Abstract
BackgroundTaurine and zinc exert neurotrophic effects in the central nervous system. Current studies demonstrate that Na+/Cl- dependent neurotransmitter transporters, similar to that of taurine, are modulated by micromolar concentrations of zinc. This study examined the effect of zinc sulfate ex vivo on [3H]taurine transport in goldfish retina.MethodsIsolated cells were incubated in Ringer with zinc (0.1–100 µM). Taurine transport was done with 50 nM [3H]taurine or by isotopic dilution with taurine (0.001–1 mM) and 50 nM [3H]taurine.ResultsZinc reduced the capacity of taurine transport without changes in affinity, and caused a noncompetitive inhibition of high affinity taurine transport, with an EC50= 0.072 µM. The mechanism by which zinc affects taurine transport is unknown at the present.ConclusionsThere may be a binding site of zinc in the transporter that affects union or translocation of taurine, or possibly the formation of taurine-zinc complexes, rather than free zinc, could affect the operation of the transporter.
Highlights
Taurine and zinc exert neurotrophic effects in the central nervous system
Zinc is essential for the normal development and function of the central nervous system (CNS) and a deficiency of this element during early development can result in gross structural defects and pronounced behavioural abnormalities [10,11]
Kinetic parameters of [3H]taurine transport The analysis of saturation experiments performed in the presence of 50 nM [3H]taurine alone and with increasing concentration of non labeled taurine from 0.001 to 1 mM resulted in a best fitting to a two site model
Summary
Current studies demonstrate that Na+/Cl- dependent neurotransmitter transporters, similar to that of taurine, are modulated by micromolar concentrations of zinc. This study examined the effect of zinc sulfate ex vivo on [3H]taurine transport in goldfish retina. Taurine (2-aminoethane sulfonic acid), a b-amino acid that contains a negatively charged sulfonic acid group, is present at high levels in the retina of many vertebrates [1] This amino acid is known to be involved in the mediation of multiple functions, such as osmoregulation, modulation of calcium fluxes, neuromodulation, protection from oxidative stress, modification of protein phosphorylation, membrane stabilization, affectation of cell migration in the brain and in the retina, regulation of axonal outgrowth, elevation in the number of regenerating retinal cells after nerve lesion, and production of neural protection in certain neuropathies [2,3,4]. The physiological functions of zinc have been studied in retina, where it is believed to interact with taurine, to modify photoreceptor plasma membranes, to modulate synaptic transmission and to serve as an antioxidant [8,9]. The trophic effect of taurine may be affected by the inhibition of its transport [22]; given that zinc, in concentrations equal to or greater than 0.06 μM, blocks the trophic function of this amino acid, that the effect of taurine could be influenced by transport inhibition, and that zinc modulates neurotransmitter transporters with the same topology, the evaluation of whether the presence or absence of zinc could affect taurine uptake was proposed as the objective of this work
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