Antioxidants, lipid peroxides and pathophysiology of male broiler chickens with ascites

Histologic findings of broiler chickens with ascites syndrome or pulmonary hypertension reveal inflammation in lung and other organs. Reactive oxygen species (ROS) generated by inflammatory cells and during hypoxia, have a wide-range adverse effects and have been implicated in the inflammatory diseases. Research results indicated that adequate antioxidant can protect the body from ROS. Four studies were designed to evaluate the involvement of antioxidants, lipid peroxidation, and pathophysiology in the etiology of ascitic broilers. In the first study, glutathione (GSH), vitamin E (vit.E) and C (vit.C) were compromised in the lung and liver of male ascitic broilers, suggesting that antioxidants play a crucial part in ascites etiology. Next, vit.E treatment delayed ascites-induced mortality, lowered plasma lipid peroxides and improved antioxidant status. Since plasma lipid peroxides were highly correlated with indices of congestive heart failure, the results again strongly implicate lipid peroxidation in the ascitic etiology. Characterization of GSH metabolism in broilers was accomplished by manipulation of GSH with a depleting agent, diethyl maleate (DEM) and by providing l-cysteine (the rate-limiting amino acid) in the diet. The effect of DEM on the GSH levels in lung, liver, heart, kidney, and brain were time-and dose-dependent. Glutathione levels increased significantly with 1% dietary cysteine supplementation. Finally, Pathophysiological changes in the lung, liver, heart, and kidney of ascitic birds induced by either low ventilation or cold stress were determined. Gross findings were ascites, hydropericardium, and right ventricular hypertrophy. Histologic examination revealed inflammation in lungs, liver, and heart and degeneration of pulmonary epithelium around parabronchi, hepatocytes and myocardium. Hypertrophy of pulmonary arterioles and right ventricle found in ascitic birds are classical indications of pulmonary hypertension. In general, pathophysiologic changes were nonspecific and similar to report by other investigators, indicating a similarity of these models of ascites with that produced in the field. In conclusion, the results of these studies; (1) confirm the suitability of cold and low ventilation models for studying ascites syndrome, (2) provide strong evidence that lipid peroxidation is involved in the ascites syndrome and (3) indicate that antioxidant therapy may be used to ameliorate this costly metabolic disease.