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Updated: Sep 11, 2025
Analysis of Oxidative Stress in Zebrafish Embryos
Published on: July 7, 2014
Colchicine induces developmental defects and renal toxicity in zebrafish by upregulating the oxidative stress
Fang Chen1, Haiyan Wei2, Dalong Liao1
1The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, Jiangxi, China.
Abstract:
Colchicine is a type of alkaloid commonly used clinically for treating diseases such as gouty arthritis. Studies suggest that colchicine is toxic to the kidneys. However, the specific mechanisms are unclear. Herein, we used zebrafish to validate the renal toxicity of colchicine and investigate the underlying mechanisms. Zebrafish larvae at 3 days post-fertilization were exposed to various concentrations (15, 20, and 25 mg/L) of colchicine solution for 72 h. Results showed that colchicine caused death, slowed heart rate, slowed growth, increased interpupillary distance, caused periorbital and renal capsule edema, caused swelling of glomerular podocytes, and disrupted the development of distal convoluted tubules of renal tubules. ROS staining revealed that colchicine increased oxidative in the glomerular. Mature zebrafish adults were exposed to colchicine solution concentrations of 0.15 and 1.5 mg/L for 4 weeks. Hematoxylin eosin staining of the kidney showed that the glomerular podocyte structure was disordered, renal tubular nuclei were irregularly arranged, and cell density was reduced. A significant increase in oxidative stress kinase activity was observed. Additionally, there was abnormal expression of genes related to kidney development and function. Abnormalities in kidney injury biomarkers were also observed in zebrafish, including urea nitrogen (BUN), creatinine (CR), and β-N-acetylglucosaminidase (NAG). These findings suggest that colchicine induced developmental defects and caused renal toxicity in zebrafish. Interestingly, treatment with astaxanthin (ASTA) partially reversed the structural and physiological damage in the kidney. Conclusively, colchicine induces developmental and renal toxicity in zebrafish by upregulating oxidative stress.
Insights
Colchicine causes kidney damage and developmental issues in zebrafish by increasing oxidative stress. Astaxanthin (ASTA) treatment showed potential in reversing some of these harmful effects.
Area of Science:
- Toxicology
- Nephrology
- Developmental Biology
Background:
- Colchicine, an alkaloid used for gouty arthritis, is suspected to cause kidney toxicity.
- The precise mechanisms underlying colchicine-induced nephrotoxicity remain largely unknown.
Purpose of the Study:
- To validate colchicine's renal toxicity in zebrafish.
- To elucidate the mechanisms of colchicine-induced kidney damage.
Main Methods:
- Zebrafish larvae and adults were exposed to varying colchicine concentrations.
- Evaluated developmental parameters, kidney structure (histopathology), oxidative stress markers, gene expression, and kidney injury biomarkers.
- Assessed the protective effects of astaxanthin (ASTA).
Main Results:
- Colchicine exposure led to increased mortality, developmental delays, edema, and significant kidney structural damage, including podocyte swelling and tubular disruption.
- Elevated reactive oxygen species (ROS) and oxidative stress kinase activity were observed.
- Abnormalities in kidney development/function genes and biomarkers (BUN, CR, NAG) were detected.
- Astaxanthin partially mitigated colchicine-induced kidney damage.
Conclusions:
- Colchicine induces developmental defects and renal toxicity in zebrafish, primarily by upregulating oxidative stress.
- Zebrafish serve as a valuable model for studying colchicine nephrotoxicity.
- Astaxanthin demonstrates potential as a therapeutic agent against colchicine-induced kidney injury.
