Physiological responses of Manila clams Venerupis (=Ruditapes) philippinarum with varying parasite Perkinsus olseni burden to toxic algal Alexandrium ostenfeldii exposure
|Author(s)||Lassudrie Malwenn1, Soudant Philippe1, Richard Gaelle1, Henry Nicolas1, Medhioub Walid1, 2, 3, Da Silva Patricia Mirella4, Donval Anne1, Bunel Melanie1, Le Goic Nelly1, Lambert Christophe1, de Montaudouin Xavier5, Fabioux Caroline1, Hegaret Helene1|
|Affiliation(s)||1 : UBO CNRS, Inst Univ Europeen Mer, Lab Sci Environm Marin LEMAR, F-29280 Plouzane, France.
2 : IFREMER, Lab Phycotoxines, F-44311 Nantes 3, France.
3 : Inst Natl Sci & Technol Mer, Lab Milieu Marin, Salammbo 2025, Tunisia.
4 : Univ Fed Paraiba, Exact & Nat Sci Ctr, Dept Mol Biol, Lab Immunol & Pathol Invertebrates, BR-58051900 Joao Pessoa, PB, Brazil.
5 : Univ Bordeaux UMR 5805 EPOC, Stn Marine Arcachon, F-33120 Arcachon, France.
|Source||Aquatic Toxicology (0166-445X) (Elsevier Science Bv), 2014-09 , Vol. 154 , P. 27-38|
|WOS© Times Cited||30|
|Keyword(s)||Bivalve, Harmful algal bloom, Oxidative stress, Venerupis philippinarum, Alexandrium ostenfeldii, Perkinsus olseni|
|Abstract||Manila clam stock from Arcachon Bay, France, is declining, as is commercial harvest. To understand the role of environmental biotic interactions in this decrease, effects of a toxic dinoflagellate, Alexandrium ostenfeldii, which blooms regularly in Arcachon bay, and the interaction with perkinsosis on clam physiology were investigated. Manila clams from Arcachon Bay, with variable natural levels of perkinsosis, were exposed for seven days to a mix of the nutritious microalga T-Iso and the toxic dinoflagellate A. ostenfeldii, a producer of spirolides, followed by seven days of depuration fed only T-Iso. Following sacrifice and quantification of protozoan parasite Perkinsus olseni burden, clams were divided into two groups according to intensity of the infection (“Light-Moderate” and “Moderate-Heavy”). Hemocyte and plasma responses, digestive enzyme activities, antioxidant enzyme activities in gills, and histopathological responses were analyzed. Reactive oxygen species (ROS) production in hemocytes and catalase (CAT) activity in gills increased with P. olseni intensity of infection in control clams fed T-Iso, but did not vary among A. ostenfeldii-exposed clams. Exposure to A. ostenfeldii caused tissue alterations associated with an inflammatory response and modifications in hemocyte morphology. In the gills, superoxide dismutase (SOD) activity decreased, and an increase in brown cell occurrence was seen, suggesting oxidative stress. Observations of hemocytes and brown cells in tissues during exposure and depuration suggest involvement of both cell types in detoxication processes. Results suggest that exposure to A. ostenfeldii disrupted the pro-/anti-oxidant response of clams to heavy P. olseni intensity. In addition, depressed mitochondrial membrane potential (MMP) in hemocytes of clams exposed to A. ostenfeldii suggests that mitochondrial functions are regulated to maintain homeostasis of digestive enzyme activity and condition index.|