Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Molecular mechanism of oxidative damage of lung in mice following exposure to lanthanum chloride
Exposure to lanthanoids (Ln) elicits an adverse response such as oxidative injury of lung in animals and human. The molecular targets of Ln remain unclear. In the present study, the function and signal pathway of nuclear factor erythroid 2 related factor 2 (Nrf2) in LaCl 3 ‐induced oxidative stress in mouse lung were investigated. Mice were exposed to 2, 5, and 10 mg/kg body weight by nasal administration for 6 consecutive months. With increased doses, La was markedly accumulated and promoted the reactive oxygen species (ROS) production in the lung, which in turn resulted in peroxidation of lipids, proteins and DNA, and severe pulmonary damages. Furthermore, LaCl 3 exposure could significantly increase levels of Nrf2, heme oxygenase 1 (HO‐1) and glutamate‐cysteine ligase catalytic subunit (GCLC) expressions in the LaCl 3 ‐exposed lung. These findings imply that the induction of Nrf2 expression is an adaptive intracellular response to LaCl 3 ‐induced oxidative stress in mouse lung, and that Nrf2 may regulate the LaCl 3 ‐induced pulmonary damages. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 357–365, 2015.
Molecular mechanism of oxidative damage of lung in mice following exposure to lanthanum chloride
Exposure to lanthanoids (Ln) elicits an adverse response such as oxidative injury of lung in animals and human. The molecular targets of Ln remain unclear. In the present study, the function and signal pathway of nuclear factor erythroid 2 related factor 2 (Nrf2) in LaCl 3 ‐induced oxidative stress in mouse lung were investigated. Mice were exposed to 2, 5, and 10 mg/kg body weight by nasal administration for 6 consecutive months. With increased doses, La was markedly accumulated and promoted the reactive oxygen species (ROS) production in the lung, which in turn resulted in peroxidation of lipids, proteins and DNA, and severe pulmonary damages. Furthermore, LaCl 3 exposure could significantly increase levels of Nrf2, heme oxygenase 1 (HO‐1) and glutamate‐cysteine ligase catalytic subunit (GCLC) expressions in the LaCl 3 ‐exposed lung. These findings imply that the induction of Nrf2 expression is an adaptive intracellular response to LaCl 3 ‐induced oxidative stress in mouse lung, and that Nrf2 may regulate the LaCl 3 ‐induced pulmonary damages. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 357–365, 2015.
Molecular mechanism of oxidative damage of lung in mice following exposure to lanthanum chloride
Hong, Jie (Autor:in) / Pan, Xiaoyu / Zhao, Xiaoyang / Yu, Xiaohong / Sang, Xuezi / Sheng, Lei / Wang, Xuecen / Gui, Suxin / Sun, Qingqing / Wang, Ling
2015
Aufsatz (Zeitschrift)
Englisch
Immune dysfunction and liver damage of mice following exposure to lanthanoids
| Online Contents | 2014
Differential effects of route of T‐2 toxin exposure on hepatic oxidative damage in mice
| Online Contents | 2015