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Early Genotoxic and Cytotoxic Effects of the Toxic Dinoflagellate Prorocentrum lima in the Mussel Mytilus galloprovincialis

机译:贻贝贻贝中有毒甲藻(prorocentrum lima)的早期遗传毒性和细胞毒性效应

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摘要

Okadaic acid (OA) and dinophysistoxins (DTXs) are the main toxins responsible for diarrhetic shellfish poisoning (DSP) intoxications during harmful algal blooms (HABs). Although the genotoxic and cytotoxic responses to OA have been evaluated in vitro, the in vivo effects of these toxins have not yet been fully explored. The present work fills this gap by evaluating the in vivo effects of the exposure to the DSP-toxin-producing dinoflagellate Prorocentrum lima during the simulation of an early HAB episode in the mussel Mytilus galloprovincialis. The obtained results revealed that in vivo exposure to this toxic microalgae induced early genotoxicity in hemocytes, as a consequence of oxidative DNA damage. In addition, the DNA damage observed in gill cells seems to be mainly influenced by exposure time and P. lima concentration, similarly to the case of the oxidative damage found in hemocytes exposed in vitro to OA. In both cell types, the absence of DNA damage at low toxin concentrations is consistent with the notion suggesting that this level of toxicity does not disturb the antioxidant balance. Lastly, in vivo exposure to growing P. lima cell densities increased apoptosis but not necrosis, probably due to the presence of a high number of protein apoptosis inhibitors in molluscs. Overall, this work sheds light into the in vivo genotoxic and cytotoxic effects of P. lima. In doing so, it also demonstrates for the first time the potential of the modified (OGG1) comet assay for assessing oxidative DNA damage caused by marine toxins in marine invertebrates.
机译:冈田酸(OA)和恐龙生物毒素(DTX)是造成有害藻华(HAB)期间腹泻性贝类中毒(DSP)中毒的主要毒素。尽管已在体外评估了对OA的遗传毒性和细胞毒性反应,但尚未充分探索这些毒素的体内作用。本工作通过评估贻贝贻贝贻贝中早期HAB发作的模拟过程中暴露于产生DSP毒素的鞭毛原毛利马菌的体内效应来填补这一空白。获得的结果表明,由于氧化DNA损伤,体内暴露于这种有毒微藻会导致血细胞早期遗传毒性。此外,在g细胞中观察到的DNA损伤似乎主要受到暴露时间和利马毕赤酵母浓度的影响,类似于体外暴露于OA的血细胞中发现的氧化损伤。在两种细胞类型中,在低毒素浓度下都不会破坏DNA,这与这一观点相符,表明这种毒性水平不会干扰抗氧化剂的平衡。最后,体内暴露于不断增长的利马毕赤酵母细胞密度可增加凋亡,但不增加坏死,这可能是由于软体动物中存在大量蛋白凋亡抑制剂所致。总的来说,这项工作揭示了利马毕赤酵母的体内遗传毒性和细胞毒性作用。在此过程中,它还首次证明了改良的(OGG1)彗星测定法可用于评估海洋无脊椎动物中海洋毒素引起的氧化DNA损伤的潜力。

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