TY - JOUR
T1 - Mitochondrial Dysfunction Induced by Zinc Oxide Nanoparticles
AU - Patrón-Romero, Leslie
AU - Luque-Morales, Priscy Alfredo
AU - Loera-Castañeda, Verónica
AU - Lares-Asseff, Ismael
AU - Leal-Ávila, María Ángeles
AU - Alvelais-Palacios, Jorge Arturo
AU - Plasencia-López, Ismael
AU - Almanza-Reyes, Horacio
N1 - Publisher Copyright:
© 2022 by the authors.
PY - 2022/8
Y1 - 2022/8
N2 - 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 [Zn2+] 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.
AB - 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 [Zn2+] 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.
KW - apoptosis
KW - mitochondria
KW - nanoparticles
KW - zinc oxide
UR - http://www.scopus.com/inward/record.url?scp=85137387852&partnerID=8YFLogxK
U2 - 10.3390/cryst12081089
DO - 10.3390/cryst12081089
M3 - Artículo de revisión
AN - SCOPUS:85137387852
SN - 2073-4352
VL - 12
JO - Crystals
JF - Crystals
IS - 8
M1 - 1089
ER -