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  • 标题:Effect of Magnesium Deficiency on Intracellular ATP Levels in Human Lens Epithelial Cells
  • 本地全文:下载
  • 作者:Noriaki Nagai ; Takashi Fukuhata ; Yoshimasa Ito
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:2007
  • 卷号:30
  • 期号:1
  • 页码:6-10
  • DOI:10.1248/bpb.30.6
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要:Cataractous lenses have an altered distribution of the intracellular ionic environment, and the lens ionic imbalance with increased levels of calcium (Ca2+) and sodium (Na+), coupled with decreased levels of magnesium (Mg2+) and potassium (K+), is related to cataract development in human senile cataracts. We previously found that the decrease of ATP in lenses caused lens ionic imbalance, and probably decrease in ATPase function. In this study, we investigated the effect of Mg2+ deficiency on cataract progression using human lens epithelial (HLE) cells. Expression levels of inducible nitric oxide synthase (iNOS) mRNA in HLE cells were significantly greater in Mg2+-deficient medium (Mg2+ 0.021 m M ) than in normal Mg2+ medium (Mg2+ 0.77 m M ). The NO release from the HLE cells cultured with Mg2+-deficient medium also increased. On the other hand, the ATP levels in HLE cells 24 h after incubation with Mg2+-deficient medium were lower than that with normal Mg2+ medium. The Ca2+- and Na+/K+-ATPase activities in HLE cells until 24 h incubation with normal Mg2+ or Mg2+-deficient medium did not change. Both diethyldithiocarbamate 10 μ M and aminoguanidine 250 μ M attenuated the increase of NO release, and caused an increase in ATP levels in HLE cells 24 h after incubation with Mg2+-deficient medium. These results suggest that Mg2+ deficiency enhances NO production via iNOS in the lens. It is possible that the excessive production of NO cause the decrease of ATP levels. These results show that Mg2+ deficiency in the lens may cause an acceleration of the progression of lens opacification.
  • 关键词:magnesium-deficient medium;ATP;nitric oxide;inducible nitric oxide synthase;human lens epithelial cell line SRA 01/04
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