The Investigation of the Relationship Between HSP-27 Release and Oxidative DNA Damage in Broiler Chickens with Tibial Dyschondroplasia by Using Histopathological and Immunohistochemical Methods


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Kapakin K. A. T. , KAPAKİN S., İMİK H., GÜMÜŞ R. , Eser G.

BRAZILIAN JOURNAL OF POULTRY SCIENCE, cilt.21, 2019 (SCI İndekslerine Giren Dergi) identifier

  • Cilt numarası: 21 Konu: 3
  • Basım Tarihi: 2019
  • Doi Numarası: 10.1590/1806-9061-2019-1091
  • Dergi Adı: BRAZILIAN JOURNAL OF POULTRY SCIENCE

Özet

Tibial dyschondroplasia (TD) is a skeletal disorder that occurs in the proximal metaphyses of tibiotarsus and sometimes tarsometatarsus, resulting in the development of avascularized and non-mineralized abnormal cartilage and causing significant economic loss. In this study, we aimed to show the histopathological changes and the relationship between the release of Heat-Shock Protein 27 (HSP-27) and oxidative DNA damage in broiler chickens with tibial dyschondroplasia, using histopathologic and immunohistochemical methods. Our study material consisted of totally 20 animals out of 42 days old 205 Ross 308 broiler chickens, 10 with TD lesions and 10 healthy control subjects. Tissue samples taken from animals performed necropsy was exposed to routine tissue follow-up. Macroscopically, unilateral and bilateral thickening and swelling were observed in the growth plates of tibiotarsal joints of the broiler chickens diagnosed with tibial dyscondroplasia. Histopathologic examination of the tibiotarsal joints of broiler chickens affected by TD revealed an increase in the number of immature chondrocytes, as well as deficiencies in vascularization and calcification. In the immunohistochemical study; HSP-27 and 8-OHDG release was positive in the chondrocytes located on the Proliferative Zone, Maturation Zone and Hypertrophic Zone. However, the positivity was the most profound in the PZ and MZ, while less in the HZ chondrocytes. As a result; we demonstrated by immunohistochemical methods that the increase in the HSP-27 release is parallel to the increase in 8-OHDG release in TD lesioned areas and this may be related to oxidative stress.