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. 2020 Jul 2;9(7):2081. doi: 10.3390/jcm9072081

Table 2.

Biomarkers of alcohol metabolism, oxidative stress and the inflammatory response to alcohol consumption and their relation to hangover severity.

Biomarker Time After Alcohol Consumption
0 h 0.5 h 2 h 4 h 12 h
Ethanol (mg/dL) 26.2 (4.5) 14.8 (3.5) 6.8 (1.0) 2.7 (0.4)
Acetaldehyde (mg/dL) 0.42 (0.03) 0.28 (0.05) 0.17 (0.02)
Interleukin (IL)-6 (pg/mL) 4.2 (0.0) 4.3 (0.8) 5.1 (1.0) 5.8 (1.0) 6.1 (1.0)
C-reactive protein (mg/L) 2.2 (0.6) 2.6 (0.7) 3.3 (0.8) 3.8 (0.7) * 3.8 (1.2)
8-isoprostane (pg/mL) 22.6 (4.5) 25.3 (3.5) 26.2 (4.8) 29.8 (7.1) 30.6 (6.5) *
Malondialdehyde (nmol/dL) 72.0 (7.3) 83.4 (7.2) * 94.4 (7.0) 95.5 (7.0) 92.6 (13.3)
Glutathione (nmol/mg Hb) 23.9 (3.4) 21.7 (3.1) 21.6 (3.9) 23.0 (2.4) 21.7 (3.5)
Superoxide dismutase (U/mL) 0.42 (0.1) 0.35 (0.1) 0.30 (0.1) 0.28 (0.1) 0.27 (0.1)

Biomarker assessments after consumption of alcohol to reach a desired BrAC of 0.03%. Mean and standard deviation (between brackets) are shown. Significant correlations with hangover severity (p < 0.05), assessed 14 h after alcohol consumption, are indicated by *. – = ethanol and acetaldehyde were not assessed at 0 h, and acetaldehyde could not be detected 12 h after alcohol consumption. Data from Mammen et al. [23].