Effects of feeding urea and copper sulphate in different combinations on live body weight, carcass weight, percent weight to body weight of different organs and histopathological tissue changes in broilers.
Summary of "Effects of feeding urea and copper sulphate in different combinations on live body weight, carcass weight, percent weight to body weight of different organs and histopathological tissue changes in broilers."
The study was carried out on a total of 100 broiler chicks divided into six equal groups at day 7 of age. Birds were fed copper sulphate and urea in different combinations for up to 37 days and then the birds of all the groups were fed plan feed for one week. The general signs were an increased water intake, ruffled feathering, watery droppings along with salivation in treatment groups. These signs were mild in groups fed low level of urea, while were severe in fed higher levels of these compounds together. Mild to moderate gross changes were observed in the birds of group B, C and D, while more pronounced changes were seen in birds of group E and F. In the latter groups, the liver was pale to yellowish and fragile. Kidneys were enlarged, swollen, congested and sometimes hemorrhagic. Histologically, mild cytoplasmic vacuolation and condensation/pyknosis or disappearance of the nucleus in the cells of the liver and kidney were the salient changes observed in the treatment groups, those were severe in birds fed higher levels of the two compounds. Changes in lungs were congestion and edema. Changes in the bursa of Fabricius were mild cytoplasmic vacuolation, cell depletion and chromatolysis. The live and carcass weights were lower in broilers fed higher levels of both copper and urea than the control group. The weights of kidney and heart were higher in birds fed higher levels of both of the compounds than the control group. It can be concluded from the present study that urea above 2% and copper sulphate above 1gm in combination cause tissue damage, especially the liver and kidneys.
Department of Pathology, Faculty of Veterinary Science, University of Agriculture, Faisalabad, Pakistan.
This article was published in the following journal.
Name: Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20829007
- DOI: http://dx.doi.org/10.1016/j.etp.2010.07.009
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Medical and Biotech [MESH] Definitions
An inherited disorder of copper metabolism transmitted as an X-linked trait and characterized by the infantile onset of HYPOTHERMIA, feeding difficulties, hypotonia, SEIZURES, bony deformities, pili torti (twisted hair), and severely impaired intellectual development. Defective copper transport across plasma and endoplasmic reticulum membranes results in copper being unavailable for the synthesis of several copper containing enzymes, including PROTEIN-LYSINE 6-OXIDASE; CERULOPLASMIN; and SUPEROXIDE DISMUTASE. Pathologic changes include defects in arterial elastin, neuronal loss, and gliosis. (From Menkes, Textbook of Child Neurology, 5th ed, p125)
Unstable isotopes of copper that decay or disintegrate emitting radiation. Cu atoms with atomic weights 58-62, 64, and 66-68 are radioactive copper isotopes.
The urea concentration of the blood stated in terms of nitrogen content. Serum (plasma) urea nitrogen is approximately 12% higher than blood urea nitrogen concentration because of the greater protein content of red blood cells. Increases in blood or serum urea nitrogen are referred to as azotemia and may have prerenal, renal, or postrenal causes. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
Nutritional support given via the alimentary canal or any route connected to the gastrointestinal system (i.e., the enteral route). This includes oral feeding, sip feeding, and tube feeding using nasogastric, gastrostomy, and jejunostomy tubes.
An amino acid produced in the urea cycle by the splitting off of urea from arginine.