UC Davis

The average surface temperature is predicted to rise 0.5ºC to 6ºC by the year 2100 and will affect domesticated animals. When Japanese quail (Coturnix coturnix japonica) are subjected to heat stress (temperatures ≥ 30˚C), a variety of changes may occur including, but not limited to, their ability to regulate blood gases, blood electrolytes, tissue oxidation, and lipids, a class of nutrients that are integral to their health. Most importantly are fatty acids which are a major component of lipids and have been shown to be significantly affected by heat stress in poultry. The extent that heat stress can alter these important aspects of health depends on the length of exposure, severity of heat, and demands of the animal. In addition, poultry chosen for high performance, such as low FCR, may have negative metabolic consequences in early heat stress. By investigating the transition from a thermoneutral zone to heat stress, procedures can be implemented to mitigate heat stress at an earlier stage. To test the hypothesis that multigenerational high performance (FCR) can mitigate the responses to heat stress, FCR of 4 treatment groups were repeated for 10 generations: (1) thermoneutral (TN, 22.2˚C), (2) thermoneutral siblings (TNS, 22.2˚C), (3) heat stress (HS, 31.1˚C), and (4) heat stress siblings (HSS, 31.1˚C). TN and HS were random bred in their respective temperatures. TNS and HSS were siblings reared at the two temperatures. HSS quail were used to determine low FCR at 31.1˚C and their corresponding TNS were mated to create the next generation’s TNS and HSS. Body weights (BW), blood gases, blood electrolytes, and sera steroid hormones were measured during the first 4 hours (acute) and after 3 weeks (chronic) of temperature exposure in generation 10. Fatty acid compositions, lipid oxidation, and antioxidant activity of feed, yolk, and adult and embryo brain, liver and kidneys, thigh for adults were investigated. Overall protein abundance in livers of actively laying female Japanese quail was quantified. It was hypothesized that TNS would have the lowest amount of lipid oxidation, HSS would have the highest SOD and CAT activity, HS and HSS would have less PUFA in all organs due to degradation, HSS would upregulate proteins involved in β-oxidation and the TCA cycle to meet increased energy demands, and HSS would have the lowest levels of glucocorticoids. Significant differences were determined at P≤0.05. Results of Experiment 1 (Chapter 2) revealed that acute and chronic heat stress at 31.1˚C does not have a clear effect on blood electrolytes, acid-base regulation, and oxygen transport. For Experiment 2 (Chapter 3), of all adult organs analyzed, livers experienced the most variations in concentrations of fatty acids when compared by treatment and sex. Males had significantly more stearic acid in the brain, kidney, and thigh and significantly more PA in all tissues than females. TN brains had significantly less PUFA than that in both TNS and HSS. TN or TNS had significantly more long chain PUFA such as DPA n-6, DPA n-3, DHA, and ARA and significantly less SFA such as PA or stearic acid than that in HS or HSS across all tissues. As revealed in Experiment 3 (Chapter 4), HSS yolk had higher levels of LA and ARA than TN and embryo brain DHA, total PUFA, and stearic acid increased over the duration of incubation as expected for proper brain development. TNS embryo brain had more LA, ALA, DPA n-3, and total n-3 than TN and significantly more stearic acid and SFA than HSS. HS embryo kidneys and gonads had more total SFA than TNS and HSS. HS embryo livers had more stearic acid, SFA:PUFA, and total SFA than TN and TNS. TN and TNS embryo livers had more PUFA than HSS embryo livers. Results of Experiment 4 (Chapter 5) indicated that heat stress did not influence lipid oxidation in any of the tissues; however, brain had the most oxidation, followed by liver> kidney>thigh. There was no significant treatment effect on SOD and CAT activities, but kidneys had significantly more CAT activity than brain, liver, and thigh. Brain and thigh had similar CAT activity. Revealed in Experiment 5 (Chapter 6), HSS had 118 significantly down-regulated proteins and 56 significantly upregulated proteins and HS had 75 significantly down-regulated proteins and 2 significantly upregulated proteins when compared to TN. Differences in protein abundance among all other comparisons were minimal (≤5) or insignificant. TN and/or TNS had significantly less antioxidants (SOD Cu/Zn and CAT) and lipoprotein transport from liver to egg than those in a heat stress temperature. TN had significantly more proteins involved in adipogenesis, lipogenesis, and fatty acid oxidation than HSS. The lower abundance of β-oxidation enzymes for HS and HSS could indicate that heat stressed quail decreased energy production to prevent further oxidative damage. For Experiment 6 (Chapter 7), chronic males, particularly from TN, had significantly higher levels of glucocorticoids, progestogens, androgens than many of the other treatments and of the 29 sera steroid hormones analyzed, 13 were significantly higher in chronic than acute. Thus, selection for low FCR in heat stress at 31.1˚C did not incur an overall fitness advantage when considering these parameters. However, selection for low FCR in heat stress could possibly reduce oxidation of PUFA or increase retention of PUFA in the brain. Heat stressed quail, regardless of selective breeding, had significantly less health-promoting fatty acids such as DHA and DPA. More research should be conducted across many parameters at temperatures below 31.1˚C to pinpoint how soon quail health is affected and possible procedures that mitigate these effects.