Acute Cardiotoxicity Evaluation of the Marine Biotoxins OA, DTX-1 and YTX

Toxins

Sara F. Ferreiro²  Cristina Carrera²  Natalia Vilariño²  M. Carmen Louzao²  Germán Santamarina¹  Antonio G. Cantalapiedra¹  Luis M. Botana² 

[1] Hospital Veterinario Universitario Rof Codina, Facultad de Veterinaria, Universidad de Santiago de Compostela, 27002 Lugo, Spain; E-Mails:;Departamento de Farmacología, Facultad de Veterinaria, Universidad de Santiago de Compostela, 27002 Lugo, Spain; E-Mails:

关键词: okadaic acid;    dynophysistoxins;    yessotoxin;    cardiotoxicity;    hERG;    ECG;    cardiac biomarkers;   

DOI  :  10.3390/toxins7041030

来源: mdpi

【 摘 要 】

Phycotoxins are marine toxins produced by phytoplankton that can get accumulated in filter feeding shellfish. Human intoxication episodes occur due to contaminated seafood consumption. Okadaic acid (OA) and dynophysistoxins (DTXs) are phycotoxins responsible for a severe gastrointestinal syndrome called diarrheic shellfish poisoning (DSP). Yessotoxins (YTXs) are marine toxins initially included in the DSP class but currently classified as a separated group. Food safety authorities from several countries have regulated the content of DSPs and YTXs in shellfish to protect human health. In mice, OA and YTX have been associated with ultrastructural heart damage in vivo. Therefore, this study explored the potential of OA, DTX-1 and YTX to cause acute heart toxicity. Cardiotoxicity was evaluated in vitro by measuring hERG (human èter-a-go-go gene) channel activity and in vivo using electrocardiogram (ECG) recordings and cardiac damage biomarkers. The results demonstrated that these toxins do not exert acute effects on hERG channel activity. Additionally, in vivo experiments showed that these compounds do not alter cardiac biomarkers and ECG in rats acutely. Despite the ultrastructural damage to the heart reported for these toxins, no acute alterations of heart function have been detected in vivo, suggesting a functional compensation in the short term.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.