ArticleToxicology and applied pharmacology2013
The generation of 4-hydroxynonenal, an electrophilic lipid peroxidation end product, in rabbit cornea organ cultures treated with UVB light and nitrogen mustard.
Article in Toxicology and applied pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Nitrogen mustard causes progressive tissue injury, severe DNA damage, and necroptosis in the cornea.Experimental eye research · 2025Article
- Cannabinoid-2 Receptor Activation Attenuates Sulfur Mustard Analog 2-Chloroethyl-Ethyl-Sulfide-Induced Acute Lung Injury in Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- ROS-induced lipid peroxidation modulates cell death outcome: mechanisms behind apoptosis, autophagy, and ferroptosis.Archives of toxicology · 2023Review
- Sulfur mustard corneal injury is associated with alterations in the epithelial basement membrane and stromal extracellular matrix.Experimental and molecular pathology · 2022Article
- Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer's Disease?International journal of molecular sciences · 2022Review
- Targeting prominin2 transcription to overcome ferroptosis resistance in cancer.EMBO molecular medicine · 2021Article
- Article
- UV-B-Induced Inflammasome Activation Can Be Prevented by Cis-Urocanic Acid in Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2020Article
- Regulation of Macrophage Foam Cell Formation During Nitrogen Mustard (NM)-Induced Pulmonary Fibrosis by Lung Lipids.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Placental BCRP/ABCG2 Transporter Prevents Fetal Exposure to the Estrogenic Mycotoxin Zearalenone.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Anandamide down-regulates placental transporter expression through CB2 receptor-mediated inhibition of cAMP synthesis.Pharmacological research · 2019Article
- Nitrogen mustard-induced corneal injury involves the sphingomyelin-ceramide pathway.The ocular surface · 2018Article
- 4-hydroxynonenal-mediated signaling and aging.Free radical biology & medicine · 2017Review
- Localization of the placental BCRP/ABCG2 transporter to lipid rafts: Role for cholesterol in mediating efflux activity.Placenta · 2017Article
- Corneal toxicity induced by vesicating agents and effective treatment options.Annals of the New York Academy of Sciences · 2016Review
- Article
- Suppression of Hyperactive Immune Responses Protects against Nitrogen Mustard Injury.The Journal of investigative dermatology · 2015Article
- Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats.Toxicology and applied pharmacology · 2014Article
- Wounding the cornea to learn how it heals.Experimental eye research · 2014Review
- Modulation of keratinocyte expression of antioxidants by 4-hydroxynonenal, a lipid peroxidation end product.Toxicology and applied pharmacology · 2014Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The cornea is highly sensitive to oxidative stress, a process that can lead to lipid peroxidation. Ultraviolet light B (UVB) and nitrogen mustard (mechlorethamine) are corneal toxicants known to induce oxidative stress. Using a rabbit air-lifted corneal organ culture model, the oxidative stress responses to these toxicants in the corneal epithelium was characterized. Treatment of the cornea with UVB (0.5 J/cm(2)) or nitrogen mustard (100 nmol) resulted in the generation of 4-hydroxynonenal (4-HNE), a reactive lipid peroxidation end product. This was associated with increased expression of the antioxidant, heme oxygenase-1 (HO-1). In human corneal epithelial cells in culture, addition of 4-HNE or 9-nitrooleic acid, a reactive nitrolipid formed during nitrosative stress, caused a time-dependent induction of HO-1 mRNA and protein; maximal responses were evident after 10h with 30 μM 4-HNE or 6h with 10 μM 9-nitrooleic acid. 4-HNE and 9-nitrooleic acid were also found to activate Erk1/2, JNK and p38 MAP kinases, as well as phosphoinositide-3-kinase (PI3)/Akt. Inhibition of p38 blocked 4-HNE- and 9-nitrooleic acid-induced HO-1 expression. Inhibition of Erk1/2, and to a lesser extent, JNK and PI3K/Akt, suppressed only 4-HNE-induced HO-1, while inhibition of JNK and PI3K/Akt, but not Erk1/2, partly reduced 9-nitrooleic acid-induced HO-1. These data indicate that the actions of 4-HNE and 9-nitrooleic acid on corneal epithelial cells are distinct. The sensitivity of corneal epithelial cells to oxidative stress may be an important mechanism mediating tissue injury induced by UVB or nitrogen mustard.
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Registered trials
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