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Apoptotic volume decrease (AVD) in A549 cells exposed to water-soluble fraction of particulate matter (PM10).

M E Giordano1, G Udayan1, M R Guascito1

  • 1Department Biological and Environmental Sciences and Technologies (DiSTeBA), Salento University, Lecce, Italy.

Frontiers in Physiology
|July 26, 2023
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Summary

Exposure to particulate matter less than 10 micrometers (PM10) induces cell death and oxidative stress in lung cells. This study reveals PM10

Keywords:
A549 cellsAVDair pollutionapoptosisoxidative stressparticulate matter

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Area of Science:

  • Environmental Health Sciences
  • Cell Biology
  • Toxicology

Background:

  • Atmospheric particulate matter (PM) exposure poses significant human health risks.
  • Particulate matter less than 10 micrometers (PM10) is a major component of air pollution.
  • Understanding the cellular mechanisms of PM10 toxicity is crucial for public health.

Purpose of the Study:

  • To investigate the cellular mechanisms of PM10-induced cytotoxicity in A549 lung cells.
  • To determine if PM10 exposure induces Apoptotic Volume Decrease (AVD) and intracellular oxidative stress.
  • To explore the role of oxidative stress in PM10-induced apoptosis.

Main Methods:

  • Exposure of A549 cells to aqueous extracts of urban background PM10 samples.
  • Cytotoxicity assessed using MTT assay.
  • Cell volume changes monitored by morphometric analysis.
  • Apoptosis detected by Annexin V staining.
  • Intracellular oxidative stress evaluated using CM-H2DCFDA fluorescent probe.

Main Results:

  • PM10 exposure induced significant cytotoxic effects and apoptotic death in A549 cells.
  • Apoptotic Volume Decrease (AVD) was observed within 30 minutes of PM10 exposure, suggesting rapid cellular response.
  • PM10 exposure led to intracellular oxidative stress, detected as early as 15 minutes.
  • Oxidative stress was significantly correlated with reduced cell viability and apoptotic cell shrinkage.
  • AVD was preventable by SITS, indicating potential involvement of chloride efflux and VRAC channels.

Conclusions:

  • Airborne PM10, particularly from biomass burning, induces cytotoxicity in A549 cells via apoptosis.
  • PM10 exposure triggers early cellular events including Apoptotic Volume Decrease (AVD) and oxidative stress.
  • Intracellular oxidative stress plays a key role in PM10-induced AVD and subsequent cytotoxicity.