Co-Exposure to SiO2 Nanoparticles and Arsenic Induced Augmentation of Oxidative Stress and Mitochondria-Dependent Apoptosis in Human Cells
Bibliographic Data
| ID | 15496407 |
|---|---|
| Authors | Maqusood Ahamed (0000-0001-6025-1950, King Saud University, corresponding author), Mohd Javed Akhtar (0000-0002-9596-7745, King Saud University), Hisham A Alhadlaq (0000-0002-3073-7025, King Saud University) |
| Year | 2019 |
| Volume | 16 |
| Issue | 17 |
| Pages | 3199-3199 |
| Publication date | 2019-09-01 |
| Open Access | Yes |
| Type | ARTICLE |
| Venue | International Journal of Environmental Research and Public Health (JOURNAL) |
| Journal identifiers | ISSN: 1661-7827 • E-ISSN: 1660-4601 |
| Publisher | Multidisciplinary Digital Publishing Institute (PUBLISHER • CH) |
| DOI | 10.3390/ijerph16173199 |
| PMID | 31480624 |
| OpenAlex | W2970042294 |
| Language | EN |
| Citations received | 1 |
| References cited | 4 |
Widespread application of silica nanoparticles (nSiO 2 ) and ubiquitous metalloid arsenic (As) may increase their chances of co-exposure to human beings in daily life. Nonetheless, studies on combined effects of nSiO 2 and As in human cells are lacking. We investigated the co-exposure effects of nSiO 2 and As in human liver (HepG2) and human fibroblast (HT1080) cells. Results showed that nSiO 2 did not cause cytotoxicity. However, exposure of As caused oxidative stress and apoptosis in both types of cells. Interesting results were that co-exposure of a non-cytotoxic concentration of nSiO 2 significantly augmented the As induced toxicity in both cells. Intracellular level of As was higher in the co-exposure group (nSiO 2 + As) than the As group alone, suggesting that nSiO 2 facilitates the cellular uptake of As. Co-exposure of nSiO 2 and As potentiated oxidative stress indicated by pro-oxidants generation (reactive oxygen species, hydrogen peroxide and lipid peroxidation) and antioxidants depletion (glutathione level, and glutathione reductase, superoxide dismutase and catalase activities). In addition, co-exposure of nSiO 2 and As also potentiated mitochondria-mediated apoptosis suggested by increased expression of p53 , bax , caspase-3 and caspase-9 genes (pro-apoptotic) and decreased expression of bcl-2 gene (anti-apoptotic) along with depleted mitochondrial membrane potential. To the best of our knowledge, this is the first study showing that co-exposure of nSiO 2 and As induced augmentation of oxidative stress and mitochondria-mediated apoptosis in HepG2 and HT1080 cells. Hence, careful attention is required for human health assessment following combined exposure to nSiO 2 and As
Apoptosis · Biology · Catalase · Cell · Cytotoxicity · Enzyme · Glutathione · HT1080 · In vitro · Intracellular · Mitochondrion · Oxidative stress · Reactive oxygen species · Superoxide dismutase · Arsenic contamination and mitigation · Chemistry · Heavy Metal Exposure and Toxicity · Nanoparticles: synthesis and applications · Biochemistry · Cell Biology
| Citations per year | 0.2 |
|---|---|
| Citation span | 2021 - 2021 (1) |
| Highly cited | No |