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Role of potassium channels in chlorogenic acid-induced apoptotic volume decrease and cell cycle arrest in Candida

JiEun Yun1, Dong Gun Lee2

  • 1School of Life Sciences, BK 21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, 80 Daehakro, Bukgu, Daegu 41566, Republic of Korea.

Biochimica Et Biophysica Acta. General Subjects
|January 2, 2017
PubMed
Summary

Chlorogenic acid (CRA) triggers Candida albicans cell death by causing potassium efflux through potassium channels. This process leads to apoptosis and cell cycle arrest, revealing a novel antifungal mechanism.

Keywords:
Apoptotic volume decreaseCell cycle arrestChlorogenic acidPotassium channel

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Area of Science:

  • Mycology
  • Biochemistry
  • Cell Biology

Background:

  • Chlorogenic acid (CRA) is a dietary phenolic compound with known antifungal properties against Candida albicans.
  • The precise antifungal mechanism of CRA, particularly its interaction with ion channels, remains largely uninvestigated.

Purpose of the Study:

  • To elucidate the role of ion channels in chlorogenic acid-induced apoptosis in Candida albicans.
  • To determine if potassium or chloride channels are involved in the antifungal effects of CRA.

Main Methods:

  • Candida albicans cells were treated with chlorogenic acid and specific potassium or chloride channel blockers.
  • Flow cytometry was employed to assess apoptosis hallmarks, including cell cycle arrest, caspase activation, and DNA fragmentation.

Main Results:

  • Chlorogenic acid induced significant potassium efflux and apoptotic volume decrease (AVD) in C. albicans.
  • Potassium channel blockade inhibited CRA-induced potassium efflux and subsequent apoptotic events, including cell cycle arrest.
  • Chloride channel blockade did not affect CRA-induced apoptosis, indicating a specific role for potassium channels.

Conclusions:

  • Potassium efflux via potassium channels is a key mechanism in chlorogenic acid-induced apoptosis in C. albicans.
  • CRA disrupts ion homeostasis, leading to AVD and G2/M cell cycle arrest, ultimately causing fungal cell death.