PMID- 29463513 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20240314 IS - 2046-6390 (Print) IS - 2046-6390 (Electronic) IS - 2046-6390 (Linking) VI - 7 IP - 2 DP - 2018 Feb 20 TI - Metabolism of the Pacific oyster, Crassostrea gigas, is influenced by salinity and modulates survival to the Ostreid herpesvirus OsHV-1. LID - 10.1242/bio.028134 [doi] LID - bio028134 AB - The Pacific oyster, Crassostrea gigas, is an osmoconforming bivalve exposed to wide salinity fluctuations. The physiological mechanisms used by oysters to cope with salinity stress are energy demanding and may impair other processes, such as defense against pathogens. This oyster species has been experiencing recurrent mortality events caused by the Ostreid herpesvirus 1 (OsHV-1). The objectives of this study were to investigate the effect of salinity (10, 15, 25 and 35 per thousand) on energetic reserves, key enzyme activities and membrane fatty acids, and to identify the metabolic risk factors related to OsHV-1-induced mortality of oysters. Acclimation to low salinity led to increased water content, protein level, and energetic reserves (carbohydrates and triglycerides) of oysters. The latter was consistent with lower activity of hexokinase, the first enzyme involved in glycolysis, up-regulation of AMP-activated protein kinase, a major regulator of cellular energy metabolism, and lower activity of catalase, an antioxidant enzyme involved in management of reactive oxygen species. Acclimation to salinity also involved a major remodeling of membrane fatty acids. Particularly, 20:4n-6 decreased linearly with decreasing salinity, likely reflecting its mobilization for prostaglandin synthesis in oysters. The survival of oysters exposed to OsHV-1 varied from 43% to 96% according to salinity ( Fuhrmann et al., 2016). Risk analyses showed that activity of superoxide dismutase and levels of proteins, carbohydrates, and triglycerides were associated with a reduced risk of death. Therefore, animals with a higher antioxidant activity and a better physiological condition seemed less susceptible to OsHV-1. CI - (c) 2018. Published by The Company of Biologists Ltd. FAU - Fuhrmann, Marine AU - Fuhrmann M AUID- ORCID: 0000-0002-4828-9275 AD - Ifremer/LEMAR UMR 6539 (UBO/CNRS/IRD/Ifremer), Technopole de Brest-Iroise, 29280 Plouzane, France marine.fuhrmann@gmail.com. FAU - Delisle, Lizenn AU - Delisle L AD - Ifremer/LEMAR UMR 6539 (UBO/CNRS/IRD/Ifremer), Technopole de Brest-Iroise, 29280 Plouzane, France. FAU - Petton, Bruno AU - Petton B AD - Ifremer/LEMAR UMR 6539 (UBO/CNRS/IRD/Ifremer), Presqu'ile du vivier, 29840 Argenton, France. FAU - Corporeau, Charlotte AU - Corporeau C AD - Ifremer/LEMAR UMR 6539 (UBO/CNRS/IRD/Ifremer), Technopole de Brest-Iroise, 29280 Plouzane, France. FAU - Pernet, Fabrice AU - Pernet F AD - Ifremer/LEMAR UMR 6539 (UBO/CNRS/IRD/Ifremer), Technopole de Brest-Iroise, 29280 Plouzane, France. LA - eng PT - Journal Article DEP - 20180220 PL - England TA - Biol Open JT - Biology open JID - 101578018 PMC - PMC5861354 OTO - NOTNLM OT - Bivalve OT - Disease OT - Environment OT - Metabolism OT - Mortality risk OT - Salinity COIS- Competing interestsThe authors declare no competing or financial interests. EDAT- 2018/02/22 06:00 MHDA- 2018/02/22 06:01 PMCR- 2018/02/15 CRDT- 2018/02/22 06:00 PHST- 2018/02/22 06:00 [entrez] PHST- 2018/02/22 06:00 [pubmed] PHST- 2018/02/22 06:01 [medline] PHST- 2018/02/15 00:00 [pmc-release] AID - bio.028134 [pii] AID - BIO028134 [pii] AID - 10.1242/bio.028134 [doi] PST - epublish SO - Biol Open. 2018 Feb 20;7(2):bio028134. doi: 10.1242/bio.028134.