Involvement of oxidative stress in ZnO NPs-induced apoptosis and autophagy of mouse GC-1 spg cells

Yang, Dan; Zhang, Meijuan; Gan, Yu; Yang, Si Kyung; Wang, Jinglei; Yu, Mei; Wei, Jie; Chen, Jiaxiang

doi:10.1016/j.ecoenv.2020.110960

Cited by 33 publications

(21 citation statements)

References 42 publications

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“…In this respect, a wide variety of ZnO nanostructures can be prepared by monitoring the growth rates along those orientations [45][46][47][48]. The resulting nZnO show distinct biomedical activity, cytotoxicity, and application [49][50][51][52][53][54][55][56]. For instance, ZnO quantum dots can be employed as imaging nanoprobes for targeting cancer cells in vitro [51].…”

Section: Lattice Structurementioning

confidence: 99%

“…The ROS production due to intracellular ZnO NPs can further induce ER oxidative stress, leading to final cell death ( Figure 16a) [50,123]. The generation of ROS and oxidative stress in mammalian cells due to intracellular ZnO NPs can also induce autophagy [49]. Sharma et al indicated that the ROS generation resulting from ZnO NPs penetration leads to a decrease in mitochondrial membrane potential (MMP; ∆Ψm), upregulation of Bcl2-associated X protein (Bax) and down regulation of Bcl2 expressions, resulting in mitochondrial mediated apoptosis.…”

Section: Cytotoxicitymentioning

confidence: 99%

“…In the case of reproductive system, ZnO NPs induced significant cytotoxicity, apoptosis, and autophagy in murine Leydic, Sertoli and GC-1 spg cells [49,143,146]. Shen et al reported that ZnO NPs (30 nm) had adverse effects in Leydic cells by activating autophagy and apoptosis via oxidative stress generation [146].…”

Section: Normal Cellsmentioning

confidence: 99%

“…Yang et al indicated that ZnO NPs also induced autophagy and apoptosis in mouse-derived spermatogonial cells (GC-1 spg) due to the generation of ROS and induction of oxidative stress. The malondialdehyde (MDA) level in the ZnO NPs-treated cells was markedly increased, while the GSH and antioxidant superoxide dismutase (SOD) levels were decreased significantly, showing the oxidative effect [49]. Thus, autophagy was activated during stress conditions, facilitating the degradation of cellular components by the vacuoles or lysosomes.…”

Section: Normal Cellsmentioning

confidence: 99%

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Interactions of Zinc Oxide Nanostructures with Mammalian Cells: Cytotoxicity and Photocatalytic Toxicity

Liao

Jin

et al. 2020

IJMS

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This article presents a state-of-the-art review and analysis of literature studies on the morphological structure, fabrication, cytotoxicity, and photocatalytic toxicity of zinc oxide nanostructures (nZnO) of mammalian cells. nZnO with different morphologies, e.g., quantum dots, nanoparticles, nanorods, and nanotetrapods are toxic to a wide variety of mammalian cell lines due to in vitro cell–material interactions. Several mechanisms responsible for in vitro cytotoxicity have been proposed. These include the penetration of nZnO into the cytoplasm, generating reactive oxygen species (ROS) that degrade mitochondrial function, induce endoplasmic reticulum stress, and damage deoxyribonucleic acid (DNA), lipid, and protein molecules. Otherwise, nZnO dissolve extracellularly into zinc ions and the subsequent diffusion of ions into the cytoplasm can create ROS. Furthermore, internalization of nZnO and localization in acidic lysosomes result in their dissolution into zinc ions, producing ROS too in cytoplasm. These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions. In vivo studies on a mouse model reveal the adverse impacts of nZnO on internal organs through different administration routes. The administration of ZnO nanoparticles into mice via intraperitoneal instillation and intravenous injection facilitates their accumulation in target organs, such as the liver, spleen, and lung. ZnO is a semiconductor with a large bandgap showing photocatalytic behavior under ultraviolet (UV) light irradiation. As such, photogenerated electron–hole pairs react with adsorbed oxygen and water molecules to produce ROS. So, the ROS-mediated selective killing for human tumor cells is beneficial for cancer treatment in photodynamic therapy. The photoinduced effects of noble metal doped nZnO for creating ROS under UV and visible light for killing cancer cells are also addressed.

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Section: Lattice Structurementioning

confidence: 99%

Section: Cytotoxicitymentioning

confidence: 99%

Section: Normal Cellsmentioning

confidence: 99%

Section: Normal Cellsmentioning

confidence: 99%

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Interactions of Zinc Oxide Nanostructures with Mammalian Cells: Cytotoxicity and Photocatalytic Toxicity

Liao

Jin

et al. 2020

IJMS

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“…Elevated levels of intracellular oxidative stress are one of the major causes of cellular autophagy. Yang et al (38) found that the level of oxidative stress was remarkably elevated in gastric cancer cells of mouse after treatment with ZnO nanoparticles, along with a significant increase in intracellular autophagic vesicles, leading to an elevated level of cellular autophagy and even inducing apoptosis in cancer cells. Besides, it has also been revealed that drugs such as Oxaliplatin induce apoptosis in cancer cells by increasing the level of cellular autophagy (39).…”

Section: Discussionmentioning

confidence: 99%

A Study on Mesoporous Silica Loaded With Novel Photosensitizers HCE6 and Oxaliplatin for the Treatment of Cholangiocarcinoma

Zhang

Liu

Fan³

et al. 2021

Front. Oncol.

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PurposeCholangiocarcinoma (CCA) is a malignant tumor with a high incidence. The therapeutic effect of conventional chemotherapy and radiotherapy is not obvious. Photodynamic therapy (PDT) is an ideal modality to fight cancer, and the nature of photosensitizer limits its application in clinical therapy. The aim of this study was to explore a novel mode of drug delivery for the intervention of bile duct cancer.MethodsOxaliplatin and photosensitizer HCE6 were loaded with mesoporous silica nanoparticles (MSNs) to synthesize Oxaliplatin/HCE6-MSNs (OH-MSNs); the structure of OH-MSNs was characterized by transmission electron microscopy (TEM) and dynamic light scattering (DLS), the drug release rate was detected by high performance liquid chromatography; the cellular activity, apoptosis level, and the expression levels of intracellular apoptosis and autophagy-related factors of OH-MSNs on cholangiocarcinoma cells were observed by CCK-8, flow cytometry, colony formation assay, and Western blot; the effects of OH-MSNs on cholangioma growth were observed by mouse tumor formation, immunohistochemistry, and tissue Tunel staining.ResultsThe release of OH-MSNs to Oxaliplatin was enhanced under acidic conditions; compared with Oxaliplatin or O-MSNs, OH-MSNs showed more potent killing effects against cholangiocarcinoma cells (P<0.05), and exerted notably inhibitory effects on the activity of cholangiocarcinoma cells (P<0.05), promoted their apoptosis (P<0.05), and greatly facilitated the expression of pro-apoptotic factors and autophagic factors in cholangiocarcinoma cells (P<0.05), and markedly inhibited the expression of anti-apoptotic factors and autophagic inhibitory factors (P<0.05); moreover, OH-MSNs could significantly suppress the growth of mouse cholangiocarcinoma (P<0.05) and induce apoptosis of tumor cells compared with Oxaliplatin or O-MSNs (P<0.05).ConclusionMSNs loading greatly increases the killing effect of Oxaliplatin on cholangiocarcinoma cells and upgrades the autophagic level of cholangiocarcinoma cells, while OH-MSNs synthesized by further loading HCE6 have a more apparent killing effect on cholangiocarcinoma cells.

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Autophagy regulation by inorganic, organic, and organic/inorganic hybrid nanoparticles: Organelle damage, regulation factors, and potential pathways

Dong

Zhang

Tang

2023

J Biochem & Molecular Tox

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The rapid development of nanotechnology requires a more thorough understanding of the potential health effects caused by nanoparticles (NPs). As a programmed cell death, autophagy is one of the biological effects induced by NPs, which maintain intracellular homeostasis by degrading damaged organelles and removing aggregates of defective proteins through lysosomes. Currently, autophagy has been shown to be associated with the development of several diseases. A significant number of research have demonstrated that most NPs can regulate autophagy, and their regulation of autophagy is divided into induction and blockade. Studying the autophagy regulation by NPs will facilitate a more comprehensive understanding of the toxicity of NPs. In this review, we will illustrate the effects of different types of NPs on autophagy, including inorganic NPs, organic NPs, and organic/inorganic hybrid NPs. The potential mechanisms by which NPs regulate autophagy are highlighted, including organelle damage, oxidative stress, inducible factors, and multiple signaling pathways. In addition, we list the factors influencing NPs‐regulated autophagy. This review may provide basic information for the safety assessment of NPs.

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Involvement of oxidative stress in ZnO NPs-induced apoptosis and autophagy of mouse GC-1 spg cells

Cited by 33 publications

References 42 publications

Interactions of Zinc Oxide Nanostructures with Mammalian Cells: Cytotoxicity and Photocatalytic Toxicity

Interactions of Zinc Oxide Nanostructures with Mammalian Cells: Cytotoxicity and Photocatalytic Toxicity

A Study on Mesoporous Silica Loaded With Novel Photosensitizers HCE6 and Oxaliplatin for the Treatment of Cholangiocarcinoma

Autophagy regulation by inorganic, organic, and organic/inorganic hybrid nanoparticles: Organelle damage, regulation factors, and potential pathways

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