The Possibility of Reactive Oxygen Species (ROS)-Independent Toxic Effects of Cochlodinium polykrikoides on Damselfish ( Chromis caerulea )
ABSTRACT To elucidate the ichthyotoxic mechanism of the harmful dinoflagellate Cochlodinium polykrikoides, a bioassay using damselfish was conducted. After exposure to a live-cell suspension of C. polykrikoides, all the fish were died within 90 min. In the presence of catalase and superoxide dismutase (SOD), no significant reduction in the toxicity of C. polykrikoides on the fish was observed. Furthermore, no significant levels of reactive oxygen species (ROS) were detected in five strains of C. polykrikoides isolated in Japan. Our results support the idea that certain toxic substances, rather than ROS, are mainly responsible for the fish-killing activity of C. polykrikoides.
- SourceAvailable from: Enayatollah Seydi
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- "The three extracts were combined, decanted, and centrifuged at 3200 £ g for 15 min. The supernatant was removed and used for cytotoxicity assays (Deeds et al. 2002; Kim et al. 2009).The dinoflagellate concentration equivalent to obtained algal extract was approximately 2.4 £ 10 4 cells/ml considering that the extract at 100% was obtained from C. polykrikoides cells. "
ABSTRACT: Harmful algal blooms produced by the marine ichthyotoxic dinoflagellate Cochlodinium polykrikoides are responsible for mass mortalities of wild and farmed fish globally. This study compared the cytotoxic mechanisms of C. polykrikoides total extract on both trout and rat liver hepatocytes. Trout hepatocytes were more sensitive than rat hepatocytes against C. polykrikoides extract. The effective concentration 50 after 3 hour incubation (EC503hr) concentrations found for C. polykrikoides extract in trout and rat hepatocytes (i.e., 50% membrane lysis in 3 hr) were Eq. 1 cell/ml and Eq. 240 cell/ml, respectively. C. polykrikoides extract exposure in both isolated trout and rat hepatocytes resulted in membrane lysis, reactive oxygen species formation, glutathione depletion, collapse of mitochondrial membrane potential, ATP depletion, increase in adenosine diphosphate (ADP)/adenosine triphosphate (ATP) ratio, cytochrome c release into the hepatocyte cytosol, and activation of caspases cascade. Trout hepatocyte toxicity was also associated with lysosomal membrane injury. Mitochondrial permeability transition in both trout and rat hepatocytes produced cytochrome c release from the mitochondrial intramembrane space into the cytosol. Thus, the cytochrome c release triggered activation of caspase-3 and apoptosis. Finally, data demonstrated that C. polykrikoides extract may induce more apoptotic phenotype in rat than trout hepatocytes, which in the latter favored predominantly necrotic mode of cell death.Toxicological and Environmental Chemistry 07/2014; 96(6-ahead-of-print):1-14. DOI:10.1080/02772248.2014.980132 · 0.83 Impact Factor
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- "The three lysates were combined, decanted and centrifuged at 3200×g for 15 min. The supernatant (total algal lysate) was removed and used for the cytotoxicity assays (modified from (16, 21). "
ABSTRACT: In this research, we investigated the cytotoxic mechanisms of Cochlodinium polykrikoidescell lysate on isolated rat liver hepatocytes.This micro algae is responsible for a severe and widespread harmful algal bloom in the Persian Gulf and Gulf of Oman (2008-2009). Isolated hepatocytes were obtained by collagenase perfusion of Sprague-Dawley rat liver.According to our results, incubation of algal lysate with isolated rat hepatocytescaused hepatocyte membrane lysis, reactive oxygen species (ROS) formation, glutathione depletion, collapse of mitochondrial membrane potential,ATP depletion and increase in ADP/ATP ratio, cytochrome c release in to the hepatocyte cytosol,activation of caspase-3 (final mediator of apoptosis) and appearance of apoptosis phenotype. On the other hand, pre-treatment of antioxidants (α-tocopherol succinate and BHT), radical scavengers (mannitol and DMSO), mitochondrial permeability transition (MPT) pore sealing agents (cyclosporine A, carnitine and trifluoperazine), NADPH P450 reductase inhibitor (Diphenyliodonium chloride), CYP2E1 inhibitors (Phenylimidazole and 4-Methylpyrazole) and ATP generators (L-glutamine, Fructose and Xylitol)inhibitedcaspase-3 activation and cell death in algal lysate treated hepatocytes.Our data also confirmed that algal lysate activates apoptosis signaling via oxidative stress and mitochondrial pathway. Thus, ROS formation caused by the lysate exposure could directly be involved in mitochondrial MPT pore opening and activation of caspase-3 leading to C.polykrikoides lysateinduced apoptosis on rat hepatocytes. These findings contribute to a better understanding of C.polykrikoides-toxic effects on mammalian liver cells.Iranian journal of pharmaceutical research (IJPR) 02/2013; 12(4):829-44. · 1.07 Impact Factor
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- "The toxicity of H. akashiwo is not completely understood, but has been tentatively linked to either the production of reactive oxygen species (Yang et al., 1995) or a brevetoxin-like neurotoxin (Khan et al., 1997). The fish-killing effects of Cochlodinium species have also been attributed to the production of reactive oxygen species, although recent work by Kim et al. (2009) suggests that other toxins may be involved. The toxins of some Karenia species have been isolated and well-described, for example, the suite of lipophilic toxins called brevetoxins that become harmful to fish through ingestion or aerosolization. "
ABSTRACT: Comparison of harmful algal bloom (HAB) species in eastern boundary upwelling systems, specifically species composition, bloom densities, toxin concentrations and impacts are likely to contribute to understanding these phenomena. We identify and describe HABs in the California, Canary, Benguela and Humboldt Current systems, including those that can cause the poisoning syndromes in humans called paralytic shellfish poisoning (PSP), diarrhetic shellfish poisoning (DSP), and amnesic shellfish poisoning (ASP), as well as yessotoxins, ichthyotoxins, and high-biomass blooms resulting in hypoxia and anoxia. Such comparisons will allow identification of parameters, some unique to upwelling systems and others not, that contribute to the development of these harmful blooms.Progress In Oceanography 04/2010; 85(1-85):33-52. DOI:10.1016/j.pocean.2010.02.003 · 3.03 Impact Factor