ArticleInvestigative ophthalmology & visual science2011
Transport via SLC5A8 (SMCT1) is obligatory for 2-oxothiazolidine-4-carboxylate to enhance glutathione production in retinal pigment epithelial cells.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Hydroxycarboxylic acid receptor 2 (GPR109A) and retinopathies: pathways and prospects.Frontiers in medicine · 2026Review
- Regulation of Intestinal Butyrate Transporters by Oxidative and Inflammatory Status.Antioxidants (Basel, Switzerland) · 2025Review
- A proteogenomic signature of age-related macular degeneration in blood.Nature communications · 2022Article
- Involvement of butyrate in electrogenic KPflugers Archiv : European journal of physiology · 2019Article
- Article
- Short-Chain Fatty Acid Transporters: Role in Colonic Homeostasis.Comprehensive Physiology · 2017Review
- Slc5a8, a Na+-coupled high-affinity transporter for short-chain fatty acids, is a conditional tumour suppressor in colon that protects against colitis and colon cancer under low-fibre dietary conditions.The Biochemical journal · 2015Article
- L-2-oxothiazolidine-4-carboxylic acid attenuates oxidative stress and inflammation in retinal pigment epithelium.Molecular vision · 2014Article
- Bioreducible crosslinked polyelectrolyte complexes for MMP-2 siRNA delivery into human vascular smooth muscle cells.Pharmaceutical research · 2012Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTo evaluate the role of SLC5A8 in the transport of 2-oxothiazolidine-4-carboxylate (OTC) and to determine whether OTC augments glutathione production in RPE cells, thereby providing protection against oxidative stress.
methodsSLC5A8-mediated transport of OTC was monitored in Xenopus laevis oocytes by electrophysiological means. Saturation kinetics, Na(+)-activation kinetics, and inhibition by ibuprofen were analyzed by monitoring OTC-induced currents as a measure of transport activity. Oxidative stress was induced in ARPE-19 cells and primary RPE cells isolated from wild type and Slc5a8(-/-) mouse retinas using H(2)O(2), and the effects of OTC on cell death and intracellular glutathione concentration were examined.
resultsHeterologous expression of human SLC5A8 in X. laevis oocytes induced Na(+)-dependent inward currents in the presence of OTC under voltage-clamp conditions. The transport of OTC via SLC5A8 was saturable, with a K(t) of 104 ± 3 μM. The Na(+)-activation kinetics was sigmoidal with a Hill coefficient of 1.9 ± 0.1, suggesting involvement of two Na(+) in the activation process. Ibuprofen, a blocker of SLC5A8, inhibited SLC5A8-mediated OTC transport; the concentration necessary for half-maximal inhibition was 17 ± 1 μM. OTC increased glutathione levels and protected ARPE-19 and primary RPE cells isolated from wild type mouse retinas from H(2)O(2)-induced cell death. These effects were abolished in primary RPE isolated from Slc5a8(-/-) mouse retinas.
conclusionsOTC is a transportable substrate for SLC5A8. OTC augments glutathione production in RPE cells, thereby protecting them from oxidative damage. Transport via SLC5A8 is obligatory for this process.
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