346 / 2024-09-14 16:16:39
Mechanism and toxic effects of Haliotis discus hannai induced by yessotoxins
harmful algal toxins,Abalone,Toxic mechanism
Session 12 - Alleviating the impact of emerging Harmful Algal Blooms (HABs) to coastal ecosystems and seafood safety for a sustainable and healthy Ocean
Abstract Accepted
Yessotoxins (YTXs) are lipid-soluble algal toxins produced by certain phytoplanktonic dinoflagellates. YTX has more than 90 derivatives, which have been linked to notable mortality in farmed abalones and pose risks to human health. During harmful algal blooms, these toxins can cause considerable damage to the tissues and organs of abalones. This study examined the impact of different concentrations of homo-YTX (0, 2, 5, and 10 µg L−1) on the economically significant abalone species Haliotis discus hannai. The abalones were exposed to these concentrations for 12 h to evaluate several factors: survival rate (S), mortality rate (D), antioxidant defense capabilities, metabolic and digestive physiological responses, and expression levels of Hsp- and apoptosis-related genes in abalone gills and digestive glands. Results provided insights into the toxicity mechanism at the transcriptome level. Homo-YTX exposure led to a decrease in survival rate of abalone S and diminished the activities of various enzymes, including Na+/K+–adenosine triphosphatase, Ca2+/Mg2+–adenosine triphosphatase, superoxide dismutase, catalase, alkaline phosphatase, xanthine oxidase, lactate dehydrogenase, amylase, protease, and lipase. The expression levels of Hsp70, Hsp90, and B-cell lymphoma-2 (BCL2) in H. discus hannai were downregulated. Meanwhile abalone D, reactive oxygen species level, and malondialdehyde content increased, alongside elevated expression levels of B-cell lymphoma-2-associated X (BAX) and caspase3 (CASP3) expression levels with higher concentrations of homo-YTX. Homo-YTX induced oxidative stress, leading to enhanced lipid peroxidation, decreased energy supply, disrupted antioxidant defense and Hsp-related defense systems, and inhibited metabolic and digestive physiological activities of gills and digestive glands in abalone. The oxidative stress resulted in insufficient energy supply, impaired heat shock responses, reduced physiological activities, and ultimately cell apoptosis, contributing to abalone death. Transcriptomic analysis confirmed that the toxic effects of homo-YTX on abalone gills primarily affect cellular processes, including cell growth and death, with apoptosis being the main pathway through which these toxic effects are mediated.