Reduced heart lipid peroxidation precedes cardiac dilatation in turkeys with naturally occurring cardiomyopathy

Study objective – The aim of the study was to determine if reduced heart lipid peroxidation in 1–2 month old turkeys with furazolidone induced dilated cardiomyopathy is drug related and model dependent, a non-specific characteristic of the dilated turkey heart, or if alterations of heart lipid peroxidation can occur prior to onset of cardiac dilatation, and therefore may be involved in its pathogenesis. Design – Ventricular lipid peroxidation capacity and superoxide dismutase activity were measured in controls and in turkeys with spontaneous cardiomyopathy at various ages (newly hatched, 7–10 d, and 1–2 months) and stages of the disease. Subjects – 46 turkeys with naturally occurring dilated cardiomyopathy and 29 age matched controls were used at hatch, 7–10 d, and 1–2 months of age. Measurements and main results – Heart lipid peroxidation, measured by thiobarbituric acid reactive substances (malondialdehyde), was found to be reduced not only in the dilated hearts of 1–2 months old cardiomyopathic turkeys [114(SEM 10) v 176(21) nmol·100 mg−1 protein, p = 0.023] but also in the non-dilated hearts of 9–10 day old cardiomyopathic turkeys [135(17) v 274(35) nmol·100 mg−1 protein, p=0.004]. Ventricular superoxide dismutase activity was similar in control and cardiomyopathic turkeys at all stages and there was the expected increase with age. In control turkeys ventricular superoxide dismutase activity in 1–2 month old birds, at 718(52) nitrite units·100 mg–1 protein, was significantly higher than values in 7–10 day old turkeys [398(31) nitrite units·100 mg–1 protein, p = 0.001]. Conclusions – Decreased lipid peroxidation capacity is present in the dilated hearts of spontaneously cardiomyopathic turkeys. However, it is also decreased in cardiomyopathic turkeys at 9–10 d (the time of highest mortality) prior to the onset of cardiac dilatation. Therefore, alterations in heart lipid composition may be involved in the pathogenesis of this cardiomyopathy and not simply a result of the cardiac dilatation/hypertrophy process.