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Molecular mechanism of oxidative damage of lung in mice following exposure to lanthanum chloride
Author(s) -
Hong Jie,
Pan Xiaoyu,
Zhao Xiaoyang,
Yu Xiaohong,
Sang Xuezi,
Sheng Lei,
Wang Xuecen,
Gui Suxin,
Sun Qingqing,
Wang Ling,
Hong Fashui
Publication year - 2015
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.21913
Subject(s) - gclc , oxidative stress , heme oxygenase , reactive oxygen species , lung , heme , chemistry , pharmacology , acetylcysteine , oxidative phosphorylation , biochemistry , medicine , glutathione , biology , antioxidant , enzyme
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.