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Oxidative stress in mice treated with antileishmanial meglumine antimoniate
D B Bento1, B de Souza, A V Steckert
1Laboratório de Biologia Celular e Molecular, Unidade Acadêmica de Ciências da Saúde, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
Abstract:
In order to improve the understanding of the toxicity of pentavalent antimony (Sb(V)), we investigated the acute effects of meglumine antimoniate (MA) on the oxidative stress in heart, liver, kidney, spleen and brain tissue of mice. Levels of lipoperoxidation and protein carbonylation were measured to evaluate the oxidative status, whereas superoxide dismutase/catalase activity and glutathione levels were recorded to examine the antioxidative status. We observed that MA caused significant protein carbonylation in the heart, spleen and brain tissue. Increased lipoperoxidation was found in the liver and brain tissue. An imbalance between superoxide dismutase and catalase activities could be observed in heart, liver, spleen and brain tissue. Our results suggest that MA causes oxidative stress in several vital organs of mice. This indicates that the production of highly reactive oxygen and nitrogen species induced by MA might be involved in some of its toxic adverse effects.
Insights
Meglumine antimoniate (MA) induces oxidative stress in mice, causing damage to vital organs like the heart, liver, and brain. This research highlights the role of reactive oxygen species in MA toxicity.
Area of Science:
- Toxicology
- Biochemistry
- Pharmacology
Background:
- Pentavalent antimony (Sb(V)) compounds are used to treat leishmaniasis.
- Understanding the toxicity of Sb(V) is crucial for patient safety.
- Oxidative stress is a potential mechanism underlying drug toxicity.
Purpose of the Study:
- To investigate the acute effects of meglumine antimoniate (MA) on oxidative and antioxidative status in mice.
- To determine the specific organs affected by MA-induced oxidative stress.
- To elucidate the role of reactive oxygen species in MA's adverse effects.
Main Methods:
- Mice were treated with MA.
- Lipoperoxidation and protein carbonylation levels were measured in heart, liver, kidney, spleen, and brain tissues.
- Superoxide dismutase (SOD) and catalase (CAT) activities, along with glutathione (GSH) levels, were assessed.
Main Results:
- MA caused significant protein carbonylation in the heart, spleen, and brain.
- Increased lipoperoxidation was observed in the liver and brain tissues.
- An imbalance in SOD/CAT activities was noted in the heart, liver, spleen, and brain.
Conclusions:
- Meglumine antimoniate induces significant oxidative stress in multiple vital organs of mice.
- The findings suggest that MA-induced oxidative stress, potentially mediated by reactive oxygen and nitrogen species, contributes to its toxic adverse effects.
- This study provides insights into the mechanisms of MA toxicity, relevant for therapeutic use and risk assessment.
