The Mechanism of the Neurotoxicity Induced by Cadmium

카드뮴의 중추신경계 독성유발 기전

  • 이종화 (순천향대학교 환경보건학과) ;
  • 장봉기 (순천향대학교 환경보건학과) ;
  • 박종안 (순천향대학교 환경보건학과) ;
  • 박종영 (순천향대학교 환경보건학과) ;
  • 김완종 (순천향대학교 생물학과) ;
  • 우기민 (순천향대학교 의과대학 생화학교실)
  • Published : 2004.09.01

Abstract

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.

Keywords

References

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