ArticleProceedings of the National Academy of Sciences of the United States of America2002
Nitric oxide-induced genotoxicity, mitochondrial damage, and apoptosis in human lymphoblastoid cells expressing wild-type and mutant p53.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 77 citations in OpenAlex.
- Loss of Arginase 2 Promotes Lung Metastasis in immune-competent hosts via Nitric Oxide Synthase 2-Dependent Th17 Response.bioRxiv : the preprint server for biology · 2026Article
- NEUROCOGNITION, PLASMA LEVEL OF TUMOUR NECROSIS FACTORRELATED APOPTOSIS INDUCING LIGAND (TRAIL), AND PHAGOCYTIC ACTIVITY IN HIV PATIENTS ON LONG-TERM ANTIRETROVIRAL THERAPY.Annals of Ibadan postgraduate medicine · 2025Article
- Review
- Article
- Sp1-regulated expression of p11 contributes to motor neuron degeneration by membrane insertion of TASK1.Nature communications · 2019Article
- Intracellular and extracellular factors influencing the genotoxicity of nitric oxide and reactive oxygen species.Oncology letters · 2017Article
- Anti-Inflammatory and Neuroprotective Role of Natural Product Securinine in Activated Glial Cells: Implications for Parkinson's Disease.Mediators of inflammation · 2017Article
- Role of nitric oxide in the regulation of immune responses during rabies virus infection in mice.Virusdisease · 2016Article
- Chemistry meets biology in colitis-associated carcinogenesis.Free radical research · 2013Review
- The impact of nitric oxide toxicity on the evolution of the glutathione transferase superfamily: a proposal for an evolutionary driving force.The Journal of biological chemistry · 2013Article
- Nitric oxide produced endogenously is responsible for hypoxia-induced HIF-1α stabilization in colon carcinoma cells.Chemical research in toxicology · 2012Article
- Delivery method, target gene structure, and growth properties of target cells impact mutagenic responses to reactive nitrogen and oxygen species.Chemical research in toxicology · 2012Article
- TAp73 induction by nitric oxide: regulation by checkpoint kinase 1 (CHK1) and protection against apoptosis.The Journal of biological chemistry · 2011Article
- Transcriptional regulation of SP-B gene expression by nitric oxide in H441 lung epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- Regulation of reactive oxygen species by p53: implications for nitric oxide-mediated apoptosis.American journal of physiology. Heart and circulatory physiology · 2010Article
- Nitric oxide activation of Keap1/Nrf2 signaling in human colon carcinoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Redox control of the DNA damage-inducible protein DinG helicase activity via its iron-sulfur cluster.The Journal of biological chemistry · 2009Article
- Effect of artemisinins and other endoperoxides on nitric oxide-related signaling pathway in RAW 264.7 mouse macrophage cells.Nitric oxide : biology and chemistry · 2008Article
- Morphological characteristics of apoptosis and its significance in neurogenesis.Neuroscience and behavioral physiology · 2008Review
- Nerve growth factor potentiates p53 DNA binding but inhibits nitric oxide-induced apoptosis in neuronal PC12 cells.Neurochemical research · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO(*)) is mutagenic and, under appropriate conditions of exposure, also induces apoptosis in many in vitro and in vivo experimental models. Biochemical and cellular mechanisms through which NO(*) induces apoptosis are incompletely understood, but involve p53/mitochondria-dependent signaling pathways. In this study, we exposed human lymphoblastoid cells harboring either wild-type (TK6 cells) or mutant p53 (WTK-1 cells) to NO(*), delivered by diffusion through Silastic tubing. Cells were exposed for 2 h at constant rates of 100-533 nM/s, similar to levels estimated to occur in vivo in inflamed tissues. DNA double-strand breaks and fragmentation detected 8-48 h after NO(*) treatment were more extensive in TK6 cells than in WTK-1 cells, whereas NO(*)-induced mutant fractions in both HPRT and TK1 genes were significantly lower in TK6 cells than in WTK-1 cells (P < 0.01-0.05). Treatment of TK6 cells with NO(*) caused extensive apoptosis, but this response was delayed and greatly reduced in magnitude in WTK-1 cells. Mitochondrial membrane depolarization and cytochrome c release were induced in both cell types. However, elevation of apoptotic protease-activating factor-1 (Apaf-1) protein and reduction of X-chromosome-linked inhibitor of apoptosis (XIAP) protein were observed only in TK6 cells. These results indicate that p53 status is an important modulator of NO(*)-induced mutagenesis and apoptosis, and suggest that levels of the Apaf-1 and XIAP proteins, but not mitochondrial depolarization and cytochrome c release, are regulated by p53 in these human lymphoblastoid cells. Thus, Apaf-1 and XIAP may play important roles in the regulation of p53-mediated apoptotic responses.
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