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Metformin ameliorates cardiopulmonary toxicity induced by chlorpyrifos
Ramtin Farhadi1,2, Marzieh Daniali1,2, Maryam Baeeri1,2
1Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences (TUMS), Tehran, Iran.
Abstract:
Chlorpyrifos (CPF) is a widely used pesticide that can impair body organs. Nonetheless, metformin is known for its protective role against dysfunction at cellular and molecular levels led by inflammatory and oxidative stress. This study aimed to investigate the modulatory impacts of metformin on CPF-induced heart and lung damage. Following the treatment of Wistar rats with different combinations of metformin and CPF, plasma, as well as heart and lung tissues, were isolated to examine the level of oxidative stress biomarkers like reactive oxygen species (ROS) and malondialdehyde (MDA), inflammatory cytokines such as tumor necrosis alpha (TNF-α), high mobility group box 1 (HMGB1) gene, deoxyribonucleic acid (DNA) damage, lactate, ADP/ATP ratio, expression of relevant genes (TRADD, TERT, KL), and along with histological analysis. Based on the findings, metformin significantly modulates the impairments in heart and lung tissues induced by CPF.
Insights
Metformin protects against chlorpyrifos (CPF) pesticide-induced heart and lung damage by reducing oxidative stress and inflammation. This study shows metformin
Area of Science:
- Toxicology and Pharmacology
- Cardiovascular and Respiratory Research
Background:
- Chlorpyrifos (CPF) is a widely used organophosphate pesticide with known organ-damaging effects.
- Metformin exhibits protective properties against cellular dysfunction induced by oxidative stress and inflammation.
Purpose of the Study:
- To investigate the protective effects of metformin on chlorpyrifos-induced damage in the heart and lungs.
- To elucidate the mechanisms underlying metformin's modulatory impact on CPF toxicity.
Main Methods:
- Wistar rats were treated with varying doses of metformin and CPF.
- Analysis included oxidative stress biomarkers (ROS, MDA), inflammatory cytokines (TNF-α), HMGB1 gene expression, DNA damage, lactate levels, ADP/ATP ratio, gene expression (TRADD, TERT, KL), and histological examination of heart and lung tissues.
Main Results:
- Metformin significantly mitigated CPF-induced impairments in heart and lung tissues.
- The protective effects involved modulation of oxidative stress, inflammation, and DNA damage markers.
Conclusions:
- Metformin demonstrates significant protective potential against chlorpyrifos-induced cardiorespiratory toxicity.
- Metformin may serve as a therapeutic agent to counteract pesticide-induced organ damage.
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