Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles
The constant evolution and applications of metallic nanoparticles (NPs) make living organisms more susceptible to being exposed to them. Among the most used are zinc oxide nanoparticles (ZnO-NPs). Therefore, understanding the molecular effects of ZnO-NPs in biological systems is extremely important....
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-08-01
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| Series: | Crystals |
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| Online Access: | https://www.mdpi.com/2073-4352/12/8/1089 |
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| author | Leslie Patrón-Romero Priscy Alfredo Luque-Morales Verónica Loera-Castañeda Ismael Lares-Asseff María Ángeles Leal-Ávila Jorge Arturo Alvelais-Palacios Ismael Plasencia-López Horacio Almanza-Reyes |
| author_facet | Leslie Patrón-Romero Priscy Alfredo Luque-Morales Verónica Loera-Castañeda Ismael Lares-Asseff María Ángeles Leal-Ávila Jorge Arturo Alvelais-Palacios Ismael Plasencia-López Horacio Almanza-Reyes |
| author_sort | Leslie Patrón-Romero |
| collection | DOAJ |
| description | The constant evolution and applications of metallic nanoparticles (NPs) make living organisms more susceptible to being exposed to them. Among the most used are zinc oxide nanoparticles (ZnO-NPs). Therefore, understanding the molecular effects of ZnO-NPs in biological systems is extremely important. This review compiles the main mechanisms that induce cell toxicity by exposure to ZnO-NPs and reported in vitro research models, with special attention to mitochondrial damage. Scientific evidence indicates that in vitro ZnO-NPs have a cytotoxic effect that depends on the size, shape and method of synthesis of ZnO-NPs, as well as the function of the cells to which they are exposed. ZnO-NPs come into contact with the extracellular region, leading to an increase in intracellular [Zn<sup>2+</sup>] levels. The mechanism by which intracellular ZnO-NPs come into contact with organelles such as mitochondria is still unclear. The mitochondrion is a unique organelle considered the “power station” in the cells, participates in numerous cellular processes, such as cell survival/death, multiple biochemical and metabolic processes, and holds genetic material. ZnO-NPs increase intracellular levels of reactive oxygen species (ROS) and, in particular, superoxide levels; they also decrease mitochondrial membrane potential (MMP), which affects membrane permeability and leads to cell death. ZnO-NPs also induced cell death through caspases, which involve the intrinsic apoptotic pathway. The expression of pro-apoptotic genes after exposure to ZnO-NPs can be affected by multiple factors, including the size and morphology of the NPs, the type of cell exposed (healthy or tumor), stage of development (embryonic or differentiated), energy demand, exposure time and, no less relevant, the dose. To prevent the release of pro-apoptotic proteins, the damaged mitochondrion is eliminated by mitophagy. To replace those mitochondria that underwent mitophagy, the processes of mitochondrial biogenesis ensure the maintenance of adequate levels of ATP and cellular homeostasis. |
| first_indexed | 2024-03-09T13:36:59Z |
| format | Article |
| id | doaj.art-5779695c695d486da8fa23b78a486de3 |
| institution | Directory Open Access Journal |
| issn | 2073-4352 |
| language | English |
| last_indexed | 2024-03-09T13:36:59Z |
| publishDate | 2022-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Crystals |
| spelling | doaj.art-5779695c695d486da8fa23b78a486de32023-11-30T21:10:38ZengMDPI AGCrystals2073-43522022-08-01128108910.3390/cryst12081089Mitochondrial Dysfunction Induced by Zinc Oxide NanoparticlesLeslie Patrón-Romero0Priscy Alfredo Luque-Morales1Verónica Loera-Castañeda2Ismael Lares-Asseff3María Ángeles Leal-Ávila4Jorge Arturo Alvelais-Palacios5Ismael Plasencia-López6Horacio Almanza-Reyes7Faculty of Medicine and Psychology, Autonomous University of Baja California, Tijuana 22390, Baja California, MexicoFaculty of Engineering, Architecture and Design, Autonomous University of Baja California, Ensenada 22860, Baja California, MexicoInstituto Politécnico Nacional, CIIDIR-Unidad Durango, Durango 34220, Durango, MexicoInstituto Politécnico Nacional, CIIDIR-Unidad Durango, Durango 34220, Durango, MexicoUniversity Center for Health Education, Autonomous University of Baja California, Tijuana 22010, Baja California, MexicoSchool of Health Sciences, Valle de Las Palmas, Autonomous University of Baja California, Tijuana 22260, Baja California, MexicoFaculty of Accounting and Administration, Autonomous University of Baja California, Tijuana 22390, Baja California, MexicoFaculty of Medicine and Psychology, Autonomous University of Baja California, Tijuana 22390, Baja California, MexicoThe constant evolution and applications of metallic nanoparticles (NPs) make living organisms more susceptible to being exposed to them. Among the most used are zinc oxide nanoparticles (ZnO-NPs). Therefore, understanding the molecular effects of ZnO-NPs in biological systems is extremely important. This review compiles the main mechanisms that induce cell toxicity by exposure to ZnO-NPs and reported in vitro research models, with special attention to mitochondrial damage. Scientific evidence indicates that in vitro ZnO-NPs have a cytotoxic effect that depends on the size, shape and method of synthesis of ZnO-NPs, as well as the function of the cells to which they are exposed. ZnO-NPs come into contact with the extracellular region, leading to an increase in intracellular [Zn<sup>2+</sup>] levels. The mechanism by which intracellular ZnO-NPs come into contact with organelles such as mitochondria is still unclear. The mitochondrion is a unique organelle considered the “power station” in the cells, participates in numerous cellular processes, such as cell survival/death, multiple biochemical and metabolic processes, and holds genetic material. ZnO-NPs increase intracellular levels of reactive oxygen species (ROS) and, in particular, superoxide levels; they also decrease mitochondrial membrane potential (MMP), which affects membrane permeability and leads to cell death. ZnO-NPs also induced cell death through caspases, which involve the intrinsic apoptotic pathway. The expression of pro-apoptotic genes after exposure to ZnO-NPs can be affected by multiple factors, including the size and morphology of the NPs, the type of cell exposed (healthy or tumor), stage of development (embryonic or differentiated), energy demand, exposure time and, no less relevant, the dose. To prevent the release of pro-apoptotic proteins, the damaged mitochondrion is eliminated by mitophagy. To replace those mitochondria that underwent mitophagy, the processes of mitochondrial biogenesis ensure the maintenance of adequate levels of ATP and cellular homeostasis.https://www.mdpi.com/2073-4352/12/8/1089mitochondriaapoptosiszinc oxidenanoparticles |
| spellingShingle | Leslie Patrón-Romero Priscy Alfredo Luque-Morales Verónica Loera-Castañeda Ismael Lares-Asseff María Ángeles Leal-Ávila Jorge Arturo Alvelais-Palacios Ismael Plasencia-López Horacio Almanza-Reyes Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles Crystals mitochondria apoptosis zinc oxide nanoparticles |
| title | Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles |
| title_full | Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles |
| title_fullStr | Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles |
| title_full_unstemmed | Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles |
| title_short | Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles |
| title_sort | mitochondrial dysfunction induced by zinc oxide nanoparticles |
| topic | mitochondria apoptosis zinc oxide nanoparticles |
| url | https://www.mdpi.com/2073-4352/12/8/1089 |
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