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Time-dependent oxidative stress caused by benznidazole
R C Pedrosa1, A F De Bem, C Locatelli
1Department of Biochemistry, Federal University of Santa Catarina, Florianópolis, Brazil. roza@mbox1.ufsc.br
Redox Report : Communications in Free Radical Research
|October 20, 2001
Summary
Benznidazole (BZN) treatment for Chagas
Area of Science:
- Biochemistry
- Pharmacology
- Toxicology
Background:
- Benznidazole (BZN) is a key trypanocide for Chagas' disease treatment.
- BZN's mechanism is partly attributed to inducing oxidative stress in parasites.
- Imidazolic compounds are known to generate reactive oxygen species (ROS).
Purpose of the Study:
- To investigate the impact of BZN on ROS production.
- To assess the effect of BZN on the host's antioxidant status.
- To evaluate BZN's hepatotoxicity through oxidative stress biomarkers.
Main Methods:
- Male rats were administered 40 mg BZN/kg body weight for 2, 4, 6, 10, and 30 days.
- Hepatic homogenates were analyzed for biomarkers: CAT, SOD, GST, GR, TBARS, GSH, TG, and GSSG.
- Concentrations and activities of these biomarkers were measured to assess oxidative stress.
Main Results:
- BZN induced tissue damage, evidenced by increased TBARS, up to day 10.
- GST activity was inhibited, while CAT and GR activities showed dynamic changes.
- GSH levels initially decreased but increased by day 30; GSSG levels were elevated.
Conclusions:
- Therapeutic doses of BZN induce significant oxidative stress in rat hepatocytes.
- BZN alters antioxidant enzyme activities and glutathione status in a time-dependent manner.
- The study highlights BZN's potential hepatotoxic effects via oxidative mechanisms.