Commonly affected by changes in climate and environmental conditions, coastal areas are very dynamic environments where shellfish play an important ecological role. In this study, the oxidative stress and genotoxic responses of mussels (Mytilus galloprovincialis) exposed to paralytic shellfish toxin (PST) - producing dinoflagellates Gymnodinium catenatum were evaluated under i) current conditions (CC: 19 °C; pH 8.0), ii) warming (W: 24 °C; pH 8.0), iii) acidification (A:19 °C; pH 7.6) and iv) combined effect of warming and acidification (WA: 24 °C; pH 7.6). Mussels were fed with G. catenatum for 5 days, and to a non-toxic diet during the following 10 days. A battery of oxidative stress biomarkers and comet assay was performed at the peak of toxin accumulation and at the end of the post-exposure phase. Under CC, gills and hepatopancreas displayed different responses/vulnerabilities and mechanisms to cope with PST. While gills presented a tendency for lipid peroxidation (LPO) and genetic damage (expressed by the Genetic Damage Indicator - GDI), hepatopancreas seems to better cope with the toxins, as no LPO was observed. However, the mechanisms involved in hepatopancreas protection were not enough to maintain DNA integrity. The absence of LPO, and the antioxidant system low responsiveness, suggests DNA damage was not oxidative. When exposed to toxic algae under W, toxin-modulated antioxidant responses were observed in both gills and hepatopancreas. Simultaneous exposure to the stressors highlighted gills susceptibility with a synergistic interaction increasing DNA damage. Exposure to toxic algae under A led to genotoxicity potentiation in both organs. The combined effect of WA did not cause relevant interactions in gills antioxidant responses, but stressors interactions impacted LPO and GDI. Antioxidant responses and LPO pointed out to be modulated by the environmental conditions in hepatopancreas, while GDI results support the dominance of toxin-triggered process. Overall, these results reveal that simultaneous exposure to warming, acidification and PSTs impairs mussel DNA integrity, compromising the genetic information due to the synergetic effects. Finally, this study highlights the increasing ecological risk of harmful algal blooms to Mytilus galloprovinciallis populations.

沿海地区通常受气候和环境条件变化的影响，是非常活跃的环境，贝类在其中起着重要的生态作用。在这项研究中，氧化应激和贻贝的基因毒性反应（紫贻贝- ）暴露于麻痹性贝毒（PST）产生鞭毛藻链状裸甲藻进行了下评价我）当前条件（CC：19℃; pH 8.0）中，二）变暖（W：24℃； pH 8.0），iii）酸化（A：19℃； pH 7.6）和iv）加温和酸化（WA：24℃； pH 7.6）的联合作用。贻贝被喂以悬链线虫持续5天，然后在接下来的10天内进行无毒饮食。在毒素积累的高峰和暴露后阶段结束时进行了一系列的氧化应激生物标记和彗星分析。在CC下，g和肝胰腺表现出不同的反应/脆弱性和应对PST的机制。虽然g呈现出脂质过氧化（LPO）和遗传损伤的趋势（由遗传损伤指标-GDI表示），但由于未观察到LPO，肝胰腺似乎可以更好地应对毒素。然而，涉及肝胰腺保护的机制不足以维持DNA完整性。LPO的缺乏和抗氧化剂系统的低响应性表明DNA损伤不是氧化性的。当在W下暴露于有毒藻类时，在g和肝胰腺中均观察到毒素调节的抗氧化反应。同时暴露于应激源突显了g的易感性，并具有协同作用，增加了DNA损伤。在A下接触有毒藻类会导致两个器官的遗传毒性增强。WA的综合作用并未在g抗氧化反应中引起相关的相互作用，但应激源的相互作用影响了LPO和GDI。肝胰腺中的抗氧化反应和LPO受到环境条件的调节，而GDI结果支持了毒素触发过程的优势。总体而言，这些结果表明，同时暴露于变暖，酸化和PST会损害贻贝DNA的完整性，由于协同效应而损害了遗传信息。最后，没食子菌种群。