Oxidative stress and apoptotic changes of rat cerebral cortical neurons exposed to cadmium in vitro / 生物医学与环境科学(英文)
Biomedical and Environmental Sciences
;
(12): 172-181, 2012.
Artigo
em Inglês
| WPRIM
| ID: wpr-235538
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the cytotoxic mechanism of cadmium (Cd) on cerebral cortical neurons.</p><p><b>METHODS</b>The primary cultures of rat cerebral cortical neurons were treated with different concentrations of cadmium acetate (0, 5, 10, and 20 micromol/L), and then the cell viability, apoptosis, ultrastructure, intracellular [Ca2+], and reactive oxygen species (ROS) levels, mitochondrial membrane potential (delta psi), activities of catalase (CAT) and superoxide dismutase (SOD) were measured.</p><p><b>RESULTS</b>A progressive loss in cell viability and an increased number of apoptotic cells were observed. In addition, Cd-induced apoptotic morphological changes in cerebral cortical neurons were also demonstrated by Hoechst 33258 staining. Meanwhile, ultrastructural changes were distortion of mitochondrial cristae and an unusual arrangement. Simultaneously, elevation of intracellular [Ca2+]i and ROS levels, depletion of Delta Psi were revealed in a dose-dependent manner during the exposure. Moreover, CAT and SOD activities in the living cells increased significantly.</p><p><b>CONCLUSION</b>Exposure of cortical neurons to different doses of Cd led to cellular death, mediated by an apoptotic mechanism, and the apoptotic death induced by oxidative stress may be a potential reason. And the disorder of intracellular homeostasis caused by oxidative stress and mitochondrial dysfunction may be a trigger for apoptosis in cortical neurons.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Técnicas In Vitro
/
Cádmio
/
Córtex Cerebral
/
Espécies Reativas de Oxigênio
/
Ratos Sprague-Dawley
/
Apoptose
/
Estresse Oxidativo
/
Biologia Celular
/
Toxicidade
/
Metabolismo
Limite:
Animais
Idioma:
Inglês
Revista:
Biomedical and Environmental Sciences
Ano de publicação:
2012
Tipo de documento:
Artigo
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