N-Acetylcysteine Attenuates Hexavalent Chromium-Induced Hypersensitivity through Inhibition of Cell Death, ROS-Related Signaling and Cytokine Expression

doi:10.1371/journal.pone.0108317

CNU IR > Pharmacy and Science > Dept. of Cosmetic Science and institute of cosmetic science > Periodical Articles > Item 310902800/28628

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/28628

Title:	N-Acetylcysteine Attenuates Hexavalent Chromium-Induced Hypersensitivity through Inhibition of Cell Death, ROS-Related Signaling and Cytokine Expression
Authors:	Lee, Yu-Hsuan Su, Shih-Bin Huang, Chien-Cheng Sheu, Hamm-Ming Tsai, Jui-Chen Lin, Chia-Ho Wang, Ying-Jan Wang, Bour-Jr
Contributors:	化粧品應用與管理系
Keywords:	TUMOR-NECROSIS-FACTOR KAPPA-B OXIDATIVE STRESS MOLECULAR-MECHANISMS ARSENIC TRIOXIDE REDOX REGULATION SKIN-DISEASE CANCER-CELLS FACTOR-ALPHA TNF-ALPHA
Date:	2014-09
Issue Date:	2015-05-06 21:23:03 (UTC+8)
Publisher:	Public Library Science
Abstract:	Chromium hypersensitivity (chromium-induced allergic contact dermatitis) is an important issue in occupational skin disease. Hexavalent chromium (Cr(VI)) can activate the Akt, Nuclear factor kappa B (NF-kappa B), and Mitogen-activated protein kinase (MAPK) pathways and induce cell death, via the effects of reactive oxygen species (ROS). Recently, cell death stimuli have been proposed to regulate the release of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1). However, the exact effects of ROS on the signaling molecules and cytotoxicity involved in Cr(VI)-induced hypersensitivity have not yet been fully demonstrated. N-acetylcysteine (NAC) could increase glutathione levels in the skin and act as an antioxidant. In this study, we investigated the effects of NAC on attenuating the Cr(VI)-triggered ROS signaling in both normal keratinocyte cells (HaCaT cells) and a guinea pig (GP) model. The results showed the induction of apoptosis, autophagy and ROS were observed after different concentrations of Cr(VI) treatment. HaCaT cells pretreated with NAC exhibited a decrease in apoptosis and autophagy, which could affect cell viability. In addition, Cr (VI) activated the Akt, NF-kappa B and MAPK pathways thereby increasing IL-1 alpha and TNF-alpha production. However, all of these stimulation phenomena could be inhibited by NAC in both of in vitro and in vivo studies. These novel findings indicate that NAC may prevent the development of chromium hypersensitivity by inhibiting of ROS-induced cell death and cytokine expression.
Relation:	Plos One, v.9 n.9, e108317
Appears in Collections:	[Dept. of Cosmetic Science and institute of cosmetic science] Periodical Articles

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