Abstract
Okadaic acid (OA), produced by dinoflagellates during harmful algal blooms, is a principal diarrhetic shellfish poisoning toxin. This toxin poses a potential threat to bivalves with economic values. To better understand the toxicity mechanism of OA to bivalves, in this study, oxidative stress biomarkers (superoxide dismutase, SOD; catalase, CAT; glutathione S-transferase, GST; malondialdehyde, MDA) and the expression of detoxification genes (heat shock protein 70, HSP70; heat shock protein 90, HSP90; cytochrome P450, CYP450) were assessed in the gills of scallops Chlamys farreri after 24 h, 48 h and 96 h exposure to OA. In addition, the digestive glands of scallops exposed to OA for 96 h were dissected for an iTRAQ based quantitative proteomic analysis. The results of OA exposure experiments showed that OA induces oxidative stress and significant enhancement of the expression of detoxification genes in scallops. The proteomics analysis revealed that 159 proteins altered remarkably in OA-treated scallops, and these proteins were involved in phagosomes, regulation of actin cytoskeleton, adherens junction, tight junction, and focal adhesion. Amino acid biosynthesis, carbon metabolism, pentose phosphate pathway, fructose and mannose metabolism in the digestive glands were also significantly impacted. Our data shed new insights on the molecular responses and toxicity mechanisms of C. farreri to OA.
Highlights
In recent years, harmful algal blooms (HABs) have occurred widespread in the ocean, with higher frequency and longer periods than that in the past (Dolah, 2000; Anderson et al, 2012; Gobler et al, 2017)
One main hazard of HABs is the release of a variety of shellfish toxins, including diarrhetic shellfish toxins (DST), neurotoxic shellfish toxins (NST), paralytic shellfish toxins (PST), and forgetful shellfish toxins (AST) (Christian and Luckas, 2008)
No significant difference was detected in the physiological indexes between the solvent control group and the control group, only experimental results derived from the control group were analyzed and discussed
Summary
Harmful algal blooms (HABs) have occurred widespread in the ocean, with higher frequency and longer periods than that in the past (Dolah, 2000; Anderson et al, 2012; Gobler et al, 2017). Okadaic acid (OA) and its analogs, a typical DST, are responsible for DSP in humans (Garcia et al, 2005). Studies on mammalian or in vitro mammalian cell lines have shown that OA inhibits the serine and threonine phosphatases PP1 and PP2A (Bialojan and Takai, 1988; Honkanan et al, 1994; Maynes et al, 2001), leads to oxidative damage (Kamat et al, 2013; Vieira et al, 2013) and cytoskeleton destruction (Kreienbuhl et al, 1992; Fiorentini et al, 1996; Opsahl et al, 2013), affects the cell cycle (Messner et al, 2001; Valdiglesias et al, 2010a,b), neurotoxicity (Kamat et al, 2013) and apoptosis (Jayaraj et al, 2009; Ferron et al, 2014; Fu et al, 2019). The mode and mechanism of action of OA on mammals have been well studied, current studies on the impacts of OA on bivalves are limited and mostly confined to the physiological level
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