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ARS Home » Southeast Area » Fayetteville, Arkansas » Poultry Production and Product Safety Research » Research » Publications at this Location » Publication #286453
Title: Effect of thiram on chicken growth plate cartilage

Author
item Rath, Narayan
item RASAPUTRA, KOMAL - University Of Arkansas
item LIYANAGE, ROHANA - University Of Arkansas
item SLAVIK, MIKE - University Of Arkansas
item LAY, JACKSON - University Of Arkansas

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 8/2/2012
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Thiram is a general use dithiocarbamate pesticide. It causes tibial dyschondroplasia, a growth plate cartilage defect in poultry characterized by growth plate broadening due to the accumulation of nonviable chondrocytes which lead to lameness. Since proteins play significant roles in all aspects cell physiology including survival, growth, and differentiation, the objective of this study was to find whether thiram induces proteomic changes that may be consequential to the failure of endochondral bone development. Growth plate chondrocytes from proximal tibia of 2wk-old broiler chicks were cultured without or with a sublethal concentration of thiram (1uM) for 48 h and the cell protein extracts subjected to 2-D gel electrophoresis and silver stained. Triplicate gels from each group were compared and statistically evaluated using Melanie software to find differentially expressed protein spots. Of total 72 stained spots 3 showed down- and 2 up- regulation in thiram group. In-gel trypsin digestion followed by mass spectrometric identified only two down-regulated proteins namely a heat shock protein 70 (HSP 70) and GalE protein. The up-regulated proteins included Serpin H1 precursor protein or HSP47, and a NMRA-like protein-1. HSP70 is cytoprotective against cellular stress and GalE involved in proteoglycan metabolism. NMRAL protein acts as a redox sensor protein and HSP47 binds collagen maintaining collagen quality and their degradation. While, the exact significance of the changes in those proteins are not clear, it appears that thiram induces cellular stress modulating heat shock protein and redox regulation portals affecting both functional and structural integrity of chondrocytes which cause apoptosis and affect endochondral bone formation.