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. 2021 Oct 5;11:19701. doi: 10.1038/s41598-021-99224-w

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Effects of stress hormones on oxidative DNA damage in oral epithelial cells. (A) Norepinephrine up-regulated the 8OHdG levels in the presence or absence of carcinogen NNK. Beta-blocker propranolol inhibited the increased oxidative DNA damage caused by the hormone combined to NNK. (B) Cortisol did not change the 8OHdG levels secreted by the NOK-SI cells. The results are expressed as the mean ± standard deviation (SD). Upper- and lower cases equal letters indicate a statistically significant difference (p < 0.05). NNK = 4 (N-metil-N-nitrosamine)-1-(3-piridil)-butano-1-one). NE = norepinefrina. PROp = propranolol. CORT = cortisol. NNK, NE, PROP and RU486 were used at 10 µM. CORT was used at 100 nM. NOK-SI cells were exposed to NNK and/or stress hormones in the presence or absence of their antagonists for 72 h.