Toxicity of fatty acid 18:5n3 fromGymnodinium cf.mikimotoi: I. morphological and biochemical aspects onDicentrarchus labrax gills and intestine

Sola, F. Gil de; Masoni, A.; Fossat, B.; Porthé-Nibelle, Jacqueline; Gentien, Patrick; Bodennec, Guy

doi:10.1002/(sici)1099-1263(199907/08)19:4<279::aid-jat579>3.0.co;2-x

Cited by 40 publications

(25 citation statements)

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“…Experiments using synthetic OPA have confirmed toxicity to sea bass ) and trout hepatocytes (Fossat et al 1999) (Table 3). The toxicity of synthetic OPA to the dinoflagellate Karenia mikimotoi itself was also demonstrated, but to a lesser extent than against other algae, and has been proposed as a factor in causing dominance of K. mikimotoi biomass in the pycnocline layer (Gentien et al 2007).…”

Section: Pufasmentioning

confidence: 96%

“…A full understanding of the fishkilling mechanism has been elusive however. In the absence of a specific toxin, such as brevetoxin in Karenia brevis and karlotoxin in Karlodinium veneficum (Mooney et al 2009), research to find a toxic mechanism in other dinoflagellates such as Karenia mikimotoi has focused on lipids such as polyunsaturated fatty acids (PUFAs) (Arzul et al 1998, Fossat et al 1999, Gentien et al 2007). Cold-adapted algae often have elevated levels of PUFAs to maintain cellular function, as these molecules remain fluid at lower temperatures (Valentine & Valentine 2004).…”

Section: Introductionmentioning

confidence: 92%

“…Inactivity of OPArich MGDG was found at 50 µg ml -1 in vitro against leukemia cells L-1210 and P-338 (Oshima et al 1994) (Table 3). Conversely, cytolytic activity of OPA-rich MGDG and OPA-OTA-rich MGDG against heart cells of oysters was found at concentrations > 0.5 µg l -1 using bioassay-guided fractionation (Hiraga et al 2002).Experiments using synthetic OPA have confirmed toxicity to sea bass ) and trout hepatocytes (Fossat et al 1999) (Table 3). The toxicity of synthetic OPA to the dinoflagellate Karenia mikimotoi itself was also demonstrated, but to a lesser extent than against other algae, and has been proposed as a factor in causing dominance of K. mikimotoi biomass in the pycnocline layer (Gentien et al 2007).…”

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confidence: 96%

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Ichthyotoxicity of gymnodinioid dinoflagellates: PUFA and superoxide effects in sheepshead minnow larvae and rainbow trout gill cells

Mooney¹,

Dorantes-Aranda²,

Place³

et al. 2011

Mar. Ecol. Prog. Ser.

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While 24 h exposure of sheepshead minnow fish larvae to purified monogalactosyl diglyceride (MGDG) lipids, containing octadecapentaenoic acid (OPA) exclusively or as a mixture of octadecatetraenoic acid, eicosapentaenoic acid, and OPA (OTA-EPA-OPA), caused sluggish swimming and gulping, it produced no mortalities even at concentrations up to 120 mg l -1 . In contrast, comparable concentrations and exposure times caused significant reductions in viability of rainbow trout gill cells. Pure EPA was the most harmful to gill cells (up to 98.5% viability loss in 60 h) followed by OPA-rich MGDG (45% loss), with OTA-rich MGDG (37% loss) the least toxic. OPA-pure MGDG was non-toxic to rainbow trout gill cells; however, surprisingly, pure palmitic acid was harmful (40% viability loss), and we conclude that gill cell line toxicity of the OPA-rich MGDG fraction was caused by admixture with palmitic acid. Screening of 15 Kareniaceae dinoflagellate species demonstrated that these species are low (on average 10 times less) producers of superoxide compared to the ichthyotoxic raphidophyte Chattonella marina. No mortality of sheepshead minnow fish larvae occurred when exposed to superoxide alone or superoxide combined with either OPA-rich MGDG or OTA-rich MGDG. Superoxide showed a slight impact on viability of rainbow trout gill cells. In conclusion, synergistic interactions between free fatty acids and reactive oxygen species as previously claimed for raphidophytes could not be confirmed. Gill damaging effects from EPA were conclusively demonstrated, however; when these co-occurred with OTA, a higher loss of viability was observed (up to 37%), suggesting a magnified toxic effect. Contradictory literature claims as to the ichthyotoxicity of OPA (nontoxic in our work) may relate to the presence of chemical impurities.KEY WORDS: Kareniaceae · Ichthyotoxicity · Octadecapentaenoic acid · OPA · Polyunsaturated fatty acid · PUFA· Superoxide Resale or republication not permitted without written consent of the publisherMar Ecol Prog Ser 426: [213][214][215][216][217][218][219][220][221][222][223][224] 2011 function, as these molecules remain fluid at lower temperatures (Valentine & Valentine 2004). Using bioassay-guided fractionation, the most common PUFAs investigated for toxic activity are octadecatetraenoic acid (OTA), octadecapentaenoic acid (OPA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). These molecules are highly reactive, contain 4 to 6 double bonds, and are short-lived in the water column (Jüt-tner 2001). PUFAs are synthesized almost entirely in the plastid, with the majority of OPA and OTA present in plastid-related glycolipids, as mono-or digalactosyl diglycerides (MGDG and DGDG) (Bell et al. 1997, Leblond & Lasiter 2009, and with EPA and DHA dominant in the cell-membrane phospholipid fraction (Leblond & Chapman 2000, Adolf et al. 2007). Upon lysis of senescent cells and/or dinoflagellate cell implosion upon contact with fish gills, the algal cells may rupture and release a cocktail of reactive...

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Section: Pufasmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 92%

mentioning

confidence: 96%

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Ichthyotoxicity of gymnodinioid dinoflagellates: PUFA and superoxide effects in sheepshead minnow larvae and rainbow trout gill cells

Mooney¹,

Dorantes-Aranda²,

Place³

et al. 2011

Mar. Ecol. Prog. Ser.

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“…Karenia sp. cells are known to produce allelopathic and ichtyotoxic compounds (Gentien and Arzul 1990) but also haemolysins, which in vitro induce red blood cells lysis (Arzul et al 1995;Fossat et al 1999;Sola et al 1999;Jenkinson and Arzul 2000) and fast-degrading toxins responsible for autotoxicity in K. mikimotoi cultures (Gentien et al 2007). Cells of K. selliformis also produce a wellcharacterised toxin referred to as gymnodimine (Seki et al 1995(Seki et al , 1996Mackenzie et al 1996), which caused death of oyster larvae exposed to whole cultures, culture filtrates or sonicated cell extracts of Karenia sp.…”

Section: Effect Of Harmful Algal Cells On Bivalve Haemocytes and Theimentioning

confidence: 99%

In vitro interactions between several species of harmful algae and haemocytes of bivalve molluscs

et al. 2011

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Harmful algal blooms (HABs) can have both lethal and sublethal impacts on shellfish. To understand the possible roles of haemocytes in bivalve immune responses to HABs and how the algae are affected by these cells (haemocytes), in vitro tests between cultured harmful algal species and haemocytes of the northern quahog (= hard clam) Mercenaria mercenaria, the soft-shell clam Mya arenaria, the eastern and Pacific oysters Crassostrea virginica and Crassostrea gigas and the Manila clam Ruditapes philippinarum were carried out. Within their respective ranges of distribution, these shellfish species can experience blooms of several HAB species, including Prorocentrum minimum, Heterosigma akashiwo, Alexandrium fundyense, Alexandrium minutum and Karenia spp.; thus, these algal species were chosen for testing. Possible differences in haemocyte variables attributable to harmful algae and also effects of haemolymph and haemocytes on the algae themselves were measured. Using microscopic and flow cytometric observations, changes were measured in haemocytes, including cell morphology, mortality, phagocytosis, adhesion and reactive oxygen species (ROS) production, as well as changes in the physiology and the characteristics of the algal cells, including mortality, size, internal complexity and chlorophyll fluorescence. These experiments suggest different effects of the several species of harmful algae upon bivalve haemocytes. Some harmful algae act as immunostimulants, whereas others are immunosuppressive. P. minimum appears to activate haemocytes, but the other harmful algal species tested seem to cause a suppression of immune functions, generally consisting of decreases in phagocytosis, production of ROS and cell adhesion and besides cause an increase in the percentage of dead haemocytes, which could be attributable to the action of chemical toxins. Microalgal cells exposed to shellfish haemolymph generally showed evidence of algal degradation, e.g. loss of chlorophyll fluorescence and modification of cell shape. Thus, in vitro tests allow a better understanding of the role of the haemocytes and the haemolymph in the defence mechanisms protecting molluscan shellfish from harmful algal cells and could also be further developed to estimate the effects of HABs on bivalve molluscs in vivo.

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“…The causative hemolytic agent in Alexandrium spp. has not been identified, but all these species are known to produce polyunsaturated fatty acids that could be hemolytic and biologically toxic (Sola, 1999). Therefore, there is a possibility that polyunsaturated fatty acids are involved in the cytotoxic effects of Alexandrium spp.…”

Section: Discussionmentioning

confidence: 99%

A new simple screening method for the detection of cytotoxic substances produced by harmful red tide phytoplankton

et al. 2007

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Toxicity of fatty acid 18:5n3 fromGymnodinium cf.mikimotoi: I. morphological and biochemical aspects onDicentrarchus labrax gills and intestine

Cited by 40 publications

References 16 publications

Ichthyotoxicity of gymnodinioid dinoflagellates: PUFA and superoxide effects in sheepshead minnow larvae and rainbow trout gill cells

Ichthyotoxicity of gymnodinioid dinoflagellates: PUFA and superoxide effects in sheepshead minnow larvae and rainbow trout gill cells

In vitro interactions between several species of harmful algae and haemocytes of bivalve molluscs

A new simple screening method for the detection of cytotoxic substances produced by harmful red tide phytoplankton

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