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Background <p>Saxitoxin (STX) is a potent phycotoxin primarily known for its acute neurotoxicity. However, its chronic impacts on key metabolic organs, particularly the liver, remain poorly understood in fish models.</p> Objective <p>This study aims to investigate the potential mechanisms by which chronic STX exposure induces hepatic lipid accumulation and cellular damage in zebrafish, <i>Danio rerio</i>.</p> Methods <p>Zebrafish were exposed to STX for 90&#xa0;days, followed by lipid quantification (triglyceride, TG; total cholesterol: TC) and comprehensive analyses of hepatic biochemical markers. We also analyzed the mRNA expression levels of genes involved in major lipid metabolism (e.g., lipid synthesis, transport, oxidation, and phospholipid repair) and apoptosis.</p> Results <p>Chronic STX exposure led to a significant accumulation of TG, with a slight increase in TC. The increased malondialdehyde (MDA) content, along with elevated levels of ALT, AST, and ALP, indicated lipid peroxidation and hepatocellular injury. Transcriptional profiling revealed that while lipid synthesis genes remained unaffected, there was a marked down-regulation of genes associated with lipid transport, β-oxidation, and phospholipid repair. Finally, increased Caspase 3 enzymatic activity and mRNA expression levels of pro-apoptotic genes indicated that the accumulation of lipid peroxides and metabolic failure was associated with activation of apoptosis-related signaling.</p> Conclusion <p>These results indicate that hepatic TG accumulation after chronic STX exposure was not accompanied by transcriptional activation of de novo lipogenesis. Instead, the overall biochemical and transcriptional responses support the involvement of lipid peroxidation, reduced lipid transport, and impaired fatty acid oxidation.</p>

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Chronic exposure to saxitoxin increases hepatic triglyceride through lipid peroxidation and disruption of lipid metabolism in zebrafish

  • 期刊论文

  • 发表日期：

    2026年7月9日

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  • Young-Joo Yun,
  • Ye-Ji Rhee,
  • Daeun Ahn,
  • Jae-Sung Rhee,
  • Hyoung-Sook Park

摘要

Background

Saxitoxin (STX) is a potent phycotoxin primarily known for its acute neurotoxicity. However, its chronic impacts on key metabolic organs, particularly the liver, remain poorly understood in fish models.

Objective

This study aims to investigate the potential mechanisms by which chronic STX exposure induces hepatic lipid accumulation and cellular damage in zebrafish, Danio rerio.

Methods

Zebrafish were exposed to STX for 90 days, followed by lipid quantification (triglyceride, TG; total cholesterol: TC) and comprehensive analyses of hepatic biochemical markers. We also analyzed the mRNA expression levels of genes involved in major lipid metabolism (e.g., lipid synthesis, transport, oxidation, and phospholipid repair) and apoptosis.

Results

Chronic STX exposure led to a significant accumulation of TG, with a slight increase in TC. The increased malondialdehyde (MDA) content, along with elevated levels of ALT, AST, and ALP, indicated lipid peroxidation and hepatocellular injury. Transcriptional profiling revealed that while lipid synthesis genes remained unaffected, there was a marked down-regulation of genes associated with lipid transport, β-oxidation, and phospholipid repair. Finally, increased Caspase 3 enzymatic activity and mRNA expression levels of pro-apoptotic genes indicated that the accumulation of lipid peroxides and metabolic failure was associated with activation of apoptosis-related signaling.

Conclusion

These results indicate that hepatic TG accumulation after chronic STX exposure was not accompanied by transcriptional activation of de novo lipogenesis. Instead, the overall biochemical and transcriptional responses support the involvement of lipid peroxidation, reduced lipid transport, and impaired fatty acid oxidation.