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Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells
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Stage Specific Effects of Zn

Keiko Mitsunaga1, Ikuo Yasumasu1

  • 1Department of Biology, School of Education, Waseda University, 1-6-1, Nishiwaseda, Shinjuku-ku, Tokyo 160, Japan.

Development, Growth & Differentiation
|June 7, 2023
PubMed
Summary

Zinc exposure during specific early sea urchin development stages causes permanent abnormalities. Chelator treatment removes excess zinc, preventing further developmental issues, highlighting critical zinc-sensitive periods.

Area of Science:

  • Developmental Biology
  • Marine Biology
  • Toxicology

Background:

  • Zinc (Zn2+) is essential for biological processes but can be toxic at elevated concentrations.
  • Understanding the specific developmental stages sensitive to metal ion exposure is crucial for developmental toxicology.

Purpose of the Study:

  • To identify critical developmental stages in sea urchin embryos sensitive to Zn2+ induced abnormal differentiation.
  • To investigate the role of zinc retention in causing these developmental defects.

Main Methods:

  • Sea urchin embryos were treated with Zn2+ at various developmental stages (0-8 hr, 14-16 hr post-fertilization, gastrula stage).
  • Embryos were subsequently cultured with or without Zn2+-specific chelators (EDDA, HEDTA).
  • Zinc levels in embryos and morphological abnormalities were assessed.

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Main Results:

  • Zn2+ treatment between 0-8 hr post-fertilization induced permanent blastulae and abnormal prisms/plutei.
  • Treatment during gastrulation also resulted in abnormal spherical embryos.
  • Chelator treatment effectively reduced high intracellular zinc levels, preventing further abnormalities.

Conclusions:

  • Specific early developmental periods in sea urchin embryos are highly sensitive to Zn2+ exposure.
  • Zinc retention during these sensitive periods is the primary cause of abnormal differentiation.
  • Chelator treatment can mitigate Zn2+ toxicity if applied promptly after exposure.