Korean J Physiol Pharmacol.
1999 Oct;3(5):529-538.
Effect of ethanol on Na+-Pi uptake in opossum kidney cells: Role of membrane fluidization and reactive oxygen species
- Affiliations
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- 1)Department of Physiology, College of Medicine, Pusan National University, Pusan, 602-739 South Korea.
Abstract
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This study was undertaken to examine the effect of ethanol on
Na+-dependent phosphate (Na+-Pi) uptake in opossum kidney (OK) cells,
an established renal proximal tubular cell line. Ethanol inhibited
Na+-dependent component of phosphate uptake in a dose-dependent manner
with I50 of 8.4%, but it did not affect Na+-independent component.
Similarly, ethanol inhibited Na+-dependent uptakes of glucose and amino
acids (AIB, glycine, alanine, and leucine). Microsomal Na+-K+-ATPase
activity was not significantly altered when cells were treated with 8%
ethanol. Kinetic analysis showed that ethanol increased Km without a
change in Vmax of Na+-Pi uptake. Inhibitory effect of n-alcohols on
Na+-Pi uptake was dependent on the length of the hydrocarbon chain, and
it resulted from the binding of one molecule of alcohol, as indicated
by the Hill coefficient (n) of 0.8-1.04. Catalase significantly
prevented the inhibition, but superoxide dismutase and hydroxyl radical
scavengers did not alter the ethanol effect. A potent antioxidant DPPD
and iron chelators did not prevent the inhibition. Pyrazole, an
inhibitor of alcohol dehydrogenase, did not attenuate ethanol-induced
inhibition of Na+-Pi uptake, but it prevented ethanol-induced cell
death. These results suggest that ethanol may inhibit Na+-Pi uptake
through a direct action on the carrier protein, although the transport
system is affected by alterations in the lipid environment of the
membrane.