Abstract

In vivo, after administration by gavage to mice and rats, okadaic acid has been reported to produce lesions in liver, small intestine and forestomach. Because several reports differ in the damage detected in different organs, and on okadaic acid distribution after consumption, we determined the toxicity of this compound after oral administration to mice. After 24 hours, histopathological examination showed necrotic foci and lipid vacuoles in the livers of intoxicated animals. By immunohistochemical analysis, we detected this toxin in the liver and kidneys of intoxicated animals. Okadaic acid induces oxidative stress and can be activated in vitro into reactive compounds by the post-mitochondrial S9 fraction, so we studied the okadaic effect on the gene expression of antioxidant and phase II detoxifying enzymes in liver. We observed a downregulation in the expression of these enzymes and a reduction of protein expression of catalase and superoxide dismutase 1 in intoxicated animals.

Highlights

  • Okadaic acid (OA) is one of the toxins responsible for the human intoxication known as diarrhetic shellfish poisoning (DSP), which appears after the consumption of contaminated shellfish [1] This polyether toxin is produced by dinoflagellates of the genera Dinophysis or Prorocentrum [2]

  • [21] Taking into account these observations, and considering that OA circulates through the enterohepatic cycle, the gene expression of antioxidant and phase II enzymes was determined in the liver of both control and OA-treated mice in order to establish if it affected the expression of these detoxifying systems

  • Diarrhea was almost instantaneous in intoxicated animals, and OA could be detected in the feces at doses of 700 μg/kg and 1000 μg/kg after the first hour post-intoxication (Table 1)

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Summary

Introduction

Okadaic acid (OA) is one of the toxins responsible for the human intoxication known as diarrhetic shellfish poisoning (DSP), which appears after the consumption of contaminated shellfish [1] This polyether toxin is produced by dinoflagellates of the genera Dinophysis or Prorocentrum [2]. Some research groups have observed small intestine damage after oral administration of OA [9,11,13,14], while other groups did not report this effect [8,10,15]. Tissue damage after toxin treatment was determined by histopathological examination of intestine, liver, kidneys, heart, lungs and brain, while. The tumor promoting activity of OA and functionally related compounds was proposed to be due to a pro-oxidant activity of this toxin [21] Taking into account these observations, and considering that OA circulates through the enterohepatic cycle, the gene expression of antioxidant and phase II enzymes was determined in the liver of both control and OA-treated mice in order to establish if it affected the expression of these detoxifying systems. Based on the results obtained, the expression of superoxide dismutase-1 and catalase was determined

Results
Experiments
Discussion
Animals and Treatments
Histopathology and Immunohistochemistry
Quantitative PCR
Western Blot
Statistical Analysis
Conclusions
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