This is an image preview.
Start a Free Account
to view the full image.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Pathophysiological effects of acute carbon monoxide exposure

Download

In circulating red blood cells, carbon monoxide binds to heme sites in hemoglobin, diminishing oxygen-carrying capacity and stabilizing the high-affinity R-state. In addition to binding hemoglobin in circulation, carbon monoxide may also bind myoglobin, causing a reduction in oxygen availability in tissue. In mitochondria, carbon monoxide may directly bind the heme a₃ site in complex IV of the mitochondrial electron transport chain, inhibiting the reduction of oxygen to water. This inhibition, coupled with reduced oxygen availability, leads to membrane depolarization, reduced ATP output, and accumulation of reducing equivalents in the electron transport chain. These reducing equivalents may react with oxygen to form superoxide (O₂^•−), which may propagate cellular damage directly or through conversion to other reactive oxygen species, such as hydrogen peroxide. Abbreviations: CO, carbon monoxide; CoQ, coenzyme Q/ubiquinone; Cyt c, cytochrome c; ETC, electron transport chain; H2O2, hydrogen peroxide; Hb-R, relaxed-state hemoglobin; Hb-T, tense-state hemoglobin; pO₂, partial pressure of oxygen. (Source: Dent MR, Rose JJ, Tejero J, Gladwin MT. Carbon monoxide poisoning: from microbes to therapeutics. Annu Rev Med 2024;75:337-51. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)