0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Marine & Wildlife Policy & Risk Remediation Sign in to save

Subchronic Exposure to Microcystin-LR Induces Hepatic Inflammation, Oxidative Stress, and Lipid Metabolic Disorders in Darkbarbel Catfish (Tachysurus vachelli)

Toxins 2025 3 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Huaxing Zhou, Tong Li, Huan Wang, Ye Zhang, Yuting Hu, Amei Liu, Guoqing Duan

Summary

Researchers exposed catfish to microcystin-LR, a common water pollutant produced by algal blooms, and found it caused significant liver inflammation, oxidative stress, and disrupted fat metabolism over 28 days. The toxin triggered immune cell infiltration in the liver and altered the expression of genes involved in lipid processing. The study provides evidence that even environmentally relevant concentrations of this algal toxin can cause serious liver damage in freshwater fish.

Body Systems

Microcystin-leucine arginine (MC-LR) is a prominent water pollutant known for its potent hepatic toxicity. However, the effects of subchronic exposure to environmentally relevant concentrations of MC-LR on the fish liver remain poorly understood. This study aimed to systematically evaluate the impact of subchronic MC-LR exposure on the liver of darkbarbel catfish (Tachysurus vachelli). A total of 270 one-year-old fish were exposed to MC-LR (0, 2, and 5 μg/L) for 28 days and sampled on days 14 (D14) and 28 (D28). Histopathological analysis revealed marked hepatic inflammation in the MC-LR treatment groups, manifested as cellular degeneration, hyperemia, and inflammation. MC-LR exposure induced oxidative stress, evidenced by elevated malondialdehyde (MDA) levels and compensatory upregulation of superoxide dismutase (SOD) activity on D28. While hepatic lipid profiles were not altered by low-dose MC-LR, significant elevation of low-density lipoprotein cholesterol (LDL-C) specifically on D28 indicated incipient lipid metabolic disorder. Metabolomic analysis demonstrated a higher sensitivity, highlighting the stress response of the liver to low-dose MC-LR exposure. The results suggest MC-LR exposure disrupted hepatic phosphatidylcholine (PC) biosynthesis and inhibited lipoprotein formation, thereby impairing lipid transport and contributing to lipid metabolic disorders. In summary, subchronic exposure to environmentally relevant concentrations of MC-LR-induced hepatic tissue inflammation, oxidative stress, and lipid metabolic disorders in darkbarbel catfish.

Sign in to start a discussion.

More Papers Like This

Meta Analysis Tier 1

Hazards of microplastics exposure to liver function in fishes: A systematic review and meta-analysis

This meta-analysis found that microplastic exposure significantly impairs fish liver function, elevating key liver enzymes (AST, ALT, ALP, LDH) and triggering oxidative stress markers in liver tissue. The toxicological mechanisms include inflammation, apoptosis, and metabolic disruption, raising concerns about the health of fish populations in microplastic-contaminated waters and the safety of fish as a human food source.

Article Tier 2

Subchronic oral exposure to polystyrene microplastics affects hepatic lipid metabolism, inflammation, and oxidative balance in gilthead seabream (Sparus aurata)

Gilthead seabream fed polystyrene microplastics for 21 days developed signs of liver damage including fat buildup, inflammation, and oxidative stress -- changes similar to early-stage fatty liver disease. Since fish liver responds to microplastics in ways comparable to mammalian livers, these findings raise concerns about what chronic microplastic exposure might do to liver health in humans and other animals.

Article Tier 2

Hepatic multi-level responses to polyethylene microplastics in Lateolabrax maculatus: Insights from transcriptomics, antioxidant enzyme activity, and histopathology

Researchers exposed spotted sea bass to diets containing polyethylene microplastics for 45 days and found multiple levels of liver damage, including altered gene expression, reduced antioxidant enzyme activity, and visible tissue changes. A subsequent depuration period showed partial but incomplete recovery. The study suggests that chronic microplastic exposure through contaminated feed may pose significant risks to liver health in commercially farmed fish species.

Article Tier 2

The effects of exposure to microplastics on grass carp (Ctenopharyngodon idella) at the physiological, biochemical, and transcriptomic levels

Researchers exposed grass carp to microplastics at two concentrations for 21 days and observed liver damage, inhibited growth, and increased oxidative stress. Transcriptome analysis revealed over 1,500 differentially expressed genes related to immune response, metabolism, and cellular stress pathways. The study suggests that microplastic exposure can trigger broad physiological and molecular disruptions in freshwater fish.

Article Tier 2

Effects of Polystyrene Microplastic Exposure on Liver Cell Damage, Oxidative Stress, and Gene Expression in Juvenile Crucian Carp (Carassius auratus)

Researchers exposed young crucian carp to polystyrene microplastics at different concentrations and found dose-dependent liver damage, with higher concentrations causing more severe tissue injury and weaker antioxidant defenses. The microplastics disrupted genes involved in detoxification and stress response in liver cells. Since crucian carp is a commonly consumed freshwater fish, these findings raise questions about whether microplastic-contaminated fish could affect the health of people who eat them.

Share this paper