Shou-Cheng Wang1, Hong-Xue Ji2, Chieh-Lun Hsiao2, Tzu-Chia Wang3, Yun-Ru Syu3, Chia-En Miao3, Lin-Lin Hou3, Song-Shei Lin4, Wen-Shin Chang2, Chia-Wen Tsai5. 1. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Taichung Armed Forces General Hospital, Taichung, Taiwan, R.O.C. 2. Terry Fox Cancer Research Laboratory, China Medical University and Hospital, Taichung, Taiwan, R.O.C. Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan, R.O.C. 3. Terry Fox Cancer Research Laboratory, China Medical University and Hospital, Taichung, Taiwan, R.O.C. 4. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 5. Terry Fox Cancer Research Laboratory, China Medical University and Hospital, Taichung, Taiwan, R.O.C. artbau2@gmail.com wenwen816@gmail.com.
Abstract
BACKGROUND: Exposure to ultraviolet (UV) light is closely related to human diseases, such as skin cancer, due to irreversible injuries to the skin cells. The UV-induced DNA damage and programmed cell death are important determinants for skin carcinogenesis. The aim of the present study was to investigate the anti-ultraviolet-C (UVC) effects of pyridoxamine in human keratinocyte HaCaT cells and its mechanisms of action. RESULTS: UVC-induced programmed cell death in HaCaT cells was abrogated by treated the cells immediately after UVC irradiation with 40, 80 and 160 μM of pyridoxamine. Monitoring the UVC-induced-specific reactive oxygen species, we found that 20, 40, 80 and 160 μM of pyridoxamine was also effective in suppressing the induction of reactive oxygen species by UVC. CONCLUSION: Overall, our results provided evidence showing that pyridoxamine was effective in protecting HaCaT cells from UVC-induced programmed cell death and may be a potential anti-UVC agent in life and clinical practice.
BACKGROUND: Exposure to ultraviolet (UV) light is closely related to human diseases, such as skin cancer, due to irreversible injuries to the skin cells. The UV-induced DNA damage and programmed cell death are important determinants for skin carcinogenesis. The aim of the present study was to investigate the anti-ultraviolet-C (UVC) effects of pyridoxamine in human keratinocyte HaCaT cells and its mechanisms of action. RESULTS: UVC-induced programmed cell death in HaCaT cells was abrogated by treated the cells immediately after UVC irradiation with 40, 80 and 160 μM of pyridoxamine. Monitoring the UVC-induced-specific reactive oxygen species, we found that 20, 40, 80 and 160 μM of pyridoxamine was also effective in suppressing the induction of reactive oxygen species by UVC. CONCLUSION: Overall, our results provided evidence showing that pyridoxamine was effective in protecting HaCaT cells from UVC-induced programmed cell death and may be a potential anti-UVC agent in life and clinical practice.
Authors: William D McCaig; Payal S Patel; Sergey A Sosunov; Nicole L Shakerley; Tori A Smiraglia; Miranda M Craft; Katharine M Walker; Matthew A Deragon; Vadim S Ten; Timothy J LaRocca Journal: Cell Death Discov Date: 2018-05-10