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Effect of Exogenous Zinc on MsrB1 Expression and Protein Oxidation in Human Lens Epithelial Cells

Yi Jia1, Jie Dai2, Liangliang Zhang2

  • 1Department of Chemical Biology, School of Biology and Engineering, Guizhou Medical University, Guiyang, 550025, Guizhou, People's Republic of China. jiayiyouxiang@163.com.

Biological Trace Element Research
|October 12, 2018
PubMed

Insights

Exogenous zinc supplementation protects human lens epithelial cells from oxidative stress by increasing methionine sulfoxide reductase B1 (MsrB1) levels. This helps reduce oxidized proteins and cell death, counteracting aging-related decline.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Nutritional Science

Background:

  • Aging is linked to zinc deficiency, causing increased protein oxidation and reduced methionine sulfoxide reductase (Msr) activity.
  • Methionine sulfoxide reductase B1 (MsrB1) plays a crucial role in cellular defense against oxidative damage.

Purpose of the Study:

  • To investigate the effect of exogenous zinc on MsrB1 mRNA levels and protein oxidation in human lens epithelial (hLE) cells.
  • To elucidate the role of zinc in regulating MsrB1 gene expression and protecting against oxidative stress.

Main Methods:

  • MTT assay to assess cell viability.
  • Oxidized protein measurement kit to quantify protein carbonyl content.
  • Real-time PCR to measure MsrB1 mRNA expression.

Main Results:

  • Exogenous zinc significantly increased hLE cell viability, counteracting the decrease caused by MsrB1 gene knockdown or peroxynitrite treatment.
  • Zinc treatment reduced protein carbonyl content, indicating decreased protein oxidation, especially after MsrB1 knockdown or peroxynitrite exposure.
  • Zinc supplementation upregulated MsrB1 levels in hLE cells under both normal and oxidative stress conditions.

Conclusions:

  • Exogenous zinc protects hLE cells from cell death induced by MsrB1 gene knockdown or peroxynitrite.
  • Zinc upregulates MsrB1, enhancing the elimination of reactive oxygen species (ROS) and oxidized proteins, thereby mitigating age-related cellular damage.
Keywords:
Exogenous zincMethionine sulfoxide reductase B1Protein oxidation

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