Change of neurocytes in acute intoxicated encephalopathy induced by 1, 2-dichloroethane after intervention with antagonists / 中华劳动卫生职业病杂志
Chinese Journal of Industrial Hygiene and Occupational Diseases
;
(12): 726-729, 2007.
Artigo
em Chinês
| WPRIM
| ID: wpr-338930
ABSTRACT
<p><b>OBJECTIVE</b>To study the role of N-methyl-D-aspartate receptor and Ca(2+) in acute intoxicated encephalopathy induced by 1, 2-dichloroethane (1, 2-DCE) in vitro.</p><p><b>METHODS</b>Neurocytes of new born rats were cultured in vitro, which were administered with different doses of 1, 2-DCE, and NMDAR and Ca(2+) antagonists including Ketamine and Nimodiping respectively. The cell morphologic structures were observed under light microscope, and its proliferation was detected by Cell Counting Kit-VIII.</p><p><b>RESULTS</b>1, 2-DCE could damage the normal morphological structure of neurocytes the cell body swelled and broke down, the karyon slurred or disappeared, the axone became shorten and thick, connection of neurocytes was reduced, the cell membrane was half-baked, injury of neurocytes became severer with the increase of the dose of 1, 2-DCE. There was no statistical difference in the proliferation of neurocytes between every 1, 2-DCE groups (P > 0.05), but there was significantly statistical difference between 1, 2-DCE groups, the control group, and the retarder groups (P < 0.01).</p><p><b>CONCLUSION</b>1, 2-DCE can damage the normal morphological structure of neurocytes, and the damage will become severer with the increase of the dose of 1, 2-DCE. However, the cell morphologic structures and proliferation of antagonist groups are much better than those in the 1, 2-DCE groups.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Fisiologia
/
Células Cultivadas
/
Cálcio
/
Ratos Sprague-Dawley
/
Receptores de N-Metil-D-Aspartato
/
Dicloretos de Etileno
/
Toxicidade
/
Neurônios
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Industrial Hygiene and Occupational Diseases
Ano de publicação:
2007
Tipo de documento:
Artigo
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