Disease relevance of Iminodiproprionitrile

• Fragmentation of the Golgi apparatus of motor neurons in amyotrophic lateral sclerosis (ALS). Clinical studies in ALS of Guam and experimental studies in deafferented neurons and in beta,beta'-iminodipropionitrile axonopathy [1].
• Protection by 2-deoxy-D-glucose against beta,beta'-iminodipropionitrile-induced neurobehavioral toxicity in mice [2].
• Communicating hydrocephalus in rodents treated with beta,beta'-iminodipropionitrile (IDPN) [3].
• 3,3'-Iminodipropionitrile induces neurofilament accumulations in the perikarya of rat vestibular ganglion neurons [4].
• Degeneration and gliosis in rat retina and central nervous system following 3,3'-iminodipropionitrile exposure [5].

Psychiatry related information on Iminodiproprionitrile

• Administration of 3,3'-iminodipropionitrile (IDPN) (1 g/kg, i.p. for 3 days) in mice leads to the development of a characteristic syndrome consisting of lateral and vertical head and neck movements, hyperactivity, random circling, increased locomotor activity, and increased startle response [6].
• Quipazine (5-25 mg.kg-1, s.c.) was given to rats in which a hyperkinetic syndrome had been previously induced by administration of beta,beta'-iminodipropionitrile (IDPN) [7].
• Learning and memory deficits in rats following exposure to 3,3'-iminodipropionitrile [8].

High impact information on Iminodiproprionitrile

• Slow axonal transport of neurofilament proteins: impairment of beta,beta'-iminodipropionitrile administration [9].
• When treated with beta,beta'-iminodipropionitrile (IDPN), a neurotoxin that segregates microtubules and retards neurofilament transport, mice heterozygous or homozygous for the NF-H null mutation did not develop neurofilamentous swellings in motor neurons, unlike normal mouse littermates [10].
• Microtubule-associated protein 2 within axons of spinal motor neurons: associations with microtubules and neurofilaments in normal and beta,beta'-iminodipropionitrile-treated axons [11].
• Cytoskeletal architecture and immunocytochemical localization of microtubule-associated proteins in regions of axons associated with rapid axonal transport: the beta,beta'-iminodipropionitrile-intoxicated axon as a model system [12].
• Beta,beta'-iminodipropionitrile (IDPN) produces a rearrangement of axoplasmic organelles with displacement of microtubules, smooth endoplasmic reticulum, and mitochondria toward the center and of neurofilaments toward the periphery of the axon, whereas the rate of the fast component of axonal transport is unchanged [13].

Chemical compound and disease context of Iminodiproprionitrile

• In addition to the neurotoxic effects of beta,beta'-iminodipropionitrile (IDPN) which have been previously reported by other investigators, the olfactory toxicity of this compound has recently been uncovered in this laboratory [14].

Biological context of Iminodiproprionitrile

• Following disruption of intermediate filaments with beta,beta'-iminodipropionitrile, as confirmed by confocal microscopy, beta(3)AR-stimulated ERK activation was blocked, and lipolysis was reduced by more than 40% [15].
• Early effects of beta,beta'-iminodipropionitrile on tubulin solubility and neurofilament phosphorylation in the axon [16].
• Alterations in flash evoked potentials (FEPs) in rats produced by 3,3'-iminodipropionitrile (IDPN) [17].
• Neurofilament gene expression following beta,beta'-iminodipropionitrile (IDPN) intoxication [18].
• Adult exposure to the neurotoxicant 3,3'-iminodipropionitrile (IDPN), induces a hyperkinetic syndrome consisting of spontaneous head movements, abnormal circling, backward locomotion, and sensory disruption [19].

Anatomical context of Iminodiproprionitrile

• We have examined the distribution of microtubule-associated protein 2 (MAP2) in the lumbar segment of spinal cord, ventral and dorsal roots, and dorsal root ganglia of control and beta,beta'-iminodipropionitrile-treated rats [11].
• Disruption of the NF-H gene increases axonal microtubule content and velocity of neurofilament transport: relief of axonopathy resulting from the toxin beta,beta'-iminodipropionitrile [10].
• Actin immunoreactivity localizes with segregated microtubules and membraneous organelles and in the subaxolemmal region in the beta,beta'-iminodipropionitrile axon [20].
• Treatment of animals with beta,beta'-iminodipropionitrile (IDPN), which caused axonal atrophy, enhanced the staining intensity of all optic nerve astrocytes [21].
• Administration of 3,3'-iminodipropionitrile (IDPN) to rats results in massive accumulation of tangled neurofilaments in the proximal axons of large neurons, such as in dorsal root ganglia (DRG) and ventral horns of the lumbar spinal cord (LSC) [22].

Associations of Iminodiproprionitrile with other chemical compounds

• In addition, we report for the first time the segregation of axoplasmic organelles in animals treated with DMHD, providing further evidence that the neurofilamentous axonopathies caused by such compounds as beta,beta'-iminodipropionitrile (IDPN), 2,5-HD and CS2 share a common underlying mechanism [23].
• beta,beta'-Iminodipropionitrile-induced persistent dyskinetic syndrome in mice is transiently modified by MPTP [24].
• Spinal cords of cats treated with the neurotoxic compound beta,beta'-iminodipropionitrile (IDPN) were observed to contain rounded homogeneous bodies, 1-12 microns in diameter, termed "dense microspheres" (DMS) [25].
• Effect of methimazole, an FMO substrate and competitive inhibitor, on the neurotoxicity of 3,3'-iminodipropionitrile in male rats [26].
• The histopathology of the olfactory mucosal lesion associated with ip administration of 2,6-dichlorobenzonitrile (dichlobenil) and 3,3'-iminodipropionitrile (IDPN) has been well documented [27].

Gene context of Iminodiproprionitrile

• This study examined Schwann cell behavior during paranodal demyelination induced by beta,beta'-iminodipropionitrile (IDPN) [28].
• In the second study, we examined the Golgi apparatus of motor neurons in the spinal cord of rats with proximal axonopathy induced by beta,beta'-iminodipropionitrile [1].
• Age-related susceptibility to 3,3'-iminodipropionitrile-induced olfactory mucosal damage [29].
• We used chronically beta,beta'-iminodipropionitrile (IDPN)-intoxicated rats as a model of ALS and investigated SOD1 changes in the spinal cord by immunocytochemical and in situ hybridization techniques [30].
• The Golgi apparatus (GA) of anterior horn neurons of rats chronically intoxicated with beta,beta'-iminodipropionitrile (IDPN) in drinking water was examined with an organelle-specific antibody [31].

Analytical, diagnostic and therapeutic context of Iminodiproprionitrile

• Nevertheless, beta,beta'-iminodipropionitrile-treated nerves show constrictions in myelinated fibres when stretched [32].
• Spinal motoneurons remained unlabeled, despite procedures aimed at increasing the somal concentration of carbonic anhydrase, such as ventral root ligation and blocking of the fast or slow axoplasmic transport using colchicine or iminodiproprionitrile [33].
• By electron microscopy the degeneration appeared similar to that caused by beta,beta'-iminodipropionitrile with respect to segregation of the cytoskeleton [34].
• 3,3'-Iminodipropionitrile (IDPN) is a neurotoxicant that produces changes in flash evoked potentials (FEPs) 18 weeks after treatment [17].
• Occurrence of lipofuscin pigment granules and "dense microspheres" in the spinal cord of young cats treated with beta,beta'-iminodipropionitrile (IDPN) [25].

References