Oxidative stress reduces transintestinal transports and (Na(+), K(+))-ATPase activity in rat jejunum.

Abstract
Because oxidative stress is a component of gastrointestinal injury, we investigated the effect of H2O2 on transintestinal transport using
isolated rat jejunum incubated in vitro. Millimolar concentrations of H2O2 inhibited all the tested parameters without inducing any cytotoxic
effect. Electrophysiological experiments indicated that H2O2 decreases significantly both short circuit current and transepithelial
electrical potential difference without affecting transepithelial resistance. The possibility that H2O2 could influence (Na+, K+)-ATPase
activity was explored using isolated basolateral membranes. Besides H2O2, free radicals (O2'¯
, HO') were generated using different
iron-dependent and independent systems; (Na+, K+)-ATPase activity was inhibited after membrane exposure to all ROS tested. The inhibition
was prevented by allopurinol, superoxide dismutase or desferrioxamine. Western blot analysis showed a decreased expression of
the a1-subunit of (Na+, K+)-ATPase. We conclude that H2O2 may be a modulator of jejunal ion and water transport by multiple mechanisms,
among which a significant inhibition of the basolateral (Na+, K+)-ATPase.