Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial Cells
A review of recent literature suggests that bismuth oxide (Bi<sub>2</sub>O<sub>3</sub>, referred to as B in this article) nanoparticles (NPs) elicit an appreciable response only after a concentration above 40–50 µg/mL in different cells all having an epithelial origin, to the...
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MDPI AG
2023-04-01
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| Series: | Toxics |
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| Online Access: | https://www.mdpi.com/2305-6304/11/4/343 |
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| author | Mohd Javed Akhtar Maqusood Ahamed Hisham Alhadlaq |
| author_facet | Mohd Javed Akhtar Maqusood Ahamed Hisham Alhadlaq |
| author_sort | Mohd Javed Akhtar |
| collection | DOAJ |
| description | A review of recent literature suggests that bismuth oxide (Bi<sub>2</sub>O<sub>3</sub>, referred to as B in this article) nanoparticles (NPs) elicit an appreciable response only after a concentration above 40–50 µg/mL in different cells all having an epithelial origin, to the best of our knowledge. Here, we report the toxicological profile of Bi<sub>2</sub>O<sub>3</sub> NPs (or BNPs) (71 ± 20 nm) in a human endothelial cell (HUVE cell line) in which BNPs exerted much steeper cytotoxicity. In contrast to a high concentration of BNPs (40–50 µg/mL) required to stimulate an appreciable toxicity in epithelial cells, BNPs induced 50% cytotoxicity in HUVE cells at a very low concentration (6.7 µg/mL) when treated for 24 h. BNPs induced reactive oxygen species (ROS), lipid peroxidation (LPO), and depletion of the intracellular antioxidant glutathione (GSH). BNPs also induced nitric oxide (NO,) which can result in the formation of more harmful species in a fast reaction that occurs with superoxide (O<sub>2</sub><sup>•−</sup>). Exogenously applied antioxidants revealed that NAC (intracellular GSH precursor) was more effective than Tiron (a preferential scavenger of mitochondrial O<sub>2</sub><sup>•−</sup>) in preventing the toxicity, indicating ROS production is extra-mitochondrial. Mitochondrial membrane potential (MMP) loss mediated by BNPs was significantly less than that of exogenously applied oxidant H<sub>2</sub>O<sub>2</sub>, and MMP loss was not as intensely reduced by either of the antioxidants (NAC and Tiron), again suggesting BNP-mediated toxicity in HUVE cells is extra-mitochondrial. When we compared the inhibitory capacities of the two antioxidants on different parameters of this study, ROS, LPO, and GSH were among the strongly inhibited biomarkers, whereas MMP and NO were the least inhibited group. This study warrants further research regarding BNPs, which may have promising potential in cancer therapy, especially via angiogenesis modulation. |
| first_indexed | 2024-03-11T04:28:24Z |
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| institution | Directory Open Access Journal |
| issn | 2305-6304 |
| language | English |
| last_indexed | 2024-03-11T04:28:24Z |
| publishDate | 2023-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Toxics |
| spelling | doaj.art-bded3160c8fb4280a2ba5eedfd83cb912023-11-17T21:37:32ZengMDPI AGToxics2305-63042023-04-0111434310.3390/toxics11040343Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial CellsMohd Javed Akhtar0Maqusood Ahamed1Hisham Alhadlaq2King Abdullah Institute for Nanotechnology, King Saud University, Riyadh 11451, Saudi ArabiaKing Abdullah Institute for Nanotechnology, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Physics and Astronomy, College of Sciences, King Saud University, Riyadh 11451, Saudi ArabiaA review of recent literature suggests that bismuth oxide (Bi<sub>2</sub>O<sub>3</sub>, referred to as B in this article) nanoparticles (NPs) elicit an appreciable response only after a concentration above 40–50 µg/mL in different cells all having an epithelial origin, to the best of our knowledge. Here, we report the toxicological profile of Bi<sub>2</sub>O<sub>3</sub> NPs (or BNPs) (71 ± 20 nm) in a human endothelial cell (HUVE cell line) in which BNPs exerted much steeper cytotoxicity. In contrast to a high concentration of BNPs (40–50 µg/mL) required to stimulate an appreciable toxicity in epithelial cells, BNPs induced 50% cytotoxicity in HUVE cells at a very low concentration (6.7 µg/mL) when treated for 24 h. BNPs induced reactive oxygen species (ROS), lipid peroxidation (LPO), and depletion of the intracellular antioxidant glutathione (GSH). BNPs also induced nitric oxide (NO,) which can result in the formation of more harmful species in a fast reaction that occurs with superoxide (O<sub>2</sub><sup>•−</sup>). Exogenously applied antioxidants revealed that NAC (intracellular GSH precursor) was more effective than Tiron (a preferential scavenger of mitochondrial O<sub>2</sub><sup>•−</sup>) in preventing the toxicity, indicating ROS production is extra-mitochondrial. Mitochondrial membrane potential (MMP) loss mediated by BNPs was significantly less than that of exogenously applied oxidant H<sub>2</sub>O<sub>2</sub>, and MMP loss was not as intensely reduced by either of the antioxidants (NAC and Tiron), again suggesting BNP-mediated toxicity in HUVE cells is extra-mitochondrial. When we compared the inhibitory capacities of the two antioxidants on different parameters of this study, ROS, LPO, and GSH were among the strongly inhibited biomarkers, whereas MMP and NO were the least inhibited group. This study warrants further research regarding BNPs, which may have promising potential in cancer therapy, especially via angiogenesis modulation.https://www.mdpi.com/2305-6304/11/4/343endothelial cellsoxidative stressanti-angiogenic potentialcancer therapy |
| spellingShingle | Mohd Javed Akhtar Maqusood Ahamed Hisham Alhadlaq Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial Cells Toxics endothelial cells oxidative stress anti-angiogenic potential cancer therapy |
| title | Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial Cells |
| title_full | Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial Cells |
| title_fullStr | Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial Cells |
| title_full_unstemmed | Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial Cells |
| title_short | Bismuth Oxide (Bi<sub>2</sub>O<sub>3</sub>) Nanoparticles Cause Selective Toxicity in a Human Endothelial (HUVE) Cell Line Compared to Epithelial Cells |
| title_sort | bismuth oxide bi sub 2 sub o sub 3 sub nanoparticles cause selective toxicity in a human endothelial huve cell line compared to epithelial cells |
| topic | endothelial cells oxidative stress anti-angiogenic potential cancer therapy |
| url | https://www.mdpi.com/2305-6304/11/4/343 |
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