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Antioxidative defense against omeprazole-induced toxicogenetical effects in Swiss mice
Antonio Lima Braga1,2, Patrícia Bastos do Nascimento1, Márcia Fernanda Correia Jardim Paz1,2
1Laboratory of Genetics and Toxicology (LAPGENIC), Federal University of Piauí, 64.049-550, Teresina, Piauí, Brazil.
Background:
Omeprazole (OME), a most frequently used proton pump inhibitor in gastric acidosis, is evident to show many adverse effects, including genetic instability. This study evaluated toxicogenic effects of OME in Mus musculus.
Methods:
For this study, 40 male Swiss mice were divided into 8 groups (n = 5) and treated with OME at doses of 10, 20, and 40 mg/kg and/or treated with the antioxidants retinol palmitate (100 IU/kg) and ascorbic acid (2.0 μM/kg). Cyclophosphamide 50 mg/kg, (cytotoxic agent) and the vehicle were served as positive and negative control group, respectively. After 14 days of treatment, the stomach cells along with the bone marrow and peripheral blood lymphocytes were collected and submitted to the comet assay (alkaline version) and micronucleus test. Additionally, hematological and biochemical parameters of the animals were also determined inspect of vehicle group.
Results:
The results suggest that OME at all doses induced genotoxicity and mutagenicity in the treated cells. However, in association with the antioxidants, these effects were modulated and/or inhibited along with a DNA repair capacity.
Conclusions:
Taken together, antioxidants (such as retinol palmitate and ascorbic acid) may be one of the best options to counteract OME-induced cytogenetic instability.
Insights
Omeprazole (OME) causes genetic damage in mice, but antioxidants like retinol palmitate and ascorbic acid can protect against these toxic effects. This highlights potential strategies to mitigate OME-induced genotoxicity.
Area of Science:
- Toxicology
- Genetics
- Pharmacology
Background:
- Omeprazole (OME), a widely used proton pump inhibitor for gastric acidosis, is associated with adverse effects, including genetic instability.
- This study investigates the toxicogenic effects of OME in a mouse model (Mus musculus).
Purpose of the Study:
- To evaluate the toxicogenic and genotoxic effects of omeprazole in mice.
- To assess the potential protective role of antioxidants against omeprazole-induced genetic damage.
Main Methods:
- 40 male Swiss mice were divided into 8 groups and treated with OME (10, 20, 40 mg/kg) and/or antioxidants (retinol palmitate, ascorbic acid).
- Cytotoxic agent (cyclophosphamide) and vehicle served as positive and negative controls.
- Comet assay and micronucleus test were performed on stomach cells, bone marrow, and lymphocytes after 14 days.
- Hematological and biochemical parameters were also analyzed.
Main Results:
- Omeprazole administration induced significant genotoxicity and mutagenicity in all treated groups.
- Co-administration with antioxidants modulated and/or inhibited OME-induced genotoxic effects.
- Evidence of enhanced DNA repair capacity was observed in the presence of antioxidants.
Conclusions:
- Antioxidants, specifically retinol palmitate and ascorbic acid, demonstrate potential in counteracting omeprazole-induced cytogenetic instability.
- These findings suggest a promising therapeutic strategy for mitigating the adverse genetic effects of omeprazole.
