ArticleInternational journal of nanomedicine2015
Cross talk between poly(ADP-ribose) polymerase 1 methylation and oxidative stress involved in the toxic effect of anatase titanium dioxide nanoparticles.
Article in International journal of nanomedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 47 citations in OpenAlex.
- Immune-epigenetic convergence in biomaterial-guided tissue regeneration.Materials today. Bio · 2026Article
- Exposure to a Titanium Dioxide Product Alters DNA Methylation in Human Cells.Nanomaterials (Basel, Switzerland) · 2024Article
- Multigenerational inheritance of breathing deficits following perinatal exposure to titanium dioxide nanoparticles in the offspring of mice.Discover nano · 2024Article
- The Effect of Nanomaterials on DNA Methylation: A Review.Nanomaterials (Basel, Switzerland) · 2023Review
- Nutriepigenomics in Environmental-Associated Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- Titanium Dioxide Nanoparticles Altered the lncRNA Expression Profile in Human Lung Cells.International journal of environmental research and public health · 2023Article
- The Yin and Yang of epigenetics in the field of nanoparticles.Nanoscale advances · 2022Review
- Epigenetic Mechanisms in Understanding Nanomaterial-Induced Toxicity.Advances in experimental medicine and biology · 2022Article
- Silver, Gold, and Iron Oxide Nanoparticles Alter miRNA Expression but Do Not Affect DNA Methylation in HepG2 Cells.Materials (Basel, Switzerland) · 2019Article
- Epigenetic Aspects of Engineered Nanomaterials: Is the Collateral Damage Inevitable?Frontiers in bioengineering and biotechnology · 2019Review
- Biological monitoring of workers exposed to engineered nanomaterials.Toxicology letters · 2018Review
- Toxicological status of nanoparticles: What we know and what we don't know.Chemico-biological interactions · 2018Review
- Internalization of Titanium Dioxide Nanoparticles Is Cytotoxic for H9c2 Rat Cardiomyoblasts.Molecules (Basel, Switzerland) · 2018Article
- Applications and toxicity of graphene family nanomaterials and their composites.Nanotechnology, science and applications · 2016Review
- Article
- Unraveling the neurotoxicity of titanium dioxide nanoparticles: focusing on molecular mechanisms.Beilstein journal of nanotechnology · 2016Review
- The effect of exposure to nanoparticles and nanomaterials on the mammalian epigenome.International journal of nanomedicineReview
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Given the tremendous growth in the application of titanium dioxide nanoparticles (TNPs), concerns about the potential health hazards of TNPs to humans have been raised. Poly(ADP-ribose) polymerase 1 (PARP-1), a highly conserved DNA-binding protein, is involved in many molecular and cellular processes. Limited data demonstrated that certain nanomaterials induced the aberrant hypermethylation of PARP-1. However, the mechanism involved in TNP-induced PARP-1 abnormal methylation has not been studied. A549 cells were incubated with anatase TNPs (22.1 nm) for 24 hours pretreatment with or without methyltransferase inhibitor 5-aza-2'-deoxycytidine and the reactive oxygen species (ROS) scavenger α-lipoic acid to assess the possible role of methylation and ROS in the toxic effect of TNPs. After TNPs characterization, a battery of assays was performed to evaluate the toxic effect of TNPs, PARP-1 methylation status, and oxidative damage. Results showed that TNPs decreased the cell viability in a dose-dependent manner, in accordance with the increase of lactate dehydrogenase activity, which indicated membrane damage of cells. Similar to the high level of PARP-1 methylation, the generation of ROS was significantly increased after exposure to TNPs for 24 hours. Furthermore, α-lipoic acid decreased TNP-induced ROS generation and then attenuated TNP-triggered PARP-1 hypermethylation. Meanwhile, 5-aza-2'-deoxycytidine simultaneously decreased the ROS generation induced by TNPs, resulting in the decline of PARP-1 methylation. In summary, TNPs triggered the aberrant hypermethylation of the PARP-1 promoter and there was a cross talk between oxidative stress and PARP-1 methylation in the toxic effect of TNPs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.