Effects of the toxic dinoflagellate Alexandrium catenella on histopathogical and escape responses of the Northern scallop Argopecten purpuratus

Hégaret, Hélène; Brokordt, Katherina; Gaymer, Carlos F.; Lohrmann, Karin B.; Garcı́a, Carlos; Varela, Daniel

doi:10.1016/j.hal.2012.04.006

Cited by 35 publications

(26 citation statements)

References 61 publications

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“…infestation and A. fundyense exposure was degeneration of adductor muscle fibers. Paralytic Shellfish Toxins (PSTs) and bucephalids individually are known to affect adductor muscles of bivalves (Calvo-Ugarteburu and McQuaid, 1998;Haberkorn et al, 2010b;Hégaret et al, 2012;Howell, 1967); however, in the present experiment, only the interaction of both led to a significant increase in myodegeneration. Again, suppression of hemocyte responses could have a role in this pathology.…”

Section: Effects Of the Interaction Between Parasitic Infestations Ancontrasting

confidence: 60%

Physiological and pathological changes in the eastern oyster Crassostrea virginica infested with the trematode Bucephalus sp. and exposed to the toxic dinoflagellate Alexandrium fundyense

Lassudrie

Wikfors

Sunila

et al. 2015

Journal of Invertebrate Pathology

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Section: Effects Of the Interaction Between Parasitic Infestations Ancontrasting

confidence: 60%

Physiological and pathological changes in the eastern oyster Crassostrea virginica infested with the trematode Bucephalus sp. and exposed to the toxic dinoflagellate Alexandrium fundyense

Lassudrie

Wikfors

Sunila

et al. 2015

Journal of Invertebrate Pathology

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“…Effects of other HAB species upon bivalves have been reported at different biological levels. Various effects upon general physiological processes (Cucci et al, 1985;Shumway, 1988a, 1988b;Landsberg, 2002;Leverone et al, 2007;Shumway, 1990), on behavior (Gainey and Shumway, 1988b;Haberkorn et al, 2011;Hégaret et al, 2012;Shumway and Cucci, 1987;Tran et al, 2010), at tissue and cellular levels (da Silva et al, 2008;Galimany et al, 2008aGalimany et al, , 2008bGalimany et al, , 2008cHaberkorn et al, 2010aHaberkorn et al, , 2010bHégaret et al, 2007aHégaret et al, , 2007bHégaret et al, , 2007c, and more recently at the a molecular level (Estrada et al, 2007;Fabioux et al, subm. ;Mello et al, 2013Mello et al, , 2012Romero-Geraldo and Hernández-Saavedra, 2012) have been observed.…”

Section: Introductionmentioning

confidence: 99%

Physiological responses of Manila clams Venerupis (=Ruditapes) philippinarum with varying parasite Perkinsus olseni burden to toxic algal Alexandrium ostenfeldii exposure

et al. 2014

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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.

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“…Immune system alteration has been reported by phagocytic capacity inhibition and hemocyte adhesion [14]–[16]. Effects of Alexandrium minutum exposure caused generalized tissue inflammation, principally of digestive organs, and biochemical alterations, such as amylase activity changes, reactive oxygen species production, and phenol oxidase activities [15]. However, few studies have addressed gene expression changes in C. gigas in response to toxic algal exposure or to their toxins.…”

Section: Introductionmentioning

confidence: 99%

Genomics Study of the Exposure Effect of Gymnodinium catenatum, a Paralyzing Toxin Producer, on Crassostrea gigas' Defense System and Detoxification Genes

García-Lagunas¹,

Romero-Geraldo²,

Hernández-Saavedra³

2013

PLoS ONE

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Background Crassostrea gigas accumulates paralytic shellfish toxins (PST) associated with red tide species as Gymnodinium catenatum. Previous studies demonstrated bivalves show variable feeding responses to toxic algae at physiological level; recently, only one study has reported biochemical changes in the transcript level of the genes involved in C. gigas stress response.Principal FindingsWe found that 24 h feeding on toxic dinoflagellate cells (acute exposure) induced a significant decrease in clearance rate and expression level changes of the genes involved in antioxidant defense (copper/zinc superoxide dismutase, Cu/Zn-SOD), cell detoxification (glutathione S-transferase, GST and cytochrome P450, CPY450), intermediate immune response activation (lipopolysaccharide and beta glucan binding protein, LGBP), and stress responses (glutamine synthetase, GS) in Pacific oysters compared to the effects with the non-toxic microalga Isochrysis galbana. A sub-chronic exposure feeding on toxic dinoflagellate cells for seven and fourteen days (30×103 cells mL−1) showed higher gene expression levels. A significant increase was observed in Cu/Zn-SOD, GST, and LGBP at day 7 and a major increase in GS and CPY450 at day 14. We also observed that oysters fed only with G. catenatum (3×103 cells mL−1) produced a significant increase on the transcription level than in a mixed diet (3×103 cells mL−1 of G. catenatum+0.75×106 cells mL−1 I. galbana) in all the analyzed genes.ConclusionsOur results provide gene expression data of PST producer dinoflagellate G. catenatum toxic effects on C. gigas, a commercially important bivalve. Over expressed genes indicate the activation of a potent protective mechanism, whose response depends on both cell concentration and exposure time against these toxic microalgae. Given the importance of dinoflagellate blooms in coastal environments, these results provide a more comprehensive overview of how oysters respond to stress generated by toxic dinoflagellate exposure.

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Effects of the toxic dinoflagellate Alexandrium catenella on histopathogical and escape responses of the Northern scallop Argopecten purpuratus

Cited by 35 publications

References 61 publications

Physiological and pathological changes in the eastern oyster Crassostrea virginica infested with the trematode Bucephalus sp. and exposed to the toxic dinoflagellate Alexandrium fundyense

Physiological and pathological changes in the eastern oyster Crassostrea virginica infested with the trematode Bucephalus sp. and exposed to the toxic dinoflagellate Alexandrium fundyense

Physiological responses of Manila clams Venerupis (=Ruditapes) philippinarum with varying parasite Perkinsus olseni burden to toxic algal Alexandrium ostenfeldii exposure

Genomics Study of the Exposure Effect of Gymnodinium catenatum, a Paralyzing Toxin Producer, on Crassostrea gigas' Defense System and Detoxification Genes

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