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카드뮴의 중추신경계 독성유발 기전
논문 개요
| 기관명 | NDSL |
|---|---|
| 저널명 | 환경독성학회지 = Journal of environmental toxicology |
| ISSN | 1226-9158, |
| ISBN |
논문저자 및 소속기관 정보
| 저자(한글) | 이종화,장봉기,박종안,박종영,김완종,우기민 |
|---|---|
| 저자(영문) | |
| 소속기관 | |
| 소속기관(영문) | |
| 출판인 | |
| 간행물 번호 | |
| 발행연도 | 2004-01-01 |
| 초록 | Although numerous studies have shown that cadmium disturbs the normal biological processes in central nervous system, the mechanism of toxicity is not well understood. The present study has investigated the effect of cadmium on oxidative stress, Na $^{+}$ K $^{+}$ ATPase activity and the aggregation of amyloid beta peptide ( $ beta$ -amyloid) in neuronal cell line, HT22 cell. LC $_{5}$ and LC $_{50}$ of cadmium for HT22 cell resulted from MTT assay was 4.1 uM and 9.5 uM, respectively. Cadmium (2 to 8 uM) dose-dependently increased the lipid peroxidation and decreased the content of glutathione. Cadmium 4 uM showed a significant decrease in Na $^{+}$ /K $^{+}$ ATPase activity as compared with control group. The aggregation of $ beta$ -amyloid was accelerated in a dose-dependent manner by the treatment with 2 to 8 uM cadmium. These results suggest that the neurotoxicity of cadmium can be mediated by the increase in oxidative stress and decrease in Na $^{+}$ /K $^{+}$ ATPase activity.se activity. |
| 원문URL | http://click.ndsl.kr/servlet/OpenAPIDetailView?keyValue=03553784&target=NART&cn=JAKO200412910518953 |
| 첨부파일 |
추가정보
| 과학기술표준분류 | |
|---|---|
| ICT 기술분류 | |
| DDC 분류 | |
| 주제어 (키워드) | cadmium,lipid peroxidation,glutathione,Na lt,TEX gt,$^{}$ lt,/TEX gt,+//K lt,TEX gt,$^{}$ lt,/TEX gt,+/ ATPase, lt,TEX gt,${ beta}$ lt,/TEX gt,-amyloid |