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Updated: Aug 15, 2026

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
Low dose exposure of diethylnitrosamine affects mice liver thymidine kinase
1Department of Biochemistry, School of Life Sciences, North-Eastern Hill University, Umshing, Shillong, India.
Abstract:
Swiss albino mice exposed to 5 and 10 mg diethylnitrosamine kg-1 body weight by intravenous route up to four weeks showed cyto- and genotoxic effects. Distortion of cell and nucleus shapes and extensive necrosis were observed. Thymidine kinase activity in the liver declined in diethylnitrosamine dose and duration dependent manners. The adult-form of thymidine kinase isozyme declined continuously during this period. Simultaneously, two isozymic forms of thymidine kinase, with small anodic migrations in an electrophoretic field, were gradually induced. Significance of theses changes in diethylnitrosamine induced precarcinogenic toxicity has been discussed.
Insights
Diethylnitrosamine exposure in mice caused cell damage and genetic toxicity. Liver thymidine kinase activity changed, indicating precarcinogenic toxicity.
Area of Science:
- Toxicology
- Biochemistry
- Genetics
Background:
- Diethylnitrosamine is a known carcinogen.
- Understanding its early toxic effects is crucial for cancer research.
Purpose of the Study:
- To investigate the cyto- and genotoxic effects of diethylnitrosamine in Swiss albino mice.
- To analyze changes in liver thymidine kinase activity and isozyme patterns.
Main Methods:
- Swiss albino mice were intravenously administered diethylnitrosamine (5 and 10 mg/kg) for up to four weeks.
- Cytological and genotoxic assessments were performed.
- Liver thymidine kinase activity and isozyme profiles were analyzed using electrophoresis.
Main Results:
- Diethylnitrosamine exposure resulted in cellular damage, including distorted cell/nucleus shapes and necrosis.
- A dose- and duration-dependent decline in overall liver thymidine kinase activity was observed.
- The adult thymidine kinase isozyme decreased, while two new isozymes with altered electrophoretic mobility were induced.
Conclusions:
- Diethylnitrosamine induces significant cyto- and genotoxic effects in mice.
- Alterations in thymidine kinase isozymes suggest a role in diethylnitrosamine-induced precarcinogenic toxicity.
- These findings contribute to understanding early molecular events in chemical carcinogenesis.

