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Mepanipyrim induces fatty liver in rats but not in mice and dogs
M Terada1, F Mizuhashi, T Tomita
1Life Science Research Institute, Kumiai Chemical Industry Co., Ltd., Shizuoka, Japan.
Abstract:
Mepanipyrim, a new fungicide, was administered orally to rats, mice and dogs for 13 weeks to clarify its toxic profiles. Hepatotoxicities were observed characteristically in these species with high concentrations of mepanipyrim; more than 200 ppm in rats, more than 1,000 ppm in mice, and more than 50 mg/kg/day in dogs. In rats, obvious fatty vacuolation in the perilobular hepatocytes and changes in the serum-lipid concentrations such as total cholesterol (TC), triglyceride (TG), phospholipid (PL) and non-esterified fatty acid (NEFA) were observed. This fatty liver appeared to be based on the alteration of lipid metabolism. In contrast, no remarkable changes were observed in mice and dogs except for an enhancement of anisonucleosis in mice or a lipofuscin deposition in Kupffer cells and hepatocytes in dogs. It appeared that there were species differences in the hepatotoxicities of mepanipyrim.
Insights
Mepanipyrim, a new fungicide, causes liver toxicity in rats at high doses by altering lipid metabolism. Species differences in hepatotoxicity were observed in rats, mice, and dogs during a 13-week oral study.
Area of Science:
- Toxicology
- Fungicide Safety
- Animal Studies
Background:
- Mepanipyrim is a novel fungicide.
- Understanding its toxicological profile is crucial for risk assessment.
Purpose of the Study:
- To investigate the toxicological profiles of mepanipyrim.
- To clarify the species-specific hepatotoxicities of mepanipyrim.
Main Methods:
- Oral administration of mepanipyrim to rats, mice, and dogs for 13 weeks.
- Observation of toxicological effects, particularly hepatotoxicity.
- Analysis of serum lipid concentrations (total cholesterol, triglyceride, phospholipid, non-esterified fatty acid).
Main Results:
- Hepatotoxicity was observed in rats at concentrations >200 ppm, characterized by fatty vacuolation and altered lipid metabolism.
- Mice showed enhanced anisonucleosis at >1,000 ppm.
- Dogs exhibited lipofuscin deposition in Kupffer cells and hepatocytes at >50 mg/kg/day.
- Significant species differences in mepanipyrim-induced hepatotoxicity were evident.
Conclusions:
- Mepanipyrim exhibits dose-dependent hepatotoxicity with distinct species-specific effects.
- Lipid metabolism alterations are a key mechanism of rat hepatotoxicity.
- Further research may be needed to fully elucidate the toxicological impact across species.
