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Mechanisms of Cd-Induced Cytotoxicity in Normal Human Skin Keratinocytes: Implication for Human Health
by
Cui, Dao-Lei
, Su, Jin-Zhou
, Xiang, Ping
, Xie, Yu-Mei
, Zhang, Meng-Yan
, Niu, You-Ya
, Li, Jing-Ya
in
Apoptosis
/ Cancer
/ Cell cycle
/ Cell growth
/ Cytotoxicity
/ DNA damage
/ Fibroblasts
/ Heavy metals
/ Morphology
/ Phosphorylation
/ Skin
/ Soil contamination
/ Sperm
2022
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Mechanisms of Cd-Induced Cytotoxicity in Normal Human Skin Keratinocytes: Implication for Human Health
by
Cui, Dao-Lei
, Su, Jin-Zhou
, Xiang, Ping
, Xie, Yu-Mei
, Zhang, Meng-Yan
, Niu, You-Ya
, Li, Jing-Ya
in
Apoptosis
/ Cancer
/ Cell cycle
/ Cell growth
/ Cytotoxicity
/ DNA damage
/ Fibroblasts
/ Heavy metals
/ Morphology
/ Phosphorylation
/ Skin
/ Soil contamination
/ Sperm
2022
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Do you wish to request the book?
Mechanisms of Cd-Induced Cytotoxicity in Normal Human Skin Keratinocytes: Implication for Human Health
by
Cui, Dao-Lei
, Su, Jin-Zhou
, Xiang, Ping
, Xie, Yu-Mei
, Zhang, Meng-Yan
, Niu, You-Ya
, Li, Jing-Ya
in
Apoptosis
/ Cancer
/ Cell cycle
/ Cell growth
/ Cytotoxicity
/ DNA damage
/ Fibroblasts
/ Heavy metals
/ Morphology
/ Phosphorylation
/ Skin
/ Soil contamination
/ Sperm
2022
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Mechanisms of Cd-Induced Cytotoxicity in Normal Human Skin Keratinocytes: Implication for Human Health
Journal Article
Mechanisms of Cd-Induced Cytotoxicity in Normal Human Skin Keratinocytes: Implication for Human Health
2022
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Overview
Cadmium (Cd) is one of the toxic heavy metals found widely in the environment. Skin is an important target organ of Cd exposure. However, the adverse effects of Cd on human skin are still not well known. In this study, normal human skin keratinocytes (HaCaT cells) were studied for changes in cell viability, morphology, DNA damage, cycle, apoptosis, and the expression of endoplasmic reticulum (ER) stress-related genes (XBP-1, BiP, ATF-4, and CHOP) after exposure to Cd for 24 h. We found that Cd decreased cell viability in a concentration-dependent manner, with a median lethal concentration (LC50) of 11 µM. DNA damage induction was evidenced by upregulation of the level of γ-H2AX. Furthermore, Cd induced G0/G1 phase cell cycle arrest and apoptosis in a dose-dependent manner and upregulated the mRNA levels of ER stress biomarker genes (XBP-1, BiP, ATF4, and CHOP). Taken together, our results showed that Cd induced cytotoxicity and DNA damage in HaCaT cells, eventually resulting in cell cycle arrest in the G0/G1 phase and apoptosis. In addition, ER stress may be involved in Cd-induced HaCaT apoptosis. Our data imply the importance of reducing Cd pollution in the environment to reduce its adverse impacts on human skin.
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