Table 1.

Characteristics of the included studies investigating the association between oxidative stress biomarkers in CVD.

Biomarkers	Study design	Pathway involvement	Laboratory methods	Model	Findings	Specificity	Reference
Isoprostane	Case-control	Peroxidation of polyunsaturated fatty acid catalyzed by free radical	GC/MS, ELISA, urine sample, radioimmune assay	In vivo, in vitro, ex vivo	F2-isoprostanes are predictive of peripheral and coronary artery disease	Nonspecific	[105, 126–128]
Malondialdehyde (MDA)	Cross-sectional	Peroxidation of polyunsaturated fatty acid, a side product of the thromboxane A2 pathway	Calorimetric assay, TBRS assay, ELISA, HPLC	In vivo	TRBAS blood serum levels in cardiovascular event	Specific	[103, 104, 109]
S-Glutathionylation	Case-control	Protein oxidation, glutathionylation pathway of protein	Western blotting, ELISA with monoclonal anti-glutathione antibody, MS	In vivo	It causes changes in intracellular Na+ and Ca2+ processing and other critical signaling pathways of CVD	Specific	[129–131]
Nitrotyrosine	Case-control	Tyrosine nitrate-mediated protein oxidation. ERK1/2 pathway	MS/MS, GC/MS, HPLC, immunocytochemical and immune histochemical assay based on monoclonal and polyclonal antibodies	In vivo	Nitrotyrosine enhanced fibrinogen activity and clot formation speed. Plasma protein-bound nitrotyrosine values are higher in coronary artery disease	Specific	[132–135]
OX-LDL	Nested case-control, cohort study	Autophagy-lysosome pathway, lipoxygenase-catalyzed oxidation of LDL	Monoclonal antibody technique, OX-LDL-EO6, LFL-DLH 3, OX-LDL-4E6 sandwich ELISA	In vivo	CVD endpoint predicted by OX-LDL; its level also indicates MI. In vivo OX-LDL link to atherosclerosis and its level in CVD individuals is more	Specificity of OXLDL is questionable	[113, 136–139]
Myeloperoxidase	Cohort study, case-control	Inflammatory neutrophil and basophil activate MPO, MAPK/NF-κB signaling	Peroxidation assay, spectrophotometrically, ELISA	In vivo and in vitro	MPO linked to acute MI, CAD	Specific	[71, 140–143]