Comparative Effects of Acrolein and Glyoxal on Redox Homeostasis, Antioxidant Defense and Membrane Properties in Human Peripheral Blood Mononuclear Cells: An In Vitro Study.
- 1Department of Oncobiology and Epigenetics, Faculty of Biology and Environmental Protection, University of Lodz, ul. Pomorska 141/143, 90-236 Lodz, Poland.
- 2Doctoral School of Exact and Natural Sciences, University of Lodz, 90-236 Lodz, Poland.
Abstract
Acrolein (ACR) and glyoxal (GO) are highly reactive carbonyls originating from endogenous metabolism, environmental pollution, and thermal food processing. This study compares the toxic mechanisms and redox effects of a 24 h exposure to ACR (30, 60, 90 µM) and GO (2, 5, 10 mM) in PBMCs. We assessed cell viability, lipid membrane fluidity, reactive oxygen/nitrogen species (ROS/RNS), free protein functional groups, reduced glutathione (GSH), non-enzymatic antioxidant capacity (NEAC), antioxidant enzyme activity (CAT, GPx), and protein expression levels (CAT, SOD1). Both aldehydes reduced viability in a concentration-dependent manner (ACR was over 30-fold more toxic than GO based on viability curves). These toxins increased membrane fluidity near the surface, while GO also altered the hydrophobic core. Both triggered a profound accumulation of ROS/RNS. At specific dose thresholds (ACR ≥ 60 µM; GO ≥ 5 mM), both toxins depleted GSH and NEAC, decreased protein thiol/amino groups, and suppressed CAT/GPx catalytic activity and CAT/SOD1 protein expression. In conclusion, ACR emerged as a markedly more potent inducer of oxidative stress and antioxidant failure than GO in PBMCs, disrupting both non-enzymatic (GSH, NEAC) and enzymatic (CAT, GPx, SOD1) defenses. These results support prioritizing ACR in exposure risk assessments and developing biomarkers of carbonyl-induced immune dysfunction.
Related
- Comparative multi-omics analysis of microbial succession, metabolite profiles, and antioxidant properties in fermented black and yellow highland barley
- Cryopreserved Peripheral Blood Mononuclear Cells Recover Mitochondrial Function Following Overnight Culture Revealed by High-Resolution Respirometry
- Expression Analysis of microRNAs in Peripheral Blood Mononuclear Cells in Type 2 Diabetes
- Quantification of Y RNAs in peripheral blood mononuclear cells from patients with ankylosing spondylitis and healthy controls.
- Lidocaine modulates interleukin-1β and interferon-α2 secretion in LPS with ATP stimulated human peripheral blood mononuclear cells
BibTeX
@article{kopera2026comparative,
title = {{Comparative Effects of Acrolein and Glyoxal on Redox Homeostasis, Antioxidant Defense and Membrane Properties in Human Peripheral Blood Mononuclear Cells: An In Vitro Study.}},
author = {Michal Kopera and Malgorzata Adamkiewicz and Joanna Bernasinska-Slomczewska and Anna Pieniazek},
journal = {International journal of molecular sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27198706},
url = {https://europepmc.org/article/MED/42883950},
note = {CC BY},
}
RIS
TY - JOUR
TI - Comparative Effects of Acrolein and Glyoxal on Redox Homeostasis, Antioxidant Defense and Membrane Properties in Human Peripheral Blood Mononuclear Cells: An In Vitro Study.
AU - Michal Kopera
AU - Malgorzata Adamkiewicz
AU - Joanna Bernasinska-Slomczewska
AU - Anna Pieniazek
PY - 2026
DA - 2026/09/29
JO - International journal of molecular sciences
DO - 10.3390/ijms27198706
UR - https://europepmc.org/article/MED/42883950
AB - Acrolein (ACR) and glyoxal (GO) are highly reactive carbonyls originating from endogenous metabolism, environmental pollution, and thermal food processing. This study compares the toxic mechanisms and redox effects of a 24 h exposure to ACR (30, 60, 90 µM) and GO (2, 5, 10 mM) in PBMCs. We assessed cell viability, lipid membrane fluidity, reactive oxygen/nitrogen species (ROS/RNS), free protein functional groups, reduced glutathione (GSH), non-enzymatic antioxidant capacity (NEAC), antioxidant enzyme activity (CAT, GPx), and protein expression levels (CAT, SOD1). Both aldehydes reduced viability in a concentration-dependent manner (ACR was over 30-fold more toxic than GO based on viability curves). These toxins increased membrane fluidity near the surface, while GO also altered the hydrophobic core. Both triggered a profound accumulation of ROS/RNS. At specific dose thresholds (ACR ≥ 60 µM; GO ≥ 5 mM), both toxins depleted GSH and NEAC, decreased protein thiol/amino groups, and suppressed CAT/GPx catalytic activity and CAT/SOD1 protein expression. In conclusion, ACR emerged as a markedly more potent inducer of oxidative stress and antioxidant failure than GO in PBMCs, disrupting both non-enzymatic (GSH, NEAC) and enzymatic (CAT, GPx, SOD1) defenses. These results support prioritizing ACR in exposure risk assessments and developing biomarkers of carbonyl-induced immune dysfunction.
SN - 1422-0067
ER -