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What does ozone react with at the air/lung interface? Model studies using human red blood cell membranes
R M Uppu1, R Cueto, G L Squadrito
1Biodynamics Institute, Louisiana State University, Baton Rouge 70803-1800, USA.
Archives of Biochemistry and Biophysics
|May 10, 1995
Summary
Human red blood cell (RBC) membranes exposed to ozone experience oxidative damage to both proteins and unsaturated lipids (UFA). Product formation from UFA ozonation is a more sensitive indicator than substrate disappearance.
Area of Science:
- Biochemistry
- Environmental Health
- Toxicology
Background:
- Ozone is a reactive oxygen species with potential health implications.
- Red blood cell (RBC) membranes contain proteins and unsaturated lipids (UFA) susceptible to oxidative damage.
Purpose of the Study:
- To investigate the oxidative damage to human RBC membranes caused by low-level ozone exposure.
- To compare the susceptibility of proteins and UFAs to ozone-induced damage.
Main Methods:
- Exposure of human RBC membranes to ozone.
- Measurement of oxidative damage markers in proteins (thiol groups, tryptophan fluorescence, acetylcholinesterase activity).
- Analysis of lipid ozonation products (hexanal, heptanal, nonanal) and UFA levels.
Main Results:
- Ozone exposure decreased thiol groups, altered tryptophan fluorescence, and reduced acetylcholinesterase activity in RBC proteins.
- Ozonation of UFAs in RBC membranes produced aldehydes like hexanal, heptanal, and nonanal.
- Nonanal formation from oleate indicated product appearance is a more sensitive measure of ozonation than UFA disappearance.
Conclusions:
- Proteins and UFAs in human RBC membranes undergo simultaneous and competitive ozonation when ozone is the limiting reactant.
- Calculations accurately predict the reaction ratios of ozone with different targets in RBC membranes.
- Similar reactions are predicted for proteins and UFAs at the air/lung interface, suggesting potential respiratory health impacts.