太赫兹辐射
热休克蛋白
体外
辐射
DNA损伤
活力测定
热休克蛋白70
生物物理学
化学
材料科学
生物
光电子学
DNA
基因
光学
生物化学
物理
作者
Gerald J. Wilmink,Benjamin D. Rivest,Caleb C. Roth,Bennett L. Ibey,Jason A. Payne,Luisiana X. Cundin,Jessica E. Grundt,Xomalin G. Peralta,Dustin G. Mixon,William P. Roach
摘要
Abstract Background Terahertz (THz) radiation sources are increasingly being used in military, defense, and medical applications. However, the biological effects associated with this type of radiation are not well characterized. In this study, we evaluated the cellular and molecular response of human dermal fibroblasts exposed to THz radiation. Methods In vitro exposures were performed in a temperature‐controlled chamber using a molecular gas THz laser (2.52 THz, 84.8 mW cm −2 , durations: 5, 10, 20, 40, or 80 minutes). Both computational and empirical dosimetric techniques were conducted using finite‐difference time‐domain (FDTD) modeling approaches, infrared cameras, and thermocouples. Cellular viability was assessed using conventional MTT assays. In addition, the transcriptional activation of protein and DNA sensing genes were evaluated using qPCR. Comparable analyses were also conducted for hyperthermic and genotoxic positive controls. Results We found that cellular temperatures increased by 3°C during all THz exposures. We also found that for each exposure duration tested, the THz and hyperthermic exposure groups exhibited equivalent levels of cell survival (≥90%) and heat shock protein expression (∼3.5‐fold increases). In addition, the expression of DNA sensing and repair genes was unchanged in both groups; however, appreciable increases were observed in the genotoxic controls. Conclusions Human dermal fibroblasts exhibit comparable cellular and molecular effects when exposed to THz radiation and hyperthermic stress. These findings suggest that radiation at 2.52 THz generates primarily thermal effects in mammalian cells. Therefore, we conclude that THz‐induced bioeffects may be accurately predicted with conventional thermal damage models. Lasers Surg. Med. 42:152–163, 2011 © 2010 Wiley‐Liss, Inc.
科研通智能强力驱动
Strongly Powered by AbleSci AI