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Related Concept Videos

Reactions at the Benzylic Position: Oxidation and Reduction00:59

Reactions at the Benzylic Position: Oxidation and Reduction

The benzylic position describes the position of a carbon atom attached directly to a benzene ring. Benzene by itself does not undergo oxidation. In contrast, the benzylic carbon is quite reactive in the presence of strong oxidizing agents such as KMnO4 or H2CrO4. Therefore, alkylbenzenes are readily oxidized to benzoic acid, irrespective of the type of alkyl groups.

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Related Experiment Video

Updated: Jul 1, 2026

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
11:39

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

Published on: July 11, 2013

Benzo[a]pyrene Aggravates Psoriasis-Like Skin Inflammation via Circulating Exosomal microRNA Modulation.

Hye Ran Kim1, Jin Seo Park1, Hye One Kim1

  • 1Department of Dermatology, Kangnam Sacred Heart Hospital, Hallym University College of Medicine, Seoul, Republic of Korea.

Experimental Dermatology
|May 14, 2026
PubMed
Summary
This summary is machine-generated.

Environmental pollutant benzo[a]pyrene (BaP) worsens psoriasis by increasing inflammation via aryl hydrocarbon receptor (AhR) signaling. Serum exosomal miR-423 may indicate environmentally induced psoriasis exacerbation.

Keywords:
benzo[a]pyreneexosomemicroRNApsoriasis

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Last Updated: Jul 1, 2026

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04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

Area of Science:

  • Environmental toxicology
  • Dermatology
  • Molecular biology

Background:

  • Psoriasis is a chronic inflammatory skin condition.
  • Polycyclic aromatic hydrocarbons like benzo[a]pyrene (BaP) are environmental pollutants linked to psoriasis exacerbation.
  • The molecular mechanisms underlying BaP's role in psoriasis remain unclear.

Purpose of the Study:

  • To investigate the role of BaP in inflammation, focusing on serum exosomes, in an imiquimod (IMQ)-induced mouse model of psoriasis.
  • To identify molecular mechanisms and potential biomarkers for environmentally induced psoriasis exacerbation.

Main Methods:

  • Utilized an IMQ-induced mouse model of psoriasis with topical BaP exposure.
  • Analyzed skin inflammation markers, including aryl hydrocarbon receptor (AhR) and proinflammatory cytokines.
  • Performed high-throughput miRNA profiling of serum exosomes.
  • Validated miRNA expression using quantitative reverse transcription-polymerase chain reaction (qRT-PCR).
  • Confirmed findings in human psoriasis patients' circulating exosomes.

Main Results:

  • Topical BaP exposure aggravated psoriatic skin inflammation and increased AhR, CYP1A1, and proinflammatory cytokine expression.
  • Serum exosomes from BaP-exposed mice enhanced cytokine expression in keratinocytes.
  • mmu-miR-423-3p was significantly upregulated in serum exosomes of IMQ- and BaP+IMQ-treated mice.
  • hsa-miR-423-5p was elevated in circulating exosomes of psoriasis patients and linked to the MAPK signaling pathway.
  • miR-423-5p increased proinflammatory cytokines and oxidative stress in psoriatic keratinocytes.

Conclusions:

  • BaP exacerbates psoriatic inflammation through AhR signaling.
  • Serum exosomal miR-423 is a potential biomarker for environmentally induced psoriasis exacerbation.
  • Understanding these mechanisms may lead to new therapeutic strategies for psoriasis.