| pubmed-article:8042409 | pubmed:abstractText | As a noncompetitive inhibitor of pig gastric H+/K(+)-ATPase, indomethacin inhibited the H+ transportation function of the enzyme, leading to not only the obvious dissipation of H+/K(+)-ATPase-generated H+ gradients, but also the decreasing of the H+ gradient formation ability of the enzyme. 4% of indomethacin was able to penetrate into the lipid bilayer of H+/K(+)-ATPase vesicles at 0.15 mg/ml protein concentration, which showed an influence of indomethacin to the membrane. Indomethacin reduced the membrane fluidity of H+/K(+)-ATPase vesicles significantly. It also damaged the conformation of membrane protein extraordinarily, which was evidenced by decreasing the intrinsic fluorescence of H+/K(+)-ATPase. From the results, we suggest that the effect of indomethacin on H+/K(+)-ATPase is taken place by its inhibition on H+/K(+)-ATPase protein, as well as by its influence on the membrane lipid bilayer of H+/K(+)-ATPase vesicles. | lld:pubmed |
