Disease relevance of Aminopropionitrile

• In addition, after the onset of hypertension, administration of beta-aminopropionitrile lowered the blood pressure [1].
• Collagen synthesis in capsules surrounding dimethylbenzanthracene-induced rat breast tumors and the effect of pretreatment with beta-aminopropionitrile [2].
• beta-Aminopropionitrile (beta APN), 500 ng/g body weight was injected intraperitoneally into male rats every 2 days between 2 and 28 days after birth [3].
• The BAPN-treated rats (lathyritic rats) died of dissecting aneurysm, and the victims with hypertensive treatment was greater in number and died earlier than those without the treatment, indicating that the rise of blood pressure promoted the onset of dissecting aneurysm [4].
• Ten patients with massive keloids, resistant to conventional therapy by excision, grafting, and/or intralesional injection of steroids, have been treated by excising the keloid, grafting the defect, inducing lathyrism with Beta aminopropionitrile fumurate or penicillamine and administering colchicine [5].

Psychiatry related information on Aminopropionitrile

• The BAPN-treated animals showed an increased density of IJs, SAs, and Ids when compared with controls but the NJs demonstrated no change [6].

High impact information on Aminopropionitrile

• Shell membranes from hens fed a copper-deficient diet or a diet supplemented with beta-aminopropionitrile had a reduced content of desmosine and isodesmosine [7].
• In the presence of the lathyrogen beta-aminopropionitrile, the smooth muscle cells incorporate [3H]lysine into a lysyl oxidase substrate that was present in the medium and associated with the cell layer [8].
• In one approach, the extracellular matrix structure of the apical half of the hydra graft was perturbed using beta-aminopropionitrile and beta-xyloside [9].
• Statistical analysis indicated that beta-aminopropionitrile, fibronectin, RGDS synthetic peptide and antibody to fibronectin all were inhibitory to I-cell migration as compared to their respective controls. beta-xyloside treatment had no effect on interstitial cell migration [9].
• The effect of BAPN was most pronounced in the submandibular gland [10].

Chemical compound and disease context of Aminopropionitrile

• We produced cerebral aneurysms in 19 rats by unilaterally ligating the common carotid artery, inducing renal hypertension, and feeding beta-aminopropionitrile fumarate [11].
• Effect of D-penicillamine and beta-aminopropionitrile on collagen breakdown of carrageenin granuloma in rats [12].
• In the present study we describe changes in aorta at the protein level associated with allylamine (AA) and beta-aminopropionitrile (beta APN) induced vascular toxicity in a rat model [13].
• Rats that were given both BAPN and phenytoin produced similar exostoses as rats that were given BAPN alone [14].
• These data show that cHyp and BAPN treatment did not prevent silica-induced pulmonary fibrosis, led to more extensive silicotic nodules, and were toxic [15].

Biological context of Aminopropionitrile

• Reduction of blood pressure and vascular collagen in hypertensive rats by beta-aminopropionitrile [1].
• Treatment of the invasive breast cancer cell lines, Hs578T and MDA-MB-231, with beta-aminopropionitrile (betaAPN), an irreversible inhibitor of LOX catalytic activity, leads to a significant decrease in cell motility/migration and adhesion formation [16].
• Suramin treatment resulted in a more normal phenotype as judged by growth rate, cell cycle parameters, and morphology. beta-aminopropionitrile, the selective inhibitor of lysyl oxidase enzyme activity, was remarkably unable to block suramin-induced reversion [17].
• BAPN exhibits a dose-dependent effect on morphogenesis, but has no effect on respiration nor on protein synthesis of the embryos throughout development [18].
• The approach taken was to disrupt collagen processing with two types of agents (a lathyritic agent, beta-aminopropionitrile (BAPN), and three types of proline analogs: dehydroproline, cis-OH-proline, and azetidine carboxylic acid) and to assess the effect on embryogenesis by morphological, immunological, and biochemical criteria [18].

Anatomical context of Aminopropionitrile

• To investigate the structure of type XI as it occurs in the matrix, sterna from chick embryos treated with beta-aminopropionitrile were solubilized without proteolysis with pepsin [19].
• Since beta-aminopropionitrile was not employed in these studies, significant accumulation of collagen chains into the insoluble extracellular matrix was observed during the chase period [20].
• To support this hypothesis, previous studies are reviewed concerning the remarkable synergistic toxic action of allylamine and beta-aminopropionitrile on the media of blood vessels [21].
• Six-month-old BN and LE rats were subjected to carotid ligation only for 11 to 13.5 months and treated or not (from 3 to 7 months of age) with an inhibitor of connective tissue fiber maturation, beta-aminopropionitrile (BAPN) [22].
• We quantified interruptions in the internal elastic lamina in certain arteries and studied the effect of beta-aminopropionitrile, an inhibitor of cross-link formation in collagen and elastic fibers, on rupture of the internal elastic lamina and on mortality in these two substrains [23].

Associations of Aminopropionitrile with other chemical compounds

• Beta-aminopropionitrile fumarate (BAPN), a potent lathyrogen that perturbs collagen cross-linking by inhibition of lysyl oxidase, also inhibited the rate of lattice cell contraction in lattices composed of native collagen [24].
• D-penicillamine and beta-aminopropionitrile effects on experimental filtering surgery [25].
• In spite of previous reports of positive results with BAPN, neither BAPN nor penicillamine was found to affect keratometry readings or corneal topography after radial keratotomy [26].
• Treatment of chick embryos with beta-aminopropionitrile, an irreversible inhibitor of lysyl oxidase, causes an inhibition of the enzyme, which begins to recover within 24 h but which is not affected by the administration of pyridoxal; with isoniazid inhibition, however, lysyl oxidase activity does not show any sign of recovery by 48 h [27].
• Protein sequence analysis of unlabeled insulin-alpha 2M complexes, together with results of beta-aminopropionitrile competition, confirmed that insulin incorporation occurs via the same gamma-glutamyl amide linkage responsible for covalent proteinase and methylamine binding to alpha 2M [28].

Gene context of Aminopropionitrile

• In addition, treatment of MDA-MB-231 and Hs578T cells with beta-aminopropionitrile (an irreversible inhibitor of LOX enzymatic activity) decreased invasive activity [29].
• The copper chelator D-penicillamine inhibits Loxl2 induced oxidation of collagen but the Lox inhibitor beta-aminopropionitrile did not inhibit the oxidation using a BAPN concentration at which Lox activity was completely inhibited [30].
• Interestingly, hsp47 gene expression but not hsp70 or BiP mRNA accumulation was enhanced by treatment with a procollagen-specific stressor, beta-aminopropionitrile [31].
• The purified LOX-p, LOXL-p1, and LOXL-p2 proteins showed specific amine oxidase activity of 0.097, 0.054, and 0.150 U/mg, respectively, which was inhibited by beta-aminopropionitrile (BAPN), a specific inhibitor of LOX [32].
• The elastic fibers that formed in fibrin treated with TGF-beta1 and insulin contained crosslinks, as evidenced by the presence of desmosine and an altered elastin labeling pattern when beta-aminopropionitrile (BAPN) was added [33].

Analytical, diagnostic and therapeutic context of Aminopropionitrile

• Pretreatment of animals with beta-aminopropionitrile to inhibit collagen cross-linking caused an 82% decrease in tumor formation and a significant reduction in tumor volume (approximately 0.4 cu cm) compared to controls (approximately 10 cu cm) [2].
• Western blots of extracted proteins from chick embryonic aortae cultured in the presence of beta-aminopropionitrile showed that the medium and a mild salt extract contained an immunoreactive protein possessing an apparent molecular mass of 58,000 whereas harsh denaturants extracted a 32,000-kDa protein [34].
• After debanding, the ratio remained lower in the banded group without beta-aminopropionitrile treatment than in the control group [35].
• BAPN was found in the urine within one hour of oral administration [36].
• Transmission electron microscopy of the media of the thoracic aorta revealed that the types of intercellular contacts seen in the controls and in the BAPN group were intermediate junctions (IJs), nexus junctions (NJs), simple appositions (SAs), and interdigitations (Ids) as in adult vessels [6].

References