Benzo(ghi)perylene (BgP) a black tattoo ingredient induced skin toxicity via direct and indirect mode of DNA damage under UVA irradiation

Negi, Sandeep; Shukla, Saumya; Patel, Sunil; Vikram, Apeksha; Gaur, Prakriti; Kamar, Mohd Danish; Pathania, Diksha; Kotian, Sumana Y.; Bala, Madhu; Rana, Priyanka S.; Bala, Lakshmi; Yadav, Akhilesh Kumar; Ray, Ratan Singh; Dwivedi, Ashish

doi:10.1016/j.cbi.2023.110508

Cited by 4 publications

(1 citation statement)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, UPM consists of three representative components such as elements, polycyclic aromatic hydrocarbons, and polychlorinated biphenyl. Elements (chromium, calcium, chlorine, and sodium), polycyclic aromatic hydrocarbons (benzo[e]pyrene and benzo[ghi] perylene) and polychlorinated biphenyl have been reported to cause skin damage 4–9 …”

Section: Introductionmentioning

confidence: 99%

Anti‐pollutant effect of oleic acid against urban particulate matter is mediated via regulation of AhR‐ and TRPV1‐mediated signaling in vitro

Choi,

Yang,

Kim

et al. 2024

Environmental Toxicology

View full text Add to dashboard Cite

Urban Particulate Matter (UPM) induces skin aging and inflammatory responses by regulating skin cells through the transient receptor potential vanilloid 1 (TRPV1). Although oleic acid, an unsaturated free fatty acid (FFA), has some functional activities, its effect on UPM‐induced skin damage has not been elucidated. Here, we investigated signaling pathways on how oleic acid is involved in attenuating UPM induced cell damage. UPM treatment increased XRE‐promoter luciferase activity and increased translocation of AhR to the nucleus, resulting in the upregulation of CYP1A1 gene. However, oleic acid treatment attenuated the UPM effects on AhR signaling. Furthermore, while UPM induced activation of TRPV1 and MAPKs signaling which activated the downstream molecules NFκB and AP‐1, these effects were reduced by cotreatment with oleic acid. UPM‐dependent generation of reactive oxygen species (ROS) and reduction of cellular proliferation were also attenuated by the treatment of oleic acid. These data reveal that cell damage induced by UPM treatment occurs through AhR signaling and TRPV1 activation which in turn activates ERK and JNK, ultimately inducing NFκB and AP‐1 activation. These effects were reduced by the cotreatment of oleic acid on HaCaT cells. These suggest that oleic acid reduces UPM‐induced cell damage through inhibiting both the AhR signaling and activation of TRPV1 and its downstream molecules, leading to a reduction of pro‐inflammatory cytokine and recovery of cell proliferation.

show abstract

Section: Introductionmentioning

confidence: 99%