Associations of dicarbonyl stress with complement activation: the CODAM study.

ABSTRACT:

Aims/hypothesis

Reactive α-dicarbonyl compounds are major precursors of AGEs and may lead to glycation of circulating and/or cell-associated complement regulators. Glycation of complement regulatory proteins can influence their capacity to inhibit complement activation. We investigated, in a human cohort, whether greater dicarbonyl stress was associated with more complement activation.

Methods

Circulating concentrations of dicarbonyl stress markers, i.e. α-dicarbonyls (methylglyoxal [MGO], glyoxal [GO] and 3-deoxyglucosone [3-DG]), and free AGEs (N^ε-(carboxymethyl)lysine [CML], N^ε-(carboxyethyl)lysine [CEL] and N^δ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine [MG-H1]), and protein-bound AGEs (CML, CEL, pentosidine), as well as the complement

SUBMITTER: Xin Y 

PROVIDER: S-EPMC7145776 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature