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ARS Home » Southeast Area » Fayetteville, Arkansas » Poultry Production and Product Safety Research » Research » Publications at this Location » Publication #189004


item Rath, Narayan
item Huff, William
item Huff, Geraldine

Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 9/15/2005
Publication Date: 1/1/2007
Citation: Rath, N.C., Huff, W.E., Huff, G.R. 2007. Regulation of avian growth plate development and its interruption by thiram, a dithiocarbamate pesticide. In: 'Hormone Biotechnology' (Ed. S.K. Maitra), Daya Publishing House, Delhi, India. p. 399-411.

Interpretive Summary: Long bone growth is a complex process which takes place in the growth plates located at the end of these bones. It consists of growth and maturation of cartilage cells which form a template over which bone is laid. Environmental chemicals such as pesticide can disrupt this process leading to bone abnormalities. This review explores some of the aspects of growth plate development in chickens and its failure induced by a common agricultural pesticide thiram that causes poultry leg problems.

Technical Abstract: Long bone growth is achieved by a process called "endochondral ossification" taking place in the growth plates located at the end of these bones. The growth plate development is a complex process which encompasses chondrocyte proliferation, maturation related differentiation, and the eventual replacement of the cartilage scaffold by bone. This process is regulated by a number of hormones, cytokines, and growth factors the interference of which can lead to growth plate abnormality and consequent bone problems. We have been studying the mechanisms underlying a growth plate abnormality in poultry called “tibial dyschondroplasia (TD)” where parts of the cartilage scaffold fail to form bone and are retained as avascular plugs of tissues that cause lameness. Using thiram, a thiocarbamate fungicide and an endocrine disruptor, to induce TD in broiler chickens, we studied its effects on the metabolism, proliferation, differentiation associated gene expression, and cell death in the growth plate to understand the mechanisms associated with this defect. The results show that thiram did not produce chondrocyte hyperplasia or changes in maturation associated gene expression that could explain an unusual increase in the growth plate size. On the other hand, it reduced cartilage glutathione levels, caused endothelial cell death and prevented angiogenesis and induced subsequent death of chondrocytes in the maturing zone cartilage. Thiram treatment also increased the blood corticosterone levels. It is concluded that thiram selectively prevents angiogenesis and induces premature chondrocyte death preventing subsequent bone formation that results in growth plate dysplasia.