Semester

Fall

Date of Graduation

2007

Document Type

Thesis

Degree Type

MS

College

Davis College of Agriculture, Natural Resources and Design

Department

Animal and Nutritional Sciences

Committee Chair

Hillar Klandorf

Abstract

Previous studies have shown that chronic treatment of broilers with hemin decreases plasma concentrations of uric acid and increases leukocyte oxidative activity (LOA) whereas the inclusion of inosine produces an inverse effect. The objective of these studies was to determine whether or not inosine could serve as a potential therapy for oxidative stress. Oxidative stress was induced in broilers by the administration of hemin. Dietary inclusion of inosine was then begun either before the onset of oxidative stress induced by hemin, or as a post treatment once oxidative stress was established. Four-week-old broilers were individually banded and divided into four treatment groups (Control, Hemin, Inosine, Hemin/Inosine). Throughout the study control birds (n=10) were injected daily intraperitoneal with a buffer solution, while hemin birds (n=10) were injected daily intraperitoneal with a 20mg/kg body weight hemin buffer solution. Leukocyte oxidative activity (LOA) and plasma uric acid (PUA) were measured on day eight. Results showed that hemin birds had higher levels of LOA (P=0.03) and lower PUA (P=0.11). On day 10, control and hemin birds were subdivided into inosine birds (n=5) and hemin/inosine birds (n=5). These birds were given 0.6M/kg of feed/day of dry inosine. Plasma concentrations of uric acid and LOA were then measured on day 15. Results showed that inosine raised concentrations of PUA (P=0.0001) and lowered LOA (P=0.004) induced by hemin. In a separate study, stereological analyses of inosine vs. control birds revealed no anatomical differences in kidney morphology between treatments (P=0.05). The results of these studies support the view that uric acid reduces oxidative stress by functioning as an antioxidant. Uric acid treatment has the potential to decrease the amount of damage generated by free radicals during times of oxidative stress associated with disease states.

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