Exposure of keratinocytes to non‑thermal dielectric barrier discharge plasma increases the level of 8‑oxoguanine via inhibition of its repair enzyme.

Abstract

Oxidative stress enhances cellular DNA oxidation and may cause mutations in DNA bases, including 8‑oxoguanine (8‑oxoG). Our recent study reported that exposure of cells to non‑thermal dielectric barrier discharge (DBD) plasma generates reactive oxygen species and damages DNA. The present study investigated the effect of non‑thermal DBD plasma exposure on the formation of 8‑oxoG in HaCaT human keratinocytes. Cells exposed to DBD plasma exhibited increased level of 8‑oxoG. In addition, mRNA and protein expression levels of 8‑oxoguanine glycosylase 1 (OGG1), an 8‑oxoG repair enzyme, were reduced in plasma‑exposed cells. Furthermore, the expression level of nuclear factor erythroid 2‑related factor 2 (Nrf2), a transcription factor that regulates OGG1 gene expression, was reduced following exposure to DBD plasma. Pretreatment of cells with an antioxidant, N‑acetyl cysteine (NAC), prior to plasma exposure suppressed the formation of 8‑oxoG and restored the expression levels of OGG1 and Nrf2. In addition, phosphorylation of protein kinaseB (Akt), which regulates the activation of Nrf2, was reduced following plasma exposure. However, phosphorylation was restored by pretreatment with NAC. These findings suggested that non‑thermal DBD plasma exposure generates 8‑oxoG via inhibition of the Akt‑Nrf2‑OGG1 signaling pathway in HaCaT cells.