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Related Experiment Video

Updated: Jun 7, 2026

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat

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Iodipamide hepatotoxicity in the rat.

R F Burk, J L Barnhart

Gastroenterology

|June 1, 1979

Summary

Iodipamide meglumine causes liver injury in rats, with age significantly impacting toxicity. Factors like selenium deficiency and specific pretreatments can alter the drug

Area of Science:

Toxicology
Hepatology
Pharmacology

Background:

Iodipamide meglumine (Cholografin) is linked to patient liver injury.
The hepatotoxic potential of iodipamide requires further investigation.

Purpose of the Study:

To assess the hepatotoxic potential of iodipamide in a rat model.
To identify factors influencing iodipamide-induced hepatotoxicity.

Main Methods:

Administration of iodipamide via intraperitoneal or intravenous routes in rats.
Evaluation of liver necrosis in rats of varying weights (200g vs 400g).
Assessment of protective effects of selenium deficiency and 3-methylcholanthrene pretreatment.

Main Results:

Iodipamide induced midzonal to centrilobular necrosis in rats weighing 400g or more at 2 mmol/kg.

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Younger rats (200g) did not develop liver necrosis, even at higher doses.

Selenium deficiency and 3-methylcholanthrene pretreatment protected against liver necrosis.

Kidney tubular necrosis was observed in younger and selenium-deficient rats.

Conclusions:

Iodipamide is a confirmed hepatotoxin in rats.
Rat age is a critical factor modifying iodipamide hepatotoxicity.
Specific physiological and pre-treatment conditions influence the drug's toxic effects.