Table 1.
Oxidative stress biomarkers levels in acute ischemic stroke.
| Biomarkers | Source Type | Study Design | Concentration | Comment | References |
|---|---|---|---|---|---|
| Lipid peroxidation | |||||
| MDA (µmol/L) | Saliva | 150 individuals: | Salivary and serum MDA levels were significantly higher in the ischemic stroke group than the healthy control and risk group. | [65] | |
| Ischemic stroke, N = 50 | 0.64 ± 0.22 | ||||
| Healthy control, N = 25 | 0.23 ± 0.07 | ||||
| Risk group, N = 75: | |||||
| Hypertension | 0.75 ± 0.21 | ||||
| Type 2 diabetes | 0.65 ± 0.22 | ||||
| Ischemic heart disease | 0.48 ± 0.13 | ||||
| Serum | 150 individuals: | ||||
| Ischemic stroke, N = 50 | 2.51 ± 1.11 | ||||
| Healthy control, N = 25 | 1.12 ± 0.35 | ||||
| Risk group, N = 75: | |||||
| Hypertension | 2.19 ± 0.83 | ||||
| Type 2 diabetes | 2.39 ± 0.97 | ||||
| Ischemic heart disease | 2.22 ± 0.73 | ||||
| Blood | 200 individuals: | MDA was significantly higher in stroke patients than in healthy controls. | [45] | ||
| Ischemic stroke, N = 100 | 7.11 ± 1.67 | ||||
| Healthy control, N = 100 | 1.64 ± 0.82 | ||||
| 4-HNE (µmol) | Plasma | 60 men: | The plasma 4-HNE concentrations in patients with ischemic stroke were higher than those in healthy control. | [74] | |
| Ischemic stroke: N = 24, | ≈11 | ||||
| Normal men, N = 36 | ≈9 | ||||
| TBARs (µmol/L) | Serum | 180 individuals: | The concentration of TBARS was significantly higher in stroke patients than in the controls. | [61] | |
| Acute ischemic stroke, N = 100: | |||||
| Small-vessel, N = 75 | 20.7 ± 2.6 | ||||
| Large-vessel, N = 25 | 19.7 ± 1.2 | ||||
| Healthy control (age- and sex-matched), N = 80 | ≈16 | ||||
| DNA oxidation | |||||
| 8-oHdG (ng/mgCr) |
Urine | 44 acute ischemic stroke patients: Lacunar, N = 9 Atherothrombotic, N = 22 Cardioembolic, N = 13 |
Day 0 15.8 ± 6.9 12.8 ± 11.7 11.8 ± 5.6 Day 7 16.1 ± 5.1 16.2 ± 15.5 13.0 ± 5.0 |
8-oHdG urinary levels increase in time, following AIS. In patients with better outcomes, the level increase is significantly slower. | [86] |
| 8-oHdG (ng/L) |
Blood | 241 acute ischemic stroke patients: | There was a difference between 8-oHdG levels and ischemic stroke severity in depressed versus non-depressed patients. Mild positive Spearman correlation between 8-oHdG levels and catalase activity. Urinary 8-oHdG levels could be used as reliable and valuable biomarkers to predict functional outcomes in stroke rehabilitation. |
[87] | |
| Depressive post-ischemic stroke, N = 70 | 218.0 (170.6–246.7) | ||||
| Non-depressive post-ischemic stroke, N = 171 | 164.8 (121.1–208.0) | ||||
| 8-oHdG (ng/mg creatinine) |
Urine | Acute ischemic stroke patients, N = 61: | There was a difference between 8-oHdG levels and ischemic stroke severity in depressed versus non-depressed patients. Mild positive Spearman correlation between 8-oHdG levels and catalase activity. Urinary 8-oHdG levels could be used as reliable and valuable biomarkers to predict functional outcomes in stroke rehabilitation. |
[88] | |
| Before rehabilitation | 5.87 ± 2.77 | ||||
| After rehabilitation | 5.60 ± 2.47 | ||||
| Protein oxidation | |||||
| Protein carbonyls (nmol/mg protein) | Plasma | 163 individuals: | Protein carbonyls were not significantly different in the experimental groups compared to the controls. | [48] | |
| Healthy control (gender and age matched), N = 81 | 0.25 ± 0.04 | ||||
| Acute ischemic stroke, N = 82 | 0.28 ± 0.04 | ||||
| Homocysteine (µmol/L) |
Plasma | 653 individuals: | The increase in total homocysteine concentrations was associated with a 6% to 7% increase in stroke risk | [89] | |
| Stroke patients (male and female), N = 120 | ≥18.6 | ||||
| Control subjects, N = 533 | 12.0 | ||||
| Serum | 225 individuals | Moderate hyperhomocysteinema has been proposed as an independent risk factor for stroke in middle-aged British men | [90] | ||
| Stroke patients (male), N = 107 | 13.7 | ||||
| Healthy subjects (male), N = 118 | 11.9 | ||||
| Blood | 71 individuals: | Hyperhomocysteinemia is independent risk factors for stroke |
[91] | ||
| Ischemic stroke patients (47 males, 24 females), N = 71 | 22.76 × 104 ± 12.67 | ||||
| Glutathion (nmol/g of brain tissue) |
Brain tissue | 36 White male rats (weighing 260–300 g; 2–3 months of age) | GSH homeostasis as an oxidative stress marker has been disturbed in global and focal ischemia. After focal and global cerebral ischemia, a significant drop was recorded in the levels of the reduced forms of GSH in blood plasma. This effect may be attributed to their oxidation. |
[92] | |
| Control: | |||||
| Reduced GSH | 592 ± 28 | ||||
| Oxidized GSH | 38 ± 4 | ||||
| Bilateral occlusion of the common carotid arteries (BCAO): | |||||
| Reduced GSH | 575 ± 24 | ||||
| Oxidized GSH | 279 ± 20 | ||||
| Middle cerebral artery occlusion (MCAO): | |||||
| Reduced GSH | 593 ± 35 | ||||
| Oxidized GSH | 204 ± 22 | ||||
| Blood | 140 Individuals (33 female, 37 male): | [93] | |||
| Control group (volunteers with similar cerebrovascular risk factors), N = 70 | 2.3 ± 0.4 | ||||
| Patients with acute ischemic stroke, N = 70 | 3.9 ± 2.5 | ||||
| S-adenosylhomocysteine methylation (%) |
Whole peripheral blood |
202 individuals: | In patients with ischemic stroke, the percentage of methylated reference AHCY was significantly higher than in controls. | [94] | |
| Patients with acute ischemic stroke, N = 64 | 0.13% (0.09%, 0.27%) | ||||
| Control group, N = 138 | 0.06% (0.00%, 0.17%) | ||||
| Methionine (odds ratios (oRs) |
Plasma | PREDIMED Cohort, 567 women: Stroke cases, N = 59 Controls, N = 508 |
OR 1.85 (95% CI 1.44–2.37) | Methionine sulfoxide was linked to an increased risk of stroke | [95] |