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Antioxidants and mitochondrial/lysosomal protective agents reverse toxicity induced by titanium dioxide nanoparticles
Evelyn Assadian1, Zhaleh Jamali2,3, Ahmad Salimi4,5
1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Most of the literature has focused on titanium dioxide (TiO2) nanoparticles (NPs) toxicity, showing the importance of oxidative stress, mitochondrial dysfunction, and cell death in TiO2-induced toxicity. For this purpose, in the current study, we investigated the protective role of antioxidant and mitochondrial/lysosomal protective agents to minimize TiO2 NPs-induced toxicity in human lymphocytes. Human lymphocytes were obtained from heathy individuals and treated with different concentrations (80, 160, and 320 µg/mL) of TiO2 NPs, and then human lymphocytes preincubated with butylated hydroxytoluene (BHT), cyclosporin A (CsA), and chloroquine separately were exposed to TiO2 NPs for 6 h. In all the above-mentioned treated groups, adverse parameters such as cytotoxicity, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), lysosomal membrane destabilization, the levels of malondialdehyde (MDA), and glutathione (GSH) were measured. The results showed that TiO2 nanoparticles induced cytotoxicity through ROS formation, MMP collapse, lysosomal damages, depletion of GSH, and lipid peroxidation. However, BHT as an antioxidant, CsA as a mitochondrial permeability transition (MPT) pore sealing agent, and chloroquine as a lysosomotropic agent, significantly inhibited all the TiO2 NPs-induced cellular and organelle toxicities. Thus, it seems that antioxidant and mitochondrial/lysosomal protective agents are promising preventive strategies against TiO2 NPs-induced toxicity.
Insights
Titanium dioxide nanoparticles (TiO2 NPs) cause cell damage via oxidative stress. Antioxidant and protective agents like BHT, CsA, and chloroquine effectively prevented TiO2 NP-induced toxicity in human lymphocytes.
Area of Science:
- Nanomaterial toxicology
- Cellular toxicology
- Biomedical science
Background:
- Titanium dioxide nanoparticles (TiO2 NPs) are widely used, but their toxicity is a concern.
- TiO2 NP toxicity mechanisms involve oxidative stress, mitochondrial dysfunction, and cell death.
Purpose of the Study:
- To investigate the protective effects of antioxidant and mitochondrial/lysosomal agents against TiO2 NP toxicity.
- To evaluate the efficacy of butylated hydroxytoluene (BHT), cyclosporin A (CsA), and chloroquine in mitigating TiO2 NP-induced damage in human lymphocytes.
Main Methods:
- Human lymphocytes were exposed to varying concentrations of TiO2 NPs.
- Cells were pre-incubated with BHT, CsA, or chloroquine before TiO2 NP exposure.
- Assessed cytotoxicity, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), lysosomal stability, malondialdehyde (MDA), and glutathione (GSH) levels.
Main Results:
- TiO2 NPs induced cytotoxicity by increasing ROS, collapsing MMP, damaging lysosomes, depleting GSH, and causing lipid peroxidation.
- BHT, CsA, and chloroquine significantly inhibited these TiO2 NP-induced toxic effects.
- These agents demonstrated protective roles against cellular and organelle damage.
Conclusions:
- Antioxidant and mitochondrial/lysosomal protective agents show promise in preventing TiO2 NP toxicity.
- Targeting oxidative stress and organelle dysfunction can mitigate nanoparticle-induced cellular damage.
- These findings suggest potential therapeutic strategies against TiO2 NP exposure.
