Histotoxic hypoxia refers to a reduction in ATP production by the mitochondria due to a defect in the cellular usage of oxygen.
Cyanide binds to the ferric ion on cytochrome oxidase a3 and prevents the fourth and final reaction in the electron transport chain.
[3] There are other chemicals that interrupt the mitochondrial electron transport chain (e.g., rotenone, antimycin A) and produce effects on tissue oxygenation similar to that of cyanide.
During a stroke, there is an interruption in the blood supply followed by reperfusion which leads to histotoxic hypoxia because of an accumulation of reactive oxygen species (ROS).
[4] In the case of inflammatory diseases, histotoxic hypoxia can also be triggered by ROS from mitochondrial damage in the active lesions of chronic multiple sclerosis.