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Life on the edge: O(2) binding in Atlantic cod red blood cells near their southern distribution limit is not sensitive to temperature or haemoglobin genotype
Atlantic cod are a commercially important species believed to be threatened by warming seas near their southern, equatorward upper thermal edge of distribution. Limitations to circulatory O(2) transport, in particular cardiac output, and the geographic distribution of functionally different haemoglo...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Company of Biologists Ltd
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5312735/ https://www.ncbi.nlm.nih.gov/pubmed/28148818 http://dx.doi.org/10.1242/jeb.141044 |
Sumario: | Atlantic cod are a commercially important species believed to be threatened by warming seas near their southern, equatorward upper thermal edge of distribution. Limitations to circulatory O(2) transport, in particular cardiac output, and the geographic distribution of functionally different haemoglobin (Hb) genotypes have separately been suggested to play a role in setting thermal tolerance in this species. The present study assessed the thermal sensitivity of O(2) binding in Atlantic cod red blood cells with different Hb genotypes near their upper thermal distribution limit and modelled its consequences for the arterio-venous O(2) saturation difference, Sa–v(O(2)), another major determinant of circulatory O(2) supply rate. The results showed statistically indistinguishable red blood cell O(2) binding between the three HbI genotypes in wild-caught Atlantic cod from the Irish Sea (53° N). Red blood cells had an unusually low O(2) affinity, with reduced or even reversed thermal sensitivity between pH 7.4 and 7.9, and 5.0 and 20.0°C. This was paired with strongly pH-dependent affinity and cooperativity of red blood cell O(2) binding (Bohr and Root effects). Modelling of Sa–v(O(2)) at physiological pH, temperature and O(2) partial pressures revealed a substantial capacity for increases in Sa–v(O(2)) to meet rising tissue O(2) demands at 5.0 and 12.5°C, but not at 20°C. Furthermore, there was no evidence for an increase of maximal Sa–v(O(2)) with temperature. It is suggested that Atlantic cod at such high temperatures may solely depend on increases in cardiac output and blood O(2) capacity, or thermal acclimatisation of metabolic rate, for matching circulatory O(2) supply to tissue demand. |
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