상위피인용논문
바이테리얼즈
Kyeong-Nam Yua,1, Tae-Jong Yoonb,1, Arash Minai-Tehrania, Ji-Eun Kima,c, Soo Jin Parkd, Min Sook Jeongd, Shin-Woo Hae, Jin-Kyu Leef, Jun Sung Kimd,*, Myung-Haing Choa,c,g,h,*
a Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Republic of Korea
b Department of Applied BioScience, CHA University, Seoul 135-907, Republic of Korea
c Department of Nano Fusion Technology, Graduate School of Convergence Science and Technology, Seoul National University, Suwon 443-270, Republic of Korea
d R&D Center, Biterials Co., Ltd., Seoul 140-200, Republic of Korea
e Division of Endocrinology, Metabolism and Lipids, Emory University School of Medicine, 101 Woodruff Circle, WMRB Room 1327 Atlanta, GA 30322, United States
f Department of Chemistry, College of Natural Sciences, Seoul National University, Seoul 151-742, Republic of Korea
g Graduate Group of Tumor Biology, Seoul National University, Seoul 151-742, Republic of Korea
h Advanced Institute of Convergence Technology, Seoul National University, Suwon 443-270, Republic of Korea
*Corresponding authors : Jun Sung Kim, Myung-Haing Cho
1These authors contributed equally.
Abstract
Zinc oxide nanoparticles (ZnO-np) are used in an increasing number of industrial products such as paint, coating and cosmetics, and in other biological applications. There have been many suggestions of a ZnO-np toxicity paradigm but the underlying molecular mechanisms about the toxicity of ZnO-np remain unclear. This study was done to determine the potential toxicity of ZnO-np and to assess the toxicity mechanism in normal skin cells. Synthesized ZnO-np generated reactive oxygen species (ROS), as determined by electron spin resonance. After uptake into cells, ZnO-np induced ROS in a concentration- and time-dependent manner. To demonstrate ZnO-np toxicity mechanism related to ROS, we detected abnormal autophagic vacuoles accumulation and mitochondria dysfunction after ZnO-np treatment. Furthermore mitochondria membrane potential and adenosine-5′-triphosphate (ATP) production are decreased for culture with ZnO-np. We conclude that ZnO-np leads to cell death through autophagic vacuole accumulation and mitochondria damage in normal skin cells via ROS induction. Accordingly, ZnO-np may cause toxicity and the results highlight and need for careful regulation of ZnO-np production and use.
Keywords : Zinc oxide nanoparticles; Cytotoxicity; Autophagy; Reactive oxygen species (ROS); Mitochondria damage
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