ArticleClinical, cosmetic and investigational dermatology2011
Cytotoxicity patterns of arsenic trioxide exposure on HaCaT keratinocytes.
Article in Clinical, cosmetic and investigational dermatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Antibiofilm, Antimicrobial, and Anti-inflammatory Potential of Rubus chamaemorus Rhizome, Leaf, and Fruit Extracts.Chemistry & biodiversity · 2026Article
- In-Vitro Safety Evaluation of Sodium Hypochlorite (NaOCl) as Part of Step 2 and Maintenance Therapy Protocols in Patients with Periodontitis Stages III-IV.Oral health & preventive dentistry · 2023Article
- Insight Into Biological Targets and Molecular Mechanisms in the Treatment of Arsenic-Related Dermatitis With Vitamin AFrontiers in nutrition · 2022Article
- The Hormetic Effect of Arsenic Trioxide on Rat Pulpal Cells: An In Vitro Preliminary Study.European journal of dentistry · 2021Article
- State of the science review of the health effects of inorganic arsenic: Perspectives for future research.Environmental toxicology · 2019Review
- Enhancement of arsenic trioxide-mediated changes in human induced pluripotent stem cells (IPS).International journal of environmental research and public health · 2014Article
- Proteomics-Based Identification of Differentially Abundant Proteins from Human Keratinocytes Exposed to Arsenic Trioxide.Journal of proteomics & bioinformatics · 2014Article
- Arsenic trioxide-mediated oxidative stress and genotoxicity in human hepatocellular carcinoma cells.OncoTargets and therapy · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundArsenic is a ubiquitous environmental toxicant, and abnormalities of the skin are the most common outcomes of long-term, low-dose, chronic arsenic exposure. If the balance between keratinocyte proliferation, differentiation, and death is perturbed, pathologic changes of the epidermis may result, including psoriasis, atopic dermatitis, and certain forms of ichthyosis. Therefore, research investigations using in vitro human epidermal cells could help elucidate cellular and molecular processes in keratinocytes affected by arsenic. Data from such investigations could also provide the basis for developing cosmetic intervention for skin diseases caused by arsenic.
methodsThe viability of HaCaT keratinocyte cultures with or without prior exposure to low-dose arsenic trioxide was compared for varying concentrations of arsenic trioxide over a time course of 14 days because in untreated control cultures, approximately 2 weeks is required to complete cell differentiation. Long-term cultures were established by culturing HaCaT cells on collagen IV, and cells were subsequently exposed to 0 parts per million (ppm), 1 ppm, 5 ppm, 7.5 ppm, 10 ppm, and 15 ppm of arsenic trioxide. The percentages of viable cells as well as DNA damage after exposure were determined on Day 2, Day 5, Day 8, and Day 14.
resultsUsing both statistical and visual analytics approaches for data analysis, we have observed a biphasic response at a 5 ppm dose with cell viability peaking on Day 8 in both chronic and acute exposures. Further, a low dose of 1 ppm arsenic trioxide enhanced HaCaT keratinocyte proliferation, whereas doses above 7.5 ppm inhibited growth.
conclusionThe time course profiling of arsenic trioxide cytotoxicity using long-term HaCaT keratinocyte cultures presents an approach to modeling the human epidermal cellular responses to varying doses of arsenic trioxide treatment or exposure. A low dose of arsenic trioxide appears to aid cell growth but concomitantly disrupts the DNA transcription process.
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