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Efficacy of taurine and hypotaurine as hydroxyl radical scavengers.

Porter DW; Shi X; Leonard SS; Vallyathan V; Castranova V

Toxicologist 1998 Mar; 42(1-S):149

https://www.toxicology.org/pubs/docs/Tox/1998Tox.pdf

20025082

We previously reported that taurine (2-aminoethanesulfonic acid) levels increase in alveolar macrophages (AM) under oxidant stress, presumably by mobilizing taurine from bound intracellular stores (Tox. Appl. Pharm. 105:55-65. 1990). In another study. AM loaded with taurine prior to oxidant stress were found to be less susceptible to oxidant injury (J. Null". Biochem. 2: 308-313. 1991). In this study. we investigated the radical scavenger activity of taurine, and its metabolic precursor hypotaurine (2-arninoethanesulfinic acid). both of which may act as radical scavengers in the cell. Electron spin resonance (ESR) was used to investigate the reoction of taurine and hypotaurine with hydroxyl radicals (OH). The Fenton-reaction (Fe(II) + H2O2 Fe(III) + OH + -OH) and the Cr(V)-mediated Fenton-like reaction (Cr(V) + H2O2-Cr(VI) + OH + -OH) were used as sources of OH radicals. To further explore the OH radical scavenger activity of taurine and hypotaurine, their ability to prevent lipid peroxidalion was evaluated using linoleic acid as a model lipid and silica as an occupational source of OH radicals and other oxidants. The results show that taurine does not scavenge OH radicals nor prevent lipid peroxidation at concentrations up to 20 roM. In contrast, hypotaurine scavenged OH radicals with reaction rate constant of k = 1.6 X 10(10)M-1S-1 and protected against lipid peroxidation in a conccn- tration-dependcnt manner from 0.5-20 mM. The rate constant for hypotaurine is comparable with other efficient cellular OH radical scavengers, such as ascorbate and glutathione. These results suggest that hypotaurine, not taurine, was responsible for the decrease in lipid peroxidation in oxidant-stressed AM whereas taurine may have contributed to membrane integrity via its interaction with membrane lipids. Further experiments are needed to explore the possible role of hypotaurine as a cellular antioxidant and whether intracellular hypotaurine oxidation accounts for the increase in intracellular taurine levels previously observed in oxidant-stressed AM.

Free-radicals; Free-radical-generation; Cell-function; Cell-damage; Cell-biology; Cellular-reactions; Lipid-peroxidation; Lipids; Silicates

107-35-7

19980301

Abstract

1998

1096-6080

HELD

The Toxicologist. Society of Toxicology 37th Annual Meeting, March 1-5,1998, Seattle, Washington

WV; WA