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Role of geraniol against lead acetate-mediated hepatic damage and their interaction with liver carboxylesterase activity in rats
30
Citations
55
References
2017
Year
Lipid PeroxidationLead Acetate GroupExperimental PharmacologyOxidative StressLiver Carboxylesterase ActivityToxicologyHepatotoxicityHealth SciencesLiver PhysiologyLead AcetateMetabolomicsExperimental ToxicologyPharmacologyDrug-induced Liver InjuryHepatologyLead Acetate CausesPhysiologyHerb-drug InteractionMedicine
In this study, the effect of geraniol (50 mg/kg for 30 d), a natural antioxidant and repellent/antifeedant monoterpene, in a rat model of lead acetate-induced (500 ppm for 30 d) liver damage was evaluated. Hepatic malondialdehyde increased in the lead acetate group. Reduced glutathione unchanged, but glutathione S-transferase, glutathione reductase, as well as carboxylesterase activities decreased in geraniol, lead acetate and geraniol + lead acetate groups. 8-OhDG immunoreactivity, mononuclear cell infiltrations and hepatic lead concentration were lower in the geraniol + lead acetate group than the lead acetate group. Serum aspartate aminotransferase and alanine aminotransferase activities increased in the Pb acetate group. In conclusion, lead acetate causes oxidative and toxic damage in the liver and this effect can reduce with geraniol treatment. However, we first observed that lead acetate, as well as geraniol, can affect liver carboxylesterase activity.
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