Effect of alpha-tocopherol on antioxidants, lipid peroxidation, and the incidence of pulmonary hypertension syndrome (ascites) in broilers.
1995
Bottje W. | Enkvetchakul B. | Moore R.
Research has demonstrated a compromised antioxidant capacity in broilers with pulmonary hypertension syndrome (PHS). Thus, the objective of the present study was to assess the effects of vitamin E on PHS-induced mortality, tissue antioxidants, and plasma lipid peroxides in male broilers. Control broilers were provided normal ventilation but others, maintained under low ventilation conditions to induce PHS, were randomly assigned to nonimplanted (NI), placebo (PL), or vitamin E (VE) implanted groups. The VE implant released a total of 15 mg of alpha-tocopherol from 0 to 3 wk of age. Tissues and blood samples were obtained at 3 and 5 wk of age from birds with (PHS+) and without (PHS-) PHS. Five-week PHS cumulative mortality was lowered by alpha-tocopherol with mortality rates of 3.6, 4.2, 11.9, and 11.8%, for Controls, VE, NI, and PL groups, respectively. The PHS+ birds exhibited lower body weights, higher hematocrit, right ventricular hypertrophy, lower tocopherol and glutathione (GSH) concentrations in liver and lung, as well as indicators of oxidative stress, including elevated plasma lipid peroxides and lower oxidized GSH in liver and erythrocytes, at 5 wk of age. All birds exhibited lower erythrocyte catalase activity at 5 than at 3 wk of age. An improved antioxidant capacity was observed in VE birds, including higher liver and lung alpha-tocopherol at 3 and 5 wk, higher liver GSH at 3 wk, and lower plasma lipid peroxide values at 5 wk of age. Direct correlations observed between body weight and plasma lipid peroxides at 3 wk (r = 0.45) and between right ventricular hypertrophy and plasma lipid peroxides at 5 wk (r = 0.48), suggests that lipid peroxidation plays a role in the etiology of PHS. The results indicate that the VE implant was effective in lowering PHS-induced mortality in broilers apparently by attenuating processes leading to lipid peroxidation.
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