Chemistry

Permanent URI for this collectionhttp://repository.kln.ac.lk/handle/123456789/3748

Browse

Search Results

Now showing 1 - 5 of 5
  • Item
    Alterations in Protein Kinase C activity after experimental brain injury
    (Brain Research, 1996) Jayawardena, B.M.; Mark, R.; Dhillon, H.S.; Mattson, M.P.; Prasad, M.R.
  • Item
    Changes in 1,4,5 inositol triphosphate receptors following experimental brain injury
    (Neuroscience research communications, 1995) Jayawardena, B.M.; Dhillon, H.S.; Carbary, T.; Prasad, M.R.
    Inositol 1,4,5-tris phosphate (IP3), a cellular second messenger of excitatory neurotransmitter system, by interacting with membrane IP3 receptor can mobilize calcium from internal stores. Regional binding properties of IP3 receptor were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, a significant decrease in the IP3 receptor density was found only in the ipsilateral left hippocampus. At 20 min after injury, significant decreases were observed in both the receptor density and the half maximal reduction of IP3, binding in both the injured left cortex and ipsilateral hippocampus. These findings suggest that increases of ligand affinity to the IP3 receptor after brain injury. This change in the IP3 receptor in concert with the increased IP3 (21) may facilitate a possible IP3 action of calcium mobilization in the brain regions that undergo neuronal cell loss after brain injury.
  • Item
    Hydrolysis of glycosylpyridinium ions by anomeric-configuration-inverting glycosidases
    (Carbohydrate Research, 1992) Jayawardena, B.M.; Sinnott, M.L.
    The hydrolyses of five ?-d-xylopyranosylpyridinium ions by the ?-d-xylosidase of Bacillus pumilus proceed with kcat values 108?109-fold larger than the rates of spontaneous hydrolysis of the same compounds. Log(kcat) values correlate well with aglycon pKa [?1g(V) = ?0.52, r = 0.99], whereas the correlation of log(kcat/Km) is poor [r = 0.77; ?1g(V/K) = ? ?0.6]. The (1 ? 3)-?-d-glucanase of Sporotrichum dimorphosporum hydrolyses 4-bromo-2-(?-d-glucopyranosyl)isoquinolinium ion with a rate enhancement of 108. The amyloglucosidase II of Aspergillus niger hydrolyses three ?-d-gluco-pyranosylpyridinium ions with rate enhancements of 105?108. The efficient hydrolysis of glycosylpyridinium ions by these three inverting glycosidases, the catalytic mechanism of which is unlikely to involve a nucleophile from the enzyme, makes it imporable that the hydrolysis of glycosylpyridinium ions by retaining glycosidases discovered some years ago, is initiated by addition of a catalytic nucleophilic carboxylate group of the enzyme to the pyridinium ring.
  • Item
    Regional Concentrations of Cyclic Nucleotides After Experimental Brain Injury
    (Journal of Neurotrauma, 1995) Dhillon, H.S.; Yang, L.; Jayawardena, B.M.; Dempsey, R.J.; Prasad, M.R.
    Regional concentrations of lactate, glucose, cAMP, and cGMP were measured after lateral fluid percussion brain injury in rats. At 5 min after injury, while tissue concentrations of lactate were elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres, those of glucose were decreased in these brain regions. By 20 min after injury, increases of lactate concentrations and decreases of glucose concentrations were observed only in the cortices and in the hippocampus of the ipsilateral hemisphere. Whereas the cAMP concentrations were unchanged in the cortices and hippocampi of the ipsilateral and contralateral hemispheres at 5 min after injury, decreases were found in the injured cortex and ipsilateral hippocampus at 20 min after injury. The tissue concentrations of cGMP were found to be elevated only in the ipsilateral hippocampus at 5 min after injury. The present observation that tissue glucose decreases in the injured cortex and the ipsilateral hippocampus are consistent with the published findings of increased hyperglycolysis and oxidative metabolism in brain immediately after injury. The present findings that the concentrations of cAMP and cGMP change in the cortex and hippocampus provide biochemical evidence for the neurotransmitter's surge after brain injury.