Cinnabarinic acid was formed in damaged mitochondria and its effect on mitochondrial respiration.

Tryptophan administration aggravates experimental mouse liver injury caused by carbon tetrachloride when 3-hydroxyanthranilic acid concentration elevates in serum. Tryptophan metabolism is changed by macrophages in injured liver. 3-Hydroxyanthranilic acid may be oxidized to cinnabarinic acid by injured mitochondria in the liver aggravating the state of injured liver. Mitochondria prepared from the liver 24 hr after CCl4 treatment have lost their ability of respiratory control. In consequence, 3-hydroxyanthranilic acid is oxidized to cinnabarinic acid by incubation with these mitochondria, whereas 3-hydroxykynurenine is not. Thus, formed cinnabarinic acid is able to inhibit completely the mitochondrial respiratory control at concentration of 10 microM.