Dietary supplementation with t-butylhydroquinone reduces cardiac hypertrophy and anemia associated with copper deficiency in rats

Abstract

The effect of dietary supplementation with the antioxidant, t-butylhydroquinone (TBHQ), on some of the cardiovascular consequences of copper deficiency was investigated. Rats were fed copper-deficient (CuD) diet containing 0.3 μg Cu/g of diet that were either nonsupplemented or supplemented with TBHQ (supplied in the dietary safflower oil at a concentration of 0.02%). Control rats were fed copper adequate (CuA) diet containing >5.0 μg Cu/g (CuA) that also were either nonsupplemented or supplemented with TBHQ. After five weeks, rats consuming CuD diet supplemented with TBHQ exihibited plasma copper concentrations, ceruloplasmin activities, and liver and heart copper concentrations that were significantly (P<0.05) lower than those of rats consuming either nonsupplemented or TBHQ supplemented CuA diet, but no different from those of rats consiming nonsupplemented CuD diet. However, rats consuming CuD diet supplemented with TBHQ had significantly (P<0.05) higher growth, hemoglobin concentrations, hematocrits, and red blood cell qistribution widths but lower heart weights than rats consuming nonsupplemented CuD diet. TBHQ supplementation had no effect on these variables in rats fed CuA diet. Thus, while TBHQ did not improve copper status, it did ameliorate the growth reduction, anemia, and cardiac hypertrophy associated with copper deficiency. These findings indirectly support the contention that oxidative damage contributes to the pathophysiological consequences of copper deficiency.