Related Experiment Video
Updated: Sep 23, 2026
Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation
Published on: July 3, 2015
The cyanobacterial toxin microcystin-LR induced DNA damage in mouse liver in vivo
1Division of Pharmacology and Toxicology, Defence Research and Development Establishment, Gwalior, India.
Abstract:
Microcystin-LR (MCLR) is a potent cyclic heptapeptidic hepatotoxin produced by the cyanobacterium Microcystis aeruginosa. Hepatotoxic and other toxic manifestations of MCLR are well documented. However, information on genotoxicity of MCLR is limited. The present investigation addresses the DNA damage induced by MCLR in mouse liver in vivo. The DNA strand breaks were measured by the fluorimetric analysis of DNA unwinding (FADU). MCLR at 0.5, 1.0 and 2.0 LD50 doses exhibited a dose and time-dependent DNA damage accompanied by similar effects on various enzymes of hepatic origin, e.g. lactate dehydrogenase, alkaline phosphatase and gamma glutamyl transferase. MCLR-induced genomic DNA fragmentation was also assessed qualitatively by agarose gel electrophoresis. MCLR induced random DNA fragmentation and DNA degradation. Glutathione (GSH) pretreatment significantly extended the survival time of animals exposed to 1.0 LD50 MCLR but offered only partial protection with regard to DNA damage. The DNA damage observed in the present study can be ascribed to activation of endonucleases.
Insights
Microcystin-LR (MCLR), a cyanobacterial toxin, causes DNA damage in mouse livers. This genotoxicity is dose-dependent and may involve endonuclease activation, though glutathione offers limited protection.
Area of Science:
- Environmental toxicology
- Molecular toxicology
- Biochemistry
Background:
- Microcystin-LR (MCLR) is a potent hepatotoxin from Microcystis aeruginosa.
- While MCLR's toxicity is known, its genotoxicity remains under-investigated.
- This study focuses on MCLR-induced DNA damage in vivo.
Purpose of the Study:
- To investigate the genotoxic effects of Microcystin-LR in mouse liver.
- To quantify DNA strand breaks and fragmentation induced by MCLR.
- To explore potential protective mechanisms against MCLR genotoxicity.
Main Methods:
- Fluorimetric analysis of DNA unwinding (FADU) for DNA strand breaks.
- Agarose gel electrophoresis for qualitative assessment of DNA fragmentation.
- Enzyme activity assays for hepatic markers (LDH, ALP, GGT).
Main Results:
- MCLR induced dose- and time-dependent DNA damage in mouse liver.
- Significant genomic DNA fragmentation and degradation were observed.
- Glutathione pretreatment partially mitigated DNA damage and extended survival time.
Conclusions:
- MCLR exhibits significant genotoxicity in mouse liver.
- DNA damage is likely mediated by endonuclease activation.
- Further research into protective strategies against MCLR genotoxicity is warranted.
