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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 #148031

Title: OXIDATIVE STRESS AND HEART FAILURE IN A MOUSE MODEL OF COPPER DEFICIENCY

Author
item ELSHERIF, LAILA
item ORTINES, RAYMOND
item Saari, Jack
item KANG, Y

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/2/2002
Publication Date: 3/14/2003
Citation: Elsherif, L., Ortines, R., Saari, J.T., Kang, Y.J. 2003. Oxidative stress and heart failure in a mouse model of copper deficiency [abstract]. The Federation of American Societies for Experimental Biology Journal 17:A229.

Interpretive Summary:

Technical Abstract: Cardiomyopathy induced by dietary copper deficiency (CuD) has been extensively studied. We have recently shown in a mouse model of CuD that heart failure occurs following hypertrophy as measured by hemodynamic and contractility parameters under physiological and stress conditions. The transition from hypertrophy to failure is thought to be due to an imbalance between oxidative stress and antioxidant capacity. We investigated whether a delay in this transition occurs in transgenic mice that overexpress metallothionein (MT) only in the heart given that MT protects from various cardiac injuries involving oxidative damage. Dams of FVB mice were fed CuD or copper-adequate diet starting from the third day post delivery and weanling wild-type (WT) and MT-transgenic (MT-TG) pups were fed the same diet for a total period of 4 wks. Significant changes in left ventricle diastolic parameters were observedin WT CuD mice including an increase in ventricular minimum diastolic pressure which occurs at the end of the isovolumetric relaxation phase of the cardiac cycle, and an increase in end-diastolic pressure which occurs at the end of diastole. Changes in these parameters were markedly inhibited in MT-TG mice. These changes are accompanied by suppression of oxidative stress in MT-TG mice. This study thus demonstrates that compromised antioxidant defense in CuD mice may be partially responsible for the development of heart failure. Supported in part by NIH grant HL63760.