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UVB exposure enhanced the dermal penetration of zinc oxide nanoparticles and induced inflammatory responses through oxidative stress mediated by MAPKs and NF-κB signaling in SKH-1 hairless mouse skin

Hairless mice received topical zinc oxide nanoparticles, with or without a UVB dose of 50 mJ/cm2.

Hairless mice received topical zinc oxide nanoparticles, with or without a UVB dose of 50 mJ/cm2. Zinc in the skin rose in a dose-dependent manner, and the combination of 10 % nanoparticles with UVB produced a significant further increase compared with 5 % nanoparticles alone. The UVB groups showed more reactive oxygen species, myeloperoxidase activity, hyperplasia and COX-2 expression through MAPK and NF-κB signalling.

Key numbers

The zinc measurements (AAS after nitric and perchloric acid digestion of skin) are shown only in electronic supplementary Figure S1 (PDF p. 4), which is not in this collection. No skin zinc concentration can be quoted from the article PDF. Doses: 5 % and 10 % zinc oxide nanoparticles (<50 nm, <100 nm) and 10 % of a <5 µm material that the paper calls bulk; UVB 50 mJ/cm2; time points 6, 24 and 48 h.

Methods (brief)

Topical application to SKH-1 mice, UVB irradiation, AAS for total skin zinc, SEM, histopathology, western blotting and immunohistochemistry. Corresponding author: kmansari@iitr.res.in.

Evidence fitness

Supports only the direction of effect: UVB-damaged mouse skin took up more zinc from nanoparticles. It is an animal model of compromised skin and cannot be converted into a human or infant value.

Limitations

Mouse skin, no formulated sunscreen, supplementary data missing. The PDF shows the Royal Society of Chemistry as publisher; Crossref now lists Oxford University Press for the journal.

Update history

No substantive edit history is available in this build. The full commit record is available in git.