Abstract

Heat stress due to high environmental temperature negatively influences animal performances. To better understand the biological impact of heat stress, laying broiler breeder chickens were subjected either to acute (step-wisely increasing temperature from 21 to 35°C within 24 hours) or chronic (32°C for 8 weeks) high temperature exposure. High temperature challenges significantly elevated body temperature of experimental birds (P<0.05). However, oxidation status of lipid and protein and expression of heat shock transcription factors (HSFs) and heat shock proteins (HSPs) 70 and 90 were differently affected by acute and chronic treatment. Tissue-specific responses to thermal challenge were also found among heart, liver and muscle. In the heart, acute heat challenge affected lipid oxidation (P = 0.05) and gene expression of all 4 HSF gene expression was upregulated (P<0.05). During chronic heat treatment, the HSP 70 mRNA level was increased (P<0.05) and HSP 90 mRNA (P<0.05) was decreased. In the liver, oxidation of protein was alleviated during acute heat challenge (P<0.05), however, gene expression HSF2, 3 and 4 and HSP 70 were highly induced (P<0.05). HSP90 expression was increased by chronic thermal treatment (P<0.05). In the muscle, both types of heat stress increased protein oxidation, but HSFs and HSPs gene expression remained unaltered. Only tendencies to increase were observed in HSP 70 (P = 0.052) and 90 (P = 0.054) gene expression after acute heat stress. The differential expressions of HSF and HSP genes in different tissues of laying broiler breeder chickens suggested that anti-heat stress mechanisms might be provoked more profoundly in the heart, by which the muscle was least protected during heat stress. In addition to HSP, HSFs gene expression could be used as a marker during acute heat stress.

Highlights

  • High environmental temperature has a harmful impact on an animal’s physiology and performance

  • heat shock proteins (HSPs) are considered as the cellular thermometer and understanding changes in HSP expression can be useful in evaluating the heat stress response [8]

  • During chronic heat stress, the rectal temperature of birds in chronic heat stress treatment (CS) was not elevated by the cyclic environmental temperature in the first week and only a tendency of increment in rectal temperature was observed in the second week

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Summary

Introduction

High environmental temperature has a harmful impact on an animal’s physiology and performance. Different mechanisms are utilized to resist the harmful effects of high temperature depending on duration of exposure. Short-term sub-lethal heat stress (acute heat stress) provokes heat shock response [1,2,3], resulting in rapid initiation of heat shock protein (HSP) synthesis and dramatic changes in gene expression [3,4,5,6]. Long-term heat exposure (chronic heat stress) induces larger scale adaptations such as enhancement of endurance by altering thermoregulatory activity (i.e., cardiovascular function). Heat acclimation is mediated by global molecular responses, including HSP expression [2,7]. HSPs are considered as the cellular thermometer and understanding changes in HSP expression can be useful in evaluating the heat stress response [8]

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