# Alterations in Lipid Metabolism and Hepatopancreatic Lipidomics Induced by Microcystin-LR Exposure in Common Carp (Cyprinus carpio)

## TL;DR

Chronic low-dose exposure to Microcystin-LR in common carp causes liver damage and disrupts lipid metabolism, offering new insights into fish hepatotoxicity.

## Contribution

This study reveals novel mechanisms of hepatic lipid metabolic disorders in fish due to chronic Microcystin-LR exposure.

## Key findings

- MC-LR exposure altered serum enzymes, lipid profiles, and caused hepatic inflammation and lipid accumulation.
- Key lipid metabolism regulators were dysregulated, indicating enhanced lipid synthesis and impaired catabolism.
- Lipidomics showed disrupted glycerophospholipids, glycerolipids, and sphingolipids, reflecting impaired lipid homeostasis.

## Abstract

Microcystin-LR is a kind of cyanotoxin. When cyanobacterial blooms occur, a large amount of cyanotoxin is produced, which poses ecological risks to aquatic organisms. In this study, we found that chronic exposure to low-dose Microcystin-LR caused oxidative stress, inflammatory responses, and hepatocyte damage. Meanwhile, the expression of genes and proteins related to lipid metabolism was disturbed. These findings deepen our understanding of the hepatotoxicity of Microcystin-LR and provide insights into hepatoprotective strategies in fish.

Microcystin-LR (MC-LR) is a hepatotoxin produced by toxic cyanobacteria such as Microcystis aeruginosa and it poses significant risks to aquatic organisms and human health. However, research on the long-term effects of environmental MC-LR exposure on lipid metabolism in fish is relatively scarce. This research investigates the effects and underlying mechanisms of chronic (one month) low-dose (3.5 μg/kg) MC-LR exposure in common carp (Cyprinus carpio) by using biochemical assays, histopathology, molecular analyses, and lipidomics. In this study, MC-LR exposure significantly altered serum enzyme activities and lipid profiles, induced hepatic inflammation and lipid accumulation, and disrupted hepatopancreatic structure. Meanwhile, key regulators of lipogenesis, fatty acid β-oxidation, and cholesterol metabolism were dysregulated, indicating enhanced lipid synthesis and impaired catabolism. Elevated oxidative stress and pro-inflammatory cytokines likely contributed to lipid metabolic disturbances, exacerbating the hepatotoxicity of MC-LR. Lipidomics profiling revealed significant disruptions in glycerophospholipids, glycerolipids, and sphingolipids, highlighting impaired lipid homeostasis. This study provides novel insights into the hepatic lipid metabolic disorders induced by MC-LR in fish.