Application of Mitochondrial and Oxidative Stress Biomarkers in the Evaluation of Neurocognitive Prognosis Following Acute Carbon Monoxide Poisoning

Yong Sung Cha, Jae Seung Chang, Hyun Kim, Kyu Sang Park

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


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.

Original languageEnglish
Article number201
Issue number3
Publication statusPublished - 2022 Mar

Bibliographical note

Funding Information:
Funding: This work was supported by the National Research Foundation of Korea, which is funded by the Korean government (Ministry of Science and Information and Communications Technology, grant no. NRF-2019R1A2C2084604 and 2017R1A5A2015369).

Publisher Copyright:
© 2022 by the authors. Licensee MDPI, Basel, Switzerland.

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Molecular Biology


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