BibTex format
@article{Eisermann:2024:10.1002/chem.202402035,
author = {Eisermann, J and Liang, Y and Wright, JJ and Clifford, E and Wilton-Ely, JDET and Kuimova, M and Roessler, M},
doi = {10.1002/chem.202402035},
journal = {Chemistry: A European Journal},
title = {The effect of reactive oxygen species on respiratory complex I activity in liposomes},
url = {http://dx.doi.org/10.1002/chem.202402035},
year = {2024}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Respiratory complex I (R-CI) is an essential enzyme in the mitochondrial electron transport chain but also a major source of reactive oxygen species (ROS), which are implicated in neurodegenerative diseases and ageing. While the mechanism of ROS production by R-CI is well-established, the feedback of ROS on R-CI activity is poorly understood. Here, we perform EPR spectroscopy on R-CI incorporated in artificial membrane vesicles to reveal that ROS (particularly hydroxyl radicals) reduce R-CI activity by making the membrane more polar and by increasing its hydrogen bonding capability. Moreover, the mechanism that we have uncovered reveals that the feedback of ROS on R-CI activity via the membrane is transient and not permanent; lipid peroxidation is negligible for the levels of ROS generated under these conditions. Our successful use of modular proteoliposome systems in conjunction with EPR spectroscopy and other biophysical techniques is a powerful approach for investigating ROS effects on other membrane proteins.
AU - Eisermann,J
AU - Liang,Y
AU - Wright,JJ
AU - Clifford,E
AU - Wilton-Ely,JDET
AU - Kuimova,M
AU - Roessler,M
DO - 10.1002/chem.202402035
PY - 2024///
SN - 0947-6539
TI - The effect of reactive oxygen species on respiratory complex I activity in liposomes
T2 - Chemistry: A European Journal
UR - http://dx.doi.org/10.1002/chem.202402035
UR - https://www.ncbi.nlm.nih.gov/pubmed/39058376
UR - https://chemistry-europe.onlinelibrary.wiley.com/doi/10.1002/chem.202402035
UR - http://hdl.handle.net/10044/1/113844
ER -