MitoQ (Mitoquinone) mesylate

Mitoquinone blocks H2O2-induced intracellular ROS responses inmurine pancreatic acinar cells. Mitoquinone does not reduce mitochondrial depolarisation induced by either cholecystokinin (CCK) or bile acid TLCS. Mitoquinone increases basal and CCK-induced cell death in a plate-reader assay.^[1]

The cells are loaded with 40 nM TMRM for 30 minutes prior incubation with either 1 μM or 10 μM of MitoQ or dTPP. Cholecystokinin-8 (CCK-8, 10 nM) or bile acid taurolithocholic acid 3-sulphate (TLCS, 500 μM) is used to induce ΔΨm depolarisation. At the end of the perfusion, the protonophore carbonyl cyanide 3-chlorophenylhydrazone (CCCP, 10 μM) is added to induce complete depolarisation of ΔΨm. The fluorescence of TMRM is excited at 543 nm and the emission is collected at 560–650 nm.

In a TLCS-induced AP model Mitoquinone treatment is not protective. In AP induced by caerulein hyperstimulation (CER-AP), Mitoquinone exerts mixed effects. Thus, partial amelioration of histopathology scores is observed but without reduction of the biochemical markers pancreatic trypsin or serumamylase. Lungmyeloperoxidase and interleukin-6 are concurrently increased by Mitoquinone in CER-AP. Mitoquinone causes biphasic effects on ROS production in isolated polymorphonuclear leukocytes, inhibiting an acute increase but elevating later levels.^[1]