期刊
JOURNAL OF GENERAL PHYSIOLOGY
卷 117, 期 2, 页码 181-190出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1085/jgp.117.2.181
关键词
potassium-chloride cotransport; red blood cell; Fenton reaction; Oncorhynchus mykiss; oxygen-sensitive ion transport
类别
In the present study we have investigated if reactive oxygen species are involved in the oxygen-dependent regulation of potassium-chloride cotransport activity in trout erythrocyte membrane. An increase in the oxygen level caused an increase in chloride-sensitive potassium transport (K+-Cl- cotransport). 5 mM hydrogen peroxide caused an increase in K+-Cl- cotransport at 5% oxygen. The increase in flux could be inhibited by adding extracellular catalase in the incubation. Pretreatment of the cells with mercaptopropionyl glycine (MPG), a scavenger of reactive oxygen species showing preference for hydroxyl radicals, abolished the activation of the K+-Cl- cotransporter by increased oxygen levels. The inhibition by MPG was due to the of transporter by the sulfhydryl reagent, N-ethylmaleimide, indicating that the effect of mPG was due to the scavenging of reactive oxygen species and not to the reaction of MPG with the cotransporter. Copper ions, which catalyze the production of hydroxyl radicals in the Fenton reaction, activated K+-Cl- cotransport significantly at hypoxic conditions (1% O-2). These data suggest that hydroxyl radicals, formed from O-2 in close vicinity to the cell membrane, play an important role in the oxygen-dependent activation of the K+-Cl- cotransporter.
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