Disease relevance of Allyl cyanide

• Allylnitrile: a compound which induces long-term dyskinesia in mice following a single administration [1].
• This inhibition was reversed by either sulpiride (0.15 mumol/kg i.v.) or haloperidol (0.13 mumol/kg i.v.) but not by yohimbine (0.14 mumol/kg i.v.). TL-350 did not change isoproterenol-induced tachycardia and hypotensive responses [2].
• In a dose-dependent manner, allylnitrile caused corneal opacity and gliosis in the retina and olfactory bulbs, decreased rearing activity and increased the rating scores in tests of vestibular dysfunction, and induced hair cell loss in both the vestibular sensory epithelia and the organ of Corti [3].
• The daily dietary intake of allylnitrile was estimated to be at least 0.12 micromol/kg body weight for Japanese, based on its generation from the vegetables, broccoli, cabbage, cauliflower and Chinese cabbage and their daily dietary consumption [4].
• A dose-dependent inhibition of cyanide formation arising from allylnitrile in the liver and a dose-dependent attenuation of acute toxicity of allylnitrile were observed when CCl4 was given just prior to the nitrile administration in rats and mice [5].

High impact information on Allyl cyanide

• Kinetics, thermodynamics, and effect of BPh3 on competitive C-C and C-H bond activation reactions in the interconversion of allyl cyanide by [Ni(dippe)] [6].
• A single oral administration of allylnitrile, crotononitrile or 2-pentenenitrile in rats induced behavioral abnormalities, such as head-twitching, head weaving, hindlimb abduction, backward pedaling and pivoting [7].
• Intravenous and intraduodenal injection of a new ergoline derivative, TL-350, produced dose-dependent inhibition of heart rate increase produced by cardioaccelerator nerve stimulation in anesthetized cats [2].
• Dopaminergic antagonists, haloperidol and sulpiride, antagonized the inhibitory effect of TL-350 in in vitro experiments [2].
• TL-350 caused dose-dependent decrease of arterial blood pressure and heart rate in anesthetized cats [2].

Chemical compound and disease context of Allyl cyanide

• The effects of allylnitrile (ALN), which induces a long-term dyskinesia in mice, on the metabolism of serotonin (5-HT) and dopamine (DA) were studied after a single administration [8].
• Straight chain aliphatic nitrile compound (propionitrile, allyl cyanide); branch chain aliphatic nitrile compound (isobutyronitrilc) and aromatic nitrile compound (benzonitrile) removal by Comamonas testosteroni and Acidovorax sp. was also investigated [9].

Biological context of Allyl cyanide

• It is conceivable that allylnitrile caused apoptotic changes in neurons but did not always lead them to cell death immediately [10].
• The results suggest that active metabolites of allylnitrile are responsible for the head twitching, and that CCl4 prevents the metabolic process in the liver by forming conjugates with allylnitrile, resulting in the inhibition of the head twitching [5].

Anatomical context of Allyl cyanide

• TL-350 induced rotation for 3 hr in rats with unilateral denervated caudate nucleus [2].
• TL-350 did not stimulate presynaptic alpha-2 adrenergic receptors in rat vas deferens and guinea-pig ileum [2].
• The present results suggest that the GABAergic systems through the medial habenula-interpeduncular nucleus-ascending raphe nuclei relay and through the substantia nigra may be involved in allylnitrile-induced behavioral abnormalities [11].
• Allylnitrile also induced changes in the amount of immunolabelling of tyrosine hydroxylase in the arcuate nucleus, substantia nigra pars compacta, locus coeruleus and caudoventrolateral reticular nucleus at either 2 or 14 days postdosing, depending on the structures [11].
• Allylnitrile produced neuronal retraction including hyperchromasia of the nuclei in the raphe nuclei, cerebral cortex, hypothalamus, hippocampal CA1 and dentate gyrus later than 30 days [10].

Associations of Allyl cyanide with other chemical compounds

• To explore what type of neuronal system is involved in these behavioral abnormalities, five neuronal markers, gamma-aminobutyric acid (GABA), tyrosine hydroxylase, serotonin, the serotonin transporter and choline acetyltransferase were immunohistochemically examined within various brain structures in allylnitrile and vehicle-treated mice [11].
• GC-MS analysis of the Bifidobacterial cultured broth showed that the major products were 3-butenenitrile (BCN) and phenylacetonitrile (PhACN), from SNG and GTL, respectively and nitriles, probably due to a decrease in the pH of the media [12].
• In liver fractions from male Sprague-Dawley rats, the metabolism of allylnitrile (ALN) to cyanide (CN-) was localized in the microsomal fraction and required NADPH and oxygen for maximal activity [13].

Gene context of Allyl cyanide

• Fos induction in the brain of mice exhibiting behavioral abnormalities following administration of allylnitrile or crotononitrile [14].

Analytical, diagnostic and therapeutic context of Allyl cyanide

• Using a combination of local -- scanning tunneling microscopy -- and spatially integrated, but chemically sensitive probes -- X-ray photoelectron spectroscopy and near edge X-ray absorption fine structure spectroscopy -- we have examined how 3-butenenitrile reacts with the Si(001)-2 x 1 surface at room temperature [15].

References