Hepatic and cardiac oxidative stress and other metabolic changes in broilers with the ascites syndrome

• Published in: Poultry science Vol. 75; no. 7; pp. 900 - 903
• Main Authors: Díaz-Cruz, A, Nava, C, Villanueva, R, Serret, M, Guinzberg, R, Piña, E
• Format: Journal Article
• Language: English
• Published: England 01.07.1996
• Subjects: Adenosine - pharmacology; Animals; Ascites - metabolism; Ascites - physiopathology; Ascites - veterinary; Chickens - metabolism; Chickens - physiology; Epinephrine - pharmacology; Free Radicals - metabolism; Glucagon - pharmacology; Glucose - metabolism; Heart - physiology; Lactates - metabolism; Lipid Peroxidation; Liver - chemistry; Liver - metabolism; Liver - physiology; Malondialdehyde - analysis; Malondialdehyde - metabolism; Myocardium - chemistry; Myocardium - metabolism; Oxidative Stress - physiology; Poultry Diseases - metabolism; Poultry Diseases - physiopathology; Quaternary Ammonium Compounds - analysis; Quaternary Ammonium Compounds - metabolism; Syndrome; Thiobarbituric Acid Reactive Substances - analysis; Thiobarbituric Acid Reactive Substances - metabolism
• ISSN: 0032-5791
• DOI: 10.3382/ps.0750900

The objective of this study was to evaluate the gluconeogenic response of in vitro stimulated hepatocytes from control broilers and broilers with clinical manifestations of the ascites syndrome. The basal rate of glucose synthesis from lactate was found to be threefold greater in sick birds than in the control group and stimulation obtained with epinephrine was found to be quantitatively similar in both groups. Under basal conditions, the hepatocytes from the sick broilers exhibited 60% more ammonium than the control birds. In addition, the quantification of thiobarbituric acid reactive substances, as indicators of cellular lipoperoxidation, showed an increase of over 100% in heart and liver of sick broilers fowl. In conclusion, the complex integrated response of gluconeogenesis to epinephrine is maintained in broilers with ascites, although their hepatocytes present changes compatible with those observed in cases of oxidative stress. It is not known whether this stress is a cause or a consequence of the ascites syndrome.