ISBN-13: 9783639168693 / Angielski / Miękka / 2009 / 188 str.
In the mammalian retina, endogenous chelatable zinc was shown to be localised mainly in the photoreceptors and retinal pigment epithelium. Zinc localisation in the photoreceptors varied in light and dark. Low (100 micromolar) levels of zinc sulphate (ZnSO4) counteracted glutamate- and NMDA-induced lactate dehydrogenase release in rat cortical cultures; as well as the changes in Gamma-aminobutyric acid (GABA)-immunoreactivity mediated by experimental ischaemia and NMDA in isolated rabbit retinas. However, high (500 micromolar) levels of ZnSO4 caused lactate dehydrogenase release and alterations in GABA-immunoreactivity, and exacerbated the effects of NMDA or ischaemia to the retina. When very low (1 micromolar) concentrations of ZnSO4 were present during ischaemia, GABA-immunoreactivity was localised to Muller cells, indicating that zinc prevents the metabolism of GABA in Muller cells in the ischaemic retina. High (500 micromolar) concentrations of ZnSO4 potentiated reactive oxygen species formation while ameliorating lipid peroxidation. When low (1 nanomol) levels of ZnSO4 were injected into the vitreous humour of the rabbit eye the retina remained unaffected."
In the mammalian retina, endogenous chelatable zincwas shown to be localised mainly in thephotoreceptors and retinal pigment epithelium. Zinclocalisation in the photoreceptors varied in lightand dark. Low (100 micromolar) levels of zincsulphate (ZnSO4) counteracted glutamate- andNMDA-induced lactate dehydrogenase release in ratcortical cultures; as well as the changes inGamma-aminobutyric acid (GABA)-immunoreactivitymediated by experimental ischaemia and NMDA inisolated rabbit retinas. However, high (500micromolar) levels of ZnSO4 caused lactatedehydrogenase release and alterations inGABA-immunoreactivity, and exacerbated the effects ofNMDA or ischaemia to the retina. When very low (1micromolar) concentrations of ZnSO4 were presentduring ischaemia, GABA-immunoreactivity was localisedto Müller cells, indicating that zinc prevents themetabolism of GABA in Müller cells in the ischaemicretina. High (500 micromolar) concentrations of ZnSO4potentiated reactive oxygen species formation whileameliorating lipid peroxidation. When low (1 nanomol)levels of ZnSO4 were injected into the vitreoushumour of the rabbit eye the retina remained unaffected.