Breath-borne
volatile organic compounds (VOCs) have been increasingly
studied as non-invasive biomarkers in both medical diagnosis and environmental
health research. Recently, changes in breath-borne VOC fingerprints
were demonstrated in rats and humans following pollutant exposures.
In this study, the eukaryotic model Saccharomyces cerevisiae was used to study the release of cellular VOCs resulting from toxicant
exposures (i.e., O3, H2O2, and CO2) and its underlying biological mechanism. Our results showed
that different toxicant exposures caused the release of distinctive
VOC profiles of yeast cells. The levels of ethyl acetate and ethyl n-propionate were altered in response to all the toxicants
used in this study and could thus be targeted for future environmental
toxicity monitoring. The RNA-seq results revealed significant changes
in the metabolic or signaling pathways related to the ribosome, carbohydrate,
and amino acid metabolisms after exposures. Notably, the shift from
glycolysis to the pentose phosphate pathway of carbohydrate metabolism
and the inhabitation of the aspartate pathway in the lysine synthesis
was essential to the cellular antioxidation by providing reduced nicotinamide
adenine dinucleotide phosphate (NADPH). The reprogrammed metabolisms
could have resulted in the observed changes of VOCs released, e.g.,
the production of ethyl acetate for detoxification from yeast cells.
This study provides further evidence that VOCs released from living
organisms could be used to monitor and guard against toxic exposures
while providing better mechanistic insights of the changes in breath-borne
VOCs previously observed in rats and humans exposed to air toxicants.