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Protective effects of curcumin on biochemical and molecular changes in sodium arsenite-induced oxidative damage in
Mehmet Can Perker1, Banu Orta Yilmaz2, Nebahat Yildizbayrak1
1Department of Biology, Institute of Graduate Studies in Sciences, Istanbul University, Istanbul, Turkey.
Abstract:
The present study was aimed at determining the oxidative damage caused by sodium arsenite in 3T3 fibroblast cells and the possible protective role of curcumin (Cur) against sodium arsenite toxicity. Embryonic fibroblast cells were exposed to sodium arsenite (0.01, 0.1, 1, and 10 μM) in the presence and absence of Cur (2.5 μM) for 24 hours. Cell viability, cytotoxicity, lipid peroxidation, hydroxyl radical, hydrogen peroxide, antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase) and expression levels of antioxidant genes (superoxide dismutase, catalase, and glutathione peroxidase) were measured in embryonic fibroblast cells. Results demonstrated that sodium arsenite directly affects antioxidant enzymes and genes in 3T3 embryonic fibroblast cells and induces oxidative damage by increasing the amount of hydrogen peroxide, hydroxyl radical, and lipid peroxidation in the cell. Furthermore, the study indicated that Cur might be a potential ameliorative antioxidant to protect the fibroblast cell toxicity induced by sodium arsenite.
Insights
Sodium arsenite causes oxidative damage in fibroblast cells by increasing harmful compounds. Curcumin may protect these cells from sodium arsenite toxicity, acting as an antioxidant.
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- Oxidative stress is implicated in various cellular dysfunctions.
- Sodium arsenite is a known environmental toxin that can induce cellular damage.
- Antioxidants play a crucial role in mitigating oxidative stress.
Purpose of the Study:
- To investigate the oxidative damage induced by sodium arsenite in 3T3 fibroblast cells.
- To evaluate the potential protective effects of curcumin against sodium arsenite toxicity.
- To understand the impact of sodium arsenite on antioxidant enzymes and gene expression.
Main Methods:
- 3T3 fibroblast cells were exposed to varying concentrations of sodium arsenite (0.01–10 μM) with or without curcumin (2.5 μM) for 24 hours.
- Assessed cell viability, cytotoxicity, lipid peroxidation, hydroxyl radical, and hydrogen peroxide levels.
- Measured the activity and gene expression of key antioxidant enzymes: superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase.
Main Results:
- Sodium arsenite exposure led to increased lipid peroxidation, hydroxyl radical, and hydrogen peroxide levels, indicating significant oxidative damage.
- The expression and activity of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) were negatively affected by sodium arsenite.
- Curcumin treatment demonstrated a protective effect, reducing the oxidative damage markers and ameliorating cytotoxicity induced by sodium arsenite.
Conclusions:
- Sodium arsenite induces oxidative damage and impairs antioxidant defense mechanisms in 3T3 fibroblast cells.
- Curcumin exhibits potential as an antioxidant agent to protect against sodium arsenite-induced cellular toxicity.
- These findings highlight the therapeutic potential of curcumin in combating arsenite poisoning.
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