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10. Para-phenylenediamine, an oxidative hair dye ingredient, increases thymic stromal lymphopoietin and proinflammatory cytokines causing acute dermatitis

Author

Lee, Jae Kwon, Lee, Hye Eun, Yang, Gabsik, Kim, Kyu-Bong, Kwack, Seung Jun, and Lee, Joo Young

Abstract

Due to high consumption of cosmetics in modern society, people are always exposed to the risk of skin damage and complications. Para-phenylenediamine (P-PD), an ingredient of hair dye, has been reported to cause allergic contact dermatitis. However, the mechanism has not been well elucidated. Here, we identify that P-PD causes dermatitis by increasing thymic stromal lymphopoietin (TSLP) and inflammatory cytokines. Topical application of P-PD to mouse ear skin in consecutive 5 days resulted in dermatitis symptoms and increased ear thickness. TSLP production in skin was upregulated by P-PD treatment alone. In addition, P-PD-induced TSLP production was potentiated by MC903, which is an in vivo TSLP inducer. P-PD increased TSLP production in keratinocytes (KCMH-1 cells and phorbol 12-myristate 13-acetate-stimulated PAM212 cells). The production of proinflammatory cytokines such as IL-1β, IL-6, IFN-γ, and CCL2, was upregulated by P-PD treatment together with MC903. The results show that repeated exposure to P-PD causes acute contact dermatitis mediated by increasing the expression of TSLP and proinflammatory cytokines.

Published
2024
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18. Effects of tobacco compound 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on the expression of epigenetically regulated genes in lung carcinogenesis

Author

Jin, Sun Woo, primary, Im, Jong Seung, additional, Park, Jae Hyeon, additional, Kim, Hyung Gyun, additional, Lee, Gi Ho, additional, Kim, Se Jong, additional, Kwack, Seung Jun, additional, Kim, Kyu-Bong, additional, Chung, Kyu Hyuck, additional, Lee, Byung Mu, additional, Kacew, Sam, additional, Jeong, Hye Gwang, additional, and Kim, Hyung Sik, additional

Published
2021
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30. Using intracellular metabolic profiling to identify novel biomarkers of cisplatin-induced acute kidney injury in NRK-52E cells.

Author

Kim, Hae Ri, Park, Jae Hyeon, Lee, Song Hee, Kwack, Seung Jun, Lee, Jaewon, Kim, Suhkmann, Yoon, Sungpil, Kim, Kyu-Bong, Lee, Byung Mu, Kacew, Sam, and Kim, Hyung Sik

Subjects
ACUTE kidney failure, LIPOCALIN-2, CISPLATIN, PROTON magnetic resonance, DRUG development, CELL death, NUCLEAR magnetic resonance, PYRUVATE kinase
Abstract

The aim of this study was to investigate changes in the intracellular metabolism resulting from cisplatin (CDDP)-induced nephrotoxicity in normal kidney tubular epithelial NRK-52E cells. Cytotoxicity, cell cycle analysis, and apoptotic cell death were all evaluated in NRK-52E cells treated with CDDP. Subsequently, proton nuclear magnetic resonance (1H-NMR) spectroscopy was used to investigate cellular metabolic profiles. CDDP-induced nephrotoxicity was determined in vivo model. Cytotoxicity in the NRK-52E cells significantly rose following treatment with CDDP and these increases were found to be concentration-dependent. Both p53 and Bax protein expression was increased in CDDP-treated NRK-52E cells, correlating with enhanced cellular apoptosis. In addition, a number of metabolites were altered in both media and cell lysates in these cells. In cell lysates, citrate, creatinine, and acetate levels were dramatically reduced following treatment with 20 µM CDDP concentrations, while glutamate level was elevated. Lactate and acetate levels were significantly increased in culture media but citrate concentrations were reduced following high 20 µM CDDP concentrations incubation. In addition, excretion of clusterin, calbindin, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), selenium binding protein 1 (SBP1), and pyruvate kinase M2 (PKM2) into the culture media was significantly increased in CDDP-treated cells while expression of acetyl CoA synthetase 1 (AceCS1) was markedly reduced in these cells. These findings suggest that acetate-dependent metabolic pathway may be a reliable and useful biomarker for detecting CDDP-induced nephrotoxicity. Taken together, data demonstrate that the discovery of novel biomarkers by metabolite profiling in target cells may contribute to the detection of nephrotoxicity and new drug development. [ABSTRACT FROM AUTHOR]

Published
2022
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42. Identification of a sensitive urinary biomarker, selenium-binding protein 1, for early detection of acute kidney injury

Author

Kim, Kyeong Seok, primary, Yang, Hun Yong, additional, Song, Hosup, additional, Kang, Ye Rim, additional, Kwon, JiHoon, additional, An, JiHye, additional, Son, Ji Yeon, additional, Kwack, Seung Jun, additional, Kim, Young-Mi, additional, Bae, Ok-Nam, additional, Ahn, Mee-Young, additional, Lee, Jaewon, additional, Yoon, Sungpil, additional, Lee, Byung Mu, additional, and Kim, Hyung Sik, additional

Published
2017
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46. Risk assessment of <italic>N</italic>-nitrosodiethylamine (NDEA) and <italic>N</italic>-nitrosodiethanolamine (NDELA) in cosmetics.

Author

Lim, Duck Soo, Roh, Tae Hyun, Kim, Min Kook, Kwon, Yong Chan, Choi, Seul Min, Kwack, Seung Jun, Kim, Kyu Bong, Yoon, Sungpil, Kim, Hyung Sik, and Lee, Byung-Mu

Subjects
RISK assessment, COSMETICS, NITROSOAMINES
Abstract

N-nitrosamines and their precursors found in cosmetics may be carcinogenic in humans. Thus the aim of this study was to carry out risk assessment for N-nitrosamines (N-nitrosodiethanolamine [NDELA], N-nitrosodiethylamine [NDEA]) and amines (triethanolamine [TEA], diethanolamine [DEA]) levels in cosmetics determined using validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) procedures. NDELA and NDEA concentrations were present at levels of “not detected” (N.D.) to 596.5 μg/kg and N.D. to 40.9 μg/kg, respectively. TEA and DEA concentrations ranged from N.D. to 860 μg/kg and N.D. to 26.22 μg/kg, respectively. The nitrite concentration (3-2250 mg/l), number of nitrosating agents to a maximum 5, and pH (3.93-10.09) were also assessed. The impact of N-nitrosamine formation on the levels of TEA, DEA, nitrite, and other nitrosating agents was also examined. N-nitrosamine concentrations correlated with the number of nitrosating agents and nitrite concentrations. Data demonstrated that higher nitrite concentrations and a greater number of nitrosating agents increased NDELA and NDEA yields. Further, the presence of TEA and DEA exerted a significant influence on N-nitrosamine formation. Risk assessments, including the margin of exposure (MOE) and lifetime cancer risk (LCR) for N-nitrosamines and margin of safety (MOS) for amines, were calculated using product type, use pattern, and concentrations. Exposure to maximum amounts of NDELA and NDEA resulted in MOE > 10,000 (based upon the benchmark dose lower confidence limit 10%) and LCR <1 × 10−5, respectively. In addition, TEA and DEA concentrations in cosmetic samples resulted in MOS values >100. Therefore, no apparent safety concerns were associated with cosmetic products containing NDELA, NDEA, TEA, and DEA in this study. However, since amines and nitrosating agents produce carcinogenic nitrosamines, their use in cosmetics needs to be minimized to levels as low as technically feasible. [ABSTRACT FROM AUTHOR]

Published
2018
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