Zinc oxide nanoparticle-triggered oxidative stress and autophagy activation in human tenon fibroblasts

Guo, Dadong; Wang, Zhe; Guo, Lijie; Yin, Xuewei; Li, Zonghong; Zhou, Mengxian; Li, Tuling; Chen, Chen

doi:10.1016/j.ejphar.2021.174294

Cited by 9 publications

(1 citation statement)

References 52 publications

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“…[ 81 ] This reduced the fecundity of female zebrafish. Guo et al [ 32 ] found that ZnONPs induced oxidative stress and autophagy in HTFs cells. Which further inhibited proliferation and caused apoptosis.…”

Section: Autophagy Regulation By Inorganic Npsmentioning

confidence: 99%

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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Section: Autophagy Regulation By Inorganic Npsmentioning

confidence: 99%

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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Mechanisms of acrolein induces toxicity in human umbilical vein endothelial cells: Oxidative stress, DNA damage response, and apoptosis

Liú

Cheng

Mei

et al. 2021

Environmental Toxicology

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Acrolein is a ubiquitous environmental pollutant that produced by the incomplete combustion of cigarette smoke, forest fires, petroleum fuels, plastic materials, and cooking fumes. Inhalation is a common form of people exposure to acrolein, increasing evidence demonstrates that acrolein impairs the cardiovascular system by targeting vascular endothelial cells. However, the molecular mechanism of the cytotoxicity of acrolein exposure on vascular endothelial cells remains unclear. This work focused on the toxicity of acrolein on human umbilical vein endothelial cells (HUVECs). The molecular mechanism was studied based on oxidative stress, DNA damage response (DDR), and mitochondrial apoptosis pathways. After HUVECs were treated with 12.5, 25, and 50 μM acrolein for 24 h, cell viability, cell colony formation, mitochondrial membrane potential, and adenosine triphosphate content significantly reduced, and acrolein increased intracellular reactive oxygen species, apoptosis rate, and 8-hydroxy-2 deoxyguanosine (8-OHdG) level. Furthermore, p38MAPK and c-Jun N-terminal kinase signaling pathways were activated in response to oxidative stress. Moreover, acrolein induced G0/G1phase arrest, promoted the expression of γ-H2AX, activated the DDR signaling pathway (Ataxia-Telangiectasia-Mutated [ATM] and Rad-3-related/Chk1 and ATM/Chk2), and triggered the consequent cell cycle checkpoints. Finally, the protein expression of Bax/Bcl-2 and cleaved Caspase-3 was up-regulated, suggesting apoptosis was induced by triggering the mitochondrial apoptosis pathway. All these results indicated that acrolein induced HUVECs cytotoxicity by regulating oxidative stress, DNA damage, and apoptosis. This study provides a novel perspective on the mechanism of acrolein-induced cardiovascular toxicity, it will be helpful for the prevention of acrolein-induced cardiovascular disease.

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Zinc Oxide Nanoparticles Trigger Autophagy in the Human Multiple Myeloma Cell Line RPMI8226: an In Vitro Study

Yin

Lyu

et al. 2023

Biol Trace Elem Res

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Zinc oxide nanoparticle-triggered oxidative stress and autophagy activation in human tenon fibroblasts

Cited by 9 publications

References 52 publications

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

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

Mechanisms of acrolein induces toxicity in human umbilical vein endothelial cells: Oxidative stress, DNA damage response, and apoptosis

Zinc Oxide Nanoparticles Trigger Autophagy in the Human Multiple Myeloma Cell Line RPMI8226: an In Vitro Study

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