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Cytotoxicity of RNases is increased by cationization and counteracted by K(Ca) channels

Olga N Ilinskaya1, Andreas Koschinski, Vladimir A Mitkevich

  • 1Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Vavilov Str. 32, 119991 Moscow, Russia.

Biochemical and Biophysical Research Communications
|January 22, 2004
PubMed

Insights

Cells with potassium calcium (K(Ca)) channels are protected from toxic microbial RNases. Without these channels, cells cannot counteract RNase cytotoxicity, highlighting the protective role of K(Ca) channels.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Toxicology

Background:

  • Potassium calcium (K(Ca)) channels regulate cell proliferation and differentiation.
  • Microbial RNases can exhibit cytotoxic effects on mammalian cells.

Purpose of the Study:

  • To investigate the role of K(Ca) channels in cellular defense against RNase-induced cytotoxicity.
  • To characterize the cytotoxic activity of Streptomyces aureofaciens RNases and their variants.

Main Methods:

  • Assessing the toxicity of various RNases (Sa, Sa2, Sa3, and Sa mutants) on human embryonic kidney cell lines.
  • Comparing cytotoxicity in cell lines with and without K(Ca) channel expression.
  • Evaluating the correlation between RNase catalytic activity, stability, charge, and cytotoxicity.

Main Results:

  • A basic variant of RNase Sa and RNase Sa3 showed significant cytotoxicity, comparable to onconase.
  • Cytotoxicity was not correlated with RNase catalytic activity or stability.
  • A positive charge on RNases enhanced their toxic effect.
  • Cells expressing K(Ca) channels demonstrated significantly lower sensitivity to cytotoxic microbial RNases.

Conclusions:

  • K(Ca) channels play a crucial role in cellular resistance to RNase-induced toxicity.
  • The positive charge of RNases is a key factor in their cytotoxic activity.
  • Cells lacking K(Ca) channel activity are unable to counteract the toxic effects of microbial RNases.

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