**PEER REVIEWED**
  
• Allylamine is a specific cardiovascular toxin that causes vascular and myocardial lesions. ... Allylamine-induced chronic lesions are markedly reduced by semicarbazide, an inhibitor of semicarbazide-sensitive amine oxidase, and that allylamine is metabolized to the aldehyde acrolein, by semicarbazide-sensitive amine oxidase, The authors hypothesized that inhibitors of semicarbazide sensitive amine oxidase might reduce the acute cardiovascular toxicity of allylamine. The authors fed 150 mg/kg allylamine to semicarbazide-pretreated (3 hr; 98 mg/kg) rats. 1 hr after allylamine treatment, Aorta, epicardiun and endocardium were assayed forsemicarbazide sensitive amine oxidase glutathione peroxidase catalase thiol status and lipid peroxidation. Semicarbazide sensitive amine oxidase activity was decreased significantly in aorta epicardium and endocardium . Activity was 30-times higher in aorta than in epicardiun and endocardium. A striking decrease in malonaldehyde level (lipid peroxidation) was found in aorta of pretreated rats as compared to allylamine-only treated rats. The reduction of free-SH content in aortic mitochondria was also attenuated in pretreated rats. Changes were not so marked in epicardium and endocardium. ... In vivo pretreatment with semicarbazide at least partially protects aortic mitochondria from allylamine toxicity. The mechanism can be explained on the basis of the fact that semicarbazide inhibits acrolein formation in allylamine-treated rats. [Awasthi S, Boor PJ; Toxl col Lett; 66 (2): 157-63 (1993)]**PEER REVIEWED**
  
• Studies were conducted to evaluate the mechanisms involved in the deregulation of proliferative control induced by allylamine in rat aortic smooth muscle cells. Subcultured smooth muscle cells from animals treated with allylamine (70 mg/kg) for 20 days were processed for measurements of [3H]thymidine incorporation and c-Ha-ras mRNA levels. Pre-confluent allylamine cells stimulated with 10 fetal bovine serum exhibited enhanced mitogenic responsiveness. Decreased [3H]thymidine incorporation was observed in post-confluent cultures relative to pre-confluent counterparts. A 5-fold increase in c-Ha-ras transcript levels was observed in pre-confluent/cycling cultures of allylamine cells relative to controls. C-Ha-ras expression was markedly reduced in post-confluent cultures of both cell types as compared to pre-confluent counterparts. No difference between control and allylamine cells was observed during GI-synchronization of pre- or post-confluent cultures. The enhanced proliferative capacity induced by allylamine is associated with alterations in cell cycle-related expression of the c-Ha-ras protooncogene.[Bowes RC 3d, Ramos KS; Toxicol Lett; 66 (3): 263-72 (1993)]**PEER REVIEWED**
  
• The cardiotoxicity of allylamine is considered to be mediated by metabolism to the highly reactive aldehyde acrolein. The toxicity of allylamine to myocardial myocyte reaggregate cultures was assessed by measuring percentage beating as a marker of functional viability. The studies demonstrated that allylamine toxicity could be prevented by inhibitors of benzylamine oxidase but not by inhibitors of nonanine oxidase A or B. Addition of exogenous markedly potentiated the toxicity the effect that could be blocked by semicarbazide an inhibitor of benzylamine oxidase. The present studies support the view that allylamine is metabolized by benylamine oxidase to the proximate toxicant acrolein. In serun-free cultures high concentrations (0.5-2.5 mM) of allylamine were required to cause any loss of viability and as the concentration of serum in the medium was increased so the loss of viability was induced by allylamine; in myocardial myocyte maintained in 50% fetal calf serum all viability was lost after 3 hr of exposure to 100 mu M-allylamine. Mercaptoethanesulphonate a scavenger of reactive species that is known not to penetrate myocytes prevented the toxicity both of 100 mu M-allylamine and 100 mu M-ACR to MMR in serum-supplemented medium. In contrast when MMR in serum-free medium were exposed to high concentrations of allylamine MESNA had no moderating effect. These findings suggest that allylamine undergoes extracellular metabolism to ACR in serum-supplemented medium because of the presence of BZO in serum. ... Extracellular metabolisn is of importance in the pathogenesis of allylamine-induced toxicity to MMR in serum-supplemented medium. The toxicity of allylamine was also prevented by the iron chelator desferrioxamine at a concentration shown not to inhibit significantly the acitivity of BZO. ACR toxicity too was inhibited by DF. This suggests a role for free radicals in the toxicity of allylamine to MMR as DF chelates iron thus preventing the catalysis of free radical reactions. Addition of alpha-tocopherol succinate an inhibitor of lipid peroxidation to the cultures also reduced the toxicity of allylamine which provides some evidence of the role of lipid peroxidation in the mechanism of allylamine toxicity of MMR. [Earl LK and et al; Toxicol in Vitro; 6 (5): 405-16 (1992)]**PEER REVIEWED**
  
• The cytotoxic responses of cultured avian and rodent aortic smooth muscle cells to allylamine were compared. Sooth muscle cells were isolated from male Japanese quail or Sprague-Dawley rats and established in culture. Cellular glutathione content and lactate dehydrogenase leakage were used as indices of cytotoxicity. Exposure of avian and rodent smooth muscle cells in primary culture to allylamine (0.2-200 uM) for 4 h was associated with a significant reduction in cellular glutathione and enzyme leakage in cultures of both cell types. Increased exposure time to 24 h further depleted cellular glutathione levels and enhanced the leakage of LDH in primary cultures of avian smooth muscle cells. In contrast enhanced LDH leakage occurred without further glutathione depletion in primary cultures of rodent smooth muscle cells upon exposure to allylamine for 24 hr. Renoval of serum did not modulate the cytotoxic response profile of primary cultures of avian SMCs treated with 200 uM allylamine but was associated with marked elevation in cellular glutathione levels and significant lactate dehydrogenase leakage in rodent smooth muscle cells cultures. The cytotoxic responses to 0.2-200 uM allylamine in secondary cultures of avian smooth muscle cells were comparable to those observed in primary culture. In contrast allylamine-induced enzyme leakage did not consistently correlate with changes in glutathione content in subcultured rodent smooth muscle cells. Challenge with 200 uM acrolein for 4 hr reduced the glutathione content in avian but not rodent subcultures of smooth muscle cells. However, significant lactate-dehydrogenase leakage occurred in subcultures of both cell types upon exposure to aclorein. Although hydrogen peroxide did not modulate glutathione levels in avian or rodentcultures leakage of lactate dehydrogenase was observed in rat smooth muscle cells challenged with 200 uM hydrogen peroxide. Removal of serum did not alter the cytotoxic responses of avian subcultures to 200 uM allylamine for 24 hr but fully prevented cytotoxicity in rodent subcultures. ... Potentially significant variations in the sequence of events leading to injury may exist between quail and rat aortic smooth muscle cells. These differences may contribute to the enhanced avian susceptibility to allylamine-induced aortic injury in vivo. [Ramos KS; Thurlow CH; J Toxicol and Environmental Health 40 (1): 61-76 (1993)]**PEER REVIEWED**
  
• The cardiotoxicity of allylamie is considered to be mediated by metabolism to the highly reactive aldehyde acrolein. The toxicity of allylamine to myocardial myocyte reaggregate cultures was assessed by measuring percentage beating as a marker of functional viability. The studies demonstrated that allylamine toxicity could be prevented by inhibitors of benzylamine oxidase but not by inhibitors of monamine oxidase A or B. Addition of exogenous benzylamine oxidase markedly potentiated the toxicity the effect that could be blocked by semicarbazide an inhibitor of benzylamine oxidase. The present studies support the view that allylamine is metabolized by benzylamine oxidase to the proximate toxicant acrolein. In serum-free cultures high concentrations (0.5-2.5 mM) of allylamine were required to cause any loss of viability and as the concentration of serum in the medium was increased so the loss of viability was induced by allylamine; in myocardial myocyte reaggregate cultures maintained in 50% fetal calf serum all viability was lost after 3 hr of exposure to 100 mu M-allylamine. Mercaptoethanesulphonate, a scavenger of reactive species that is known not to penetrate myocytes prevented the toxicity both of 100 uM allylamine and 100 uM acrolein to myocardial myocyte reaggregate cultures in serum-supplemented medium. In contrast when myocardial myocyte reaggregate cultures in serum-free medium were exposed to high concentrations of allylamine, mercaptoethanesulphonate had no moderating effect. These findings suggest that allylamine undergoes extracellular metabolism to acrolein in serum-supplemented medium because of the presence of benzylamine oxidase in serum. ... Extracellular metabolism is of importance in the pathogenesis of allylamine-induced toxicity to myocardial myocyte reaggregate cultures in serun-supplemented medium. The toxicity of allylamine was also prevented by the iron chelator desferrioxamine at a concentration shown not to inhibitsignificantly the acitivity of benzylamine oxidase. Acrolein toxicity too was inhibited by desferrioxamine. This suggests a role for free radicals in the toxicity of allylamine to myocardial myocyte reaggregate cultures as desferrioxamine chelates iron thus preventing the catalysis of free radical reactions. Addition of alpha-tocopherol succinate an inhbitor of lipid peroxidation to the cultures also reduced the toxicity of allylamine which provides some evidence of the role of lipid peroxidation in the mechanism of allylamine toxicity of myocardial myocyte reaggregate cultures. [Earl LK et al;ToxicolIn Vitro; 6 (5): 405-16 (1992)]**PEER REVIEWED**
  
• The perfused rat heart preparation was used to assess direct toxic and physiologic effects of 10 to 30 mM allylamine and 0.01 to 3.0 mM acrolein, an allylamine metabolite. No grossly apparent functional abnormality was noted in allylamine perfused hearts except at 30mM. Acrolein perfused hearts beat irregularly and stopped within 15 minutes at 0.01 to 0.3 mM and by 5 minutes at; loss. Contraction band necrosis and extensive noted in allylamine perfused hearts. Acrolein perfusion resulted in no morphological lesions or creatine-kinase loss. Contraction band necrosis and extensive mitochondraal changes were seen by electron microscopy in hemodynamic preparations of rat hearts perfused with 10 mM allylamine. A marked rise was caused by allylamine in left ventricular pressure at 5 and 10 minutes. This was followed by a slow decline to a markedly depressed level at the end of 2 hr. End diastolic pressure rose steadily throughout the 2 hr perfusion. Coronary flow was similar in control and allylamine perfused hearts for 1 hr but then declined slowly. /It was/ suggested that vascular spasm or alterations in coronary flow are not the cause of allylamine induced myocardial damage. The toxic effect on myocardium may be mediated through the metabolism of allylamine and subsequent injurious intracellular events. [Sklar JL et al; - Toxicol and Appl Pharmacol 107 (3): 535-44 (1991)]**PEER REVIEWED**
  
• This study investigated the response of chick myocardial myocyte reaggregates (MMR) to allylamine which is specifically toxic to the cardiovascular system, and its putative toxic metabolite, acrolein. Toxicity was assessed by determining cellular ATP content, spontaneous beating and ultrastructural alterations. Both allylamine and acrolein caused a dose-dependent loss of beating and depletion of cellular ATP content. Treatment with either 10 or 100 uM-allylamine produced marked alterations in reaggregate tissue morphology at all times, which was charaterized by widespread myocyte necrosis and a reduction in tissue conpactness. Exposure of aggregates to acrolein produced generalized tissue destruction following administration of either 10 or 100 uM-acrolein. The concentration of allylamine required to cause loss of myocardial myocyte reaggregates beating was greatly increased when incubations were carried out in serum-free medium. It is suggested that the presence of benzylamine oxidase in serum contributes to the toxicity of allylamine to myocardial myocyte reaggregates, by metabolizing allylamine to acrolein. This proposal is supported by the finding that the related amines n-methylallylanine and diallylamine had no effect on spontaneous beating, which may because they are very poor substrates for benzylanine oxidase. The data presented demonstrate that allylamine is highly toxic to myocardial myocyte reaggregates. [Kesingland K et al; Toxicol In Vitro 5 (2): 145-56 (1991)]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• LD50 Rat oral 102 mg/kg [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 6]**PEER REVIEWED**
  
• LD50 Mouse oral 57 mg/kg [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 6]**PEER REVIEWED**
  
• LD50 Rabbit dermal 35 mg/kg [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 6]**PEER REVIEWED**
  
• LD50 Mouse iv 49 mg/kg [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 6]**PEER REVIEWED**
  

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Absorption, Distribution and Excretion

• None found

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Metabolism/Metabolites

• ACROLEIN WAS DETECTED IN HOMOGENATES OF RAT AORTA, LUNG, SKELETAL MUSCLE & HEART INCUBATED WITH ALLYLAMINE. HYDROGEN PEROXIDE, A PRODUCT OF OXIDATIVE DEAMINATION, WAS GENERATED DURING ALLYLAMINE OXIDATION. ACROLEIN WAS ALSO PRODUCED BY BOVINE PLASMA AMINE OXIDASE & PORCINE KIDNEY DIAMINE OXIDASE BUT NOT BY RAT LIVER OR BRAIN HOMOGENATES. BENZYLAMINE OXIDASE IS ACTIVE ENZYME IN OXIDIZING ALLYLAMINE. [NELSON TJ, BOOR PJ; BIOCHEM PHARMACOL 31 (4): 509 (1982)]**PEER REVIEWED**
  

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TSCA Test Submissions

• None found

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Footnotes

¹ Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.