Cyclooxygenase-2 is Upregulated in Copper-Deficient Rats |
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Authors: | Dale A Schuschke Ayotunde S O Adeagbo Phani K Patibandla Uchechi Egbuhuzo Rafael Fernandez-Botran and W Thomas Johnson |
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Institution: | (1) Department of Physiology and Biophysics, Health Sciences Center A1111, University of Louisville School of Medicine, Louisville, KY 40292, USA;(2) Department of Pathology and Laboratory Medicine, University of Louisville School of Medicine, Louisville, KY 40292, USA;(3) Grand Forks Human Nutrition Research Center, Grand Forks, ND 58202, USA |
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Abstract: | Copper deficiency inactivates Cu/Zn-SOD and promotes accumulation of reactive oxygen species. This process likely impairs
nitric oxide (NO)-mediated relaxation as well as triggers vascular inflammation. The current study was designed to determine
whether COX-2, a proinflammatory protein, expression and activity are upregulated in the oxidative environment associated
with inadequate Cu. Weanling male Sprague Dawley rats were fed purified diets which were either Cu-adequate (Cu-A); Cu-marginal
(Cu-M), Cu-deficient (Cu-D), or the Cu-D diet combined with the SOD mimetic Tempol (Cu-D/T; 1 mM in drinking water) for 4 weeks.
COX-2 protein, PGE2 (COX-2 metabolite) and isoprostanes (index of oxidative stress) were all higher in the Cu-D group vs Cu-A group, but no significant differences occurred between the Cu-M and Cu-A groups. Tempol protected against an attenuation
of NO-mediated vasodilation in the Cu-D rats but did not prevent the elevation of PGE2 or isoprostanes. Our data suggest a role for copper as a modulator of oxidative stress and inflammation independent of SOD
activity or NO-derived oxidants. |
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