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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #234239

Title: Tempol Normalizes Aortic Relaxation But Not Elevated Isoprostanes or PGE2 in Copper-Deficient Rats

Author
item SCHUSCHKE, DALE
item Johnson, William
item ADEAGBO, AYOTUNDE

Submitted to: Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 1/7/2009
Publication Date: 4/27/2009
Citation: Schuschke, D.A., Johnson, W.T., Adeagbo, A.S. 2009. Tempol Normalizes Aortic Relaxation But Not Elevated Isoprostanes or PGE2 in Copper-Deficient Rats. Journal of Federation of American Societies for Experimental Biology. 23:727.3.

Interpretive Summary:

Technical Abstract: Copper deficiency promotes accumulation of reactive oxygen species, which likely impair nitric oxide mediated relaxation as well as trigger vascular inflammation. We hypothesize that an antioxidant supplementation would diminish oxidative stress, restore aortic relaxation, and limit pro-inflammatory prostaglandin E2 (PGE2) synthesis during Cu deficiency. Weanling male Sprague Dawley rats were fed purified diets which were either copper-adequate (Cu-A; 6.3 'g Cu/g diet); copper-deficient (Cu-D; 0.3 'g Cu/g diet), or the Cu-D diet and the SOD mimetic Tempol (Cu-D/T; 1mM in drinking water) for 4 weeks. Relaxation of aortic rings was measured with force displacement transducers coupled to a Grass polygraph. Acetylcholine-induced relaxation was significantly less in the Cu-D (pD2 = 6.77 ± 0.10) vs Cu-A (pD2 = 8.18 ± 0.30); the decrease was normalized in Cu-D/Tempol (pD2 = 7.75 ± 0.16) rats. Serum isoprostanes (index of oxidative stress) and PGE2 were higher in both the Cu-D and Cu-D/T groups vs Cu-A controls. Thus, Cu-deficency significantly impaired NO-mediated relaxation and tempol supplementation restored aortic responsiveness. Our data also suggest a role for copper as a modulator of oxidative stress and inflammation independent of SOD activity or NO-derived oxidants. Support: NIH DK055030.