The Effect of Curcumin on Acetaminophen-Induced Toxicity on Performance and some Blood Parameters of Japanese Quail from 0-37 Days of Age
الموضوعات :
M. Emadi
1
(Department of Animal Science, Facultyof Agriculture,Payame Noor University, Tehran, Iran)
A. Hadavi
2
(Department of Animal Science, Faculty of Agriculture, Ferdowsi University of Mashhad, Mashhad, Iran)
J. Ameri
3
(Department of Animal Science, Faculty of Agriculture, Ferdowsi University of Mashhad, Mashhad, Iran)
H. Kermanshahi
4
(Department of Animal Science, Faculty of Agriculture, Ferdowsi University of Mashhad, Mashhad, Iran)
الکلمات المفتاحية: Performance, quail, Acetaminophen, Curcumin, liver,
ملخص المقالة :
This study was conducted to determine the effects of supplemented curcumin (CMN), derived from plant Curcuma longa, extract on performance and blood parameters of acetaminophen (ACT) induced quail hepatic injury. 240 quails from 0-37 days of age were used in a completely randomized design with 4 treatments of 4 replicates each and 15 chickens per replicate. All groups received 750 mg/kg body weight oral doses of ACT at 12 days of age. Japanese quails were divided into four groups: control (no CMN), commercial diet with 20 g CMN per ton, commercial diet with 40 g CMN per ton and commercial diet with 60 g CMN per ton. Feed intake and body weight gain were recorded weekly. Blood albumin, glucose, total protein, triglyceride, aspartate aminotransferase, alanine aminotransferase, bilirubin, uric acid and creatinine were determined at 28 and 35 days of age. Adding curcumin to the diets significantly increased serum aspartate aminotransferase at 28 days of age (P<0.05) and decreased triglyceride and bilirubin at 35 days of age (P<0.05). There were no significant differences in performance and other blood parameters among the treatment groups at 28 and 35 days of age. The data indicated that curcumin is a natural antioxidant hepatoprotective agent against hepatotoxicity induced by acetaminophen model. Thus, curcumin may have a therapeutic value in drug-induced hepatotoxicity as well as in acetaminophen therapy.
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