Disease relevance of LMFA01090032

• The bacteria thus isolated were found to be members of the alpha division of the Proteobacteria in the Rhizobium subdivision, most likely Agrobacterium sp. They could utilize both dihaloalcohol substrates and 2-chloropropionic acid [1].
• A 3-kb EcoRI fragment of genomic DNA from a Rhizobium sp. cloned into pUC19 endowed Escherichia coli K-12 with the ability to grow, albeit slowly, with 2-chloropropionic acid as substrate [2].
• For certain chemicals, GSH provides neuroprotection, and Edward Lock discussed the selective toxicity of 2-chloropropionic acid (CPA) to the cerebellum and how its modification by modulating brain thiol status provides an example of GSH acting in neuroprotection [3].
• The neurotoxin 2-chloropropionic acid (2CPA, 750 mg/kg, per os) induces ataxia in rats causing neuropathological changes (necrosis and edema) localized mainly in the cerebellum (CB) [4].

High impact information on LMFA01090032

• Extracts were prepared from the forebrain and cerebellum of animals that had been treated with L-2-chloropropionic acid, with and without prior treatment with MK-801, and were analysed using magnetic resonance spectroscopy and amino acid analysis [5].
• Evidence for mediation of L-2-chloropropionic acid-induced delayed neuronal cell death by activation of a constitutive nitric oxide synthase [6].
• The ring opening reaction of epoxy groups of the P(GMA) main chain with 2-chloropropionic acid resulted in the immobilization of the alpha-chloroester groups (the ATRP initiators for the NIPAAm side chains) and the concomitant formation of hydroxyl groups [7].
• The derived amino acid sequence of DehE showed little identity with DehD or DehL, but there was significant identity to two other dehalogenases that act non-selectively on 2-chloropropionic acid [2].
• Calpain activation and not oxidative damage mediates L-2-chloropropionic acid-induced cerebellar granule cell necrosis [8].

Biological context of LMFA01090032

• Comparison of the deduced amino acid sequences of the two dehalogenases (18% identity) indicated with any other 2-chloropropionic acid dehalogenase studied so far [9].
• 1p4studied the effect of L-2-chloropropionic acid (L-CPA)-induced (250 mg/kg/po/day for 3 days) neurotoxicity, which results in an almost total destruction of cerebellar granule cells over 5 days, on forebrain and cerebellar neurochemistry [10].
• We have used the L-2-chloropropionic acid (L-CPA) (750 mg/kg) model of NMDA-mediated selective cerebellar granule cell necrosis in vivo to examine the role of the glycine binding site and possible effect of the NR2C subunit (which is largely expressed only in the cerebellum) on granule cell necrosis [11].

Anatomical context of LMFA01090032

• The objectives of the studies described were to assess the ultrastructural neuropathology, blood-brain barrier (BBB) integrity and calcium status of the cerebellum of rats following a single dose of 750 mg.kg-1 L-2-chloropropionic acid (L-2-CPA) [12].

Associations of LMFA01090032 with other chemical compounds

• We have used the model of L-2-chloropropionic acid (L-CPA)-induced selective cerebellar granule necrosis to study excitatory amino acid-induced necrotic cell death in vivo produced by the activation of N-methyl-D-aspartate (NMDA) receptors [13].

Analytical, diagnostic and therapeutic context of LMFA01090032

• Oral administration of L-2-chloropropionic acid (L-CPA) to rats either as a single dose (750 mg/kg) or daily doses (250 mg/kg per day for 3 days) produces selective necrosis to the granule cell layer of the cerebellum [14].

References