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Liver damage induced in rats by malathion impurities
S Keadtisuke1, W Dheranetra, T Nakatsugawa
1Department of Entomology, University of California, Riverside.
Toxicology Letters
|June 1, 1990
Summary
Malathion impurities O,O,S-trimethyl phosphorothioate and O,S,S-trimethyl phosphorodithioate cause blood clotting disorders and increase beta-glucuronidase levels in rats. The liver endoplasmic reticulum releases this enzyme, with piperonyl butoxide reducing its blood levels.
Area of Science:
- Toxicology
- Biochemistry
- Pharmacology
Background:
- Malathion impurities can exhibit significant toxicity.
- Understanding the toxicological mechanisms of these impurities is crucial for risk assessment.
Purpose of the Study:
- To investigate the hemostatic effects and beta-glucuronidase release induced by malathion impurities O,O,S-trimethyl phosphorothioate (OOS-Me) and O,S,S-trimethyl phosphorodithioate (OSS-Me).
- To identify the source of elevated beta-glucuronidase and evaluate potential modulators of toxicity.
Main Methods:
- Oral administration of OOS-Me and OSS-Me to rats.
- Assessment of blood clotting parameters (prothrombin time, thrombin time).
- Measurement of serum beta-glucuronidase levels using isoelectrofocusing electrophoresis.
- Co-treatment and pre-treatment studies with O,O,O-trimethyl phosphorothioate (OOO-Me) and piperonyl butoxide.
Main Results:
- OOS-Me and OSS-Me induced hemostatic disorders, including prolonged clotting times and deficiencies in coagulation Factors II, V, and VII.
- A dose-dependent increase in serum beta-glucuronidase was observed, with peak elevations of 15-fold (OOS-Me) and 31-fold (OSS-Me).
- The liver endoplasmic reticulum was identified as the source of released beta-glucuronidase. OOO-Me did not affect enzyme levels, while piperonyl butoxide reduced them.
Conclusions:
- Malathion impurities OOS-Me and OSS-Me possess significant toxicological potential, affecting hemostasis and causing beta-glucuronidase release from the liver.
- Piperonyl butoxide demonstrates a protective effect by reducing beta-glucuronidase levels, suggesting a role in modulating the toxicity of these compounds.
