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.
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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; · 3.99 Impact Factor
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ABSTRACT: Harmful Algal Blooms caused by the marine ichthyotoxic dinoflagellate Cochlodinium polykrikoides are responsible for mass mortalities of wild and farmed fish worldwide. In this research, we investigated the cytotoxic mechanisms of aqueous extract of C. polykrikoides on isolated Rainbow trout (Oncorhynchus mykiss) liver hepatocytes. Algal extract exposure with isolated trout hepatocytes caused hepatocyte membrane lysis, reactive oxygen species (ROS) formation, glutathione depletion, lysosomal membrane rupture, collapse of mitochondrial membrane potential, ATP depletion and increase in ADP/ATP ratio, cytochrome C release into the hepatocyte cytosol, and activation of caspases cascade. Anti-oxidants, free radical scavengers, mitochondrial permeability transition (MPT) pore sealing agents, microsomal oxidases inhibitors, ATP generators and lysosomotropic agents protected fish hepatocytes against C. polykrikoides. Fish hepatocyte toxicity was also associated with mitochondrial and lysosomal membrane injury. These events caused cytochrome C release from the mitochondrial intra-membrane space into cytosol. The cytochrome C release could trigger activation of caspase-3 and apoptosis.Marine environmental research 04/2013; · 2.34 Impact Factor
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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) 01/2013; 12(4):829-44. · 0.51 Impact Factor