Mitochondrial and oxidative stress play critical roles in the pathogenic mechanisms of
carbon monoxide (CO)-induced toxicity. This study was designed to evaluate whether the serum levels of specific stress
biomarkers might reflect
brain injury and act as prognostic markers for the development of neurocognitive sequelae following CO
poisoning. We analyzed the data from 51 adult patients admitted with acute CO
poisoning and measured the serum level expression of
growth differentiation factor 15 (GDF15) and
fibroblast growth factor 21 (
FGF21), indicators of mitochondrial stress, and
8-Oxo-2'-deoxyguanosine (8-OHdG) and
malondialdehyde (MDA), indicators of oxidative stress. Serum was collected upon arrival at the hospital, at 24 h post treatment, and within 7 days of HBO2
therapy. Global Deterioration Scale scores were measured 1 month post incident and used to place the patients in either favorable or poor outcome groups. Initial serum GDF15 and 8-OHdG concentrations were significantly increased in the poor-outcome group and all four
biomarkers decreased at 24 h post HBO2
therapy, and were then maintained or further decreased at the 1-week mark. Notably, the degree of change in these
biomarkers between baseline and 24 h post HBO2 were significantly larger in the poor-outcome group, reflecting greater CO-associated stress, confirming that post-CO
poisoning serum
biomarker levels and their response to HBO2 were proportional to the initial stress. We suggest that these
biomarkers accurately reflect neuronal toxicity in response to CO
poisoning, which is consistent with their activity in other pathologies.