期刊
JOURNAL OF THERMAL BIOLOGY
卷 100, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jtherbio.2021.103040
关键词
Heat shock; alpha-crystallins; HSP27; Oxidative stress; Glutathione; Lipid peroxidation
资金
- NKFIH grant of the Hungarian National Research, Development and Innovation Office [124586]
- NKB-PhD grant of the University of Veterinary Medicine Budapest
- New National Excellence Program of the Ministry for Innovation and Technology from the National Research, Development and Innovation Fund [UNKP-20-3-II-ATE-11]
The liver was found to be the most susceptible to heat-provoked oxidative stress, with rapid activation of protective pathways and the involvement of sHSP-s leading to an over-compensation mechanism.
As heat stress is a major emerging issue in poultry farming, investigations on the molecular mechanisms of the heat-triggered cellular response in chickens are of special importance. In the present study, 32-day-old Ross 308 broiler chickens were subjected to 37 degrees C environmental temperature combined with 50% relative humidity for 4 or 8 h respectively. Following sampling, redox parameters such as malondialdehyde (MDA), reduced glutathione (GSH), protein carbonyl levels as well as glutathione pemxidase activity were assessed in liver, spleen, and kidney homogenates. The concentrations of small heat shock proteins (sHSP-s) HSP27, alpha A- and alpha B-crystallins were also investigated. Among these organs, the liver was found the most susceptible to heat-provoked oxidative stress, indicated by enhanced lipid peroxidation and rapid activation of protective pathways, including the definite increase of glutathione peroxidase activity and the excessive utilization of (alpha A- and alpha B-crystallin proteins. Heat-associated decline of protein carbonylation and GSH content was observed in the liver in correlation with the increased involvement of (alpha A- and alpha B-crystallins in cellular defense, resulting supposedly in an over-compensation mechanism. These data highlight the hepatic sensitivity to acute heat shock, potential adaptation mechanisms, and the specific role of sHSP-s in the restoration of physiologic cell function.
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