In the previous issue of Critical Care, Donnino and colleagues [1] suggest a coenzyme Q 10 (CoQ 10 ) deficiency in patients with septic shock. Tis study provides new insights into the field of oxidative stress and mitochon- drial dysfunction during septic shock. Tough extensively studied, the pathophysiology of sepsis-associated multi- organ failure (MOF) remains unknown. Sepsis is charac- terized by a systemic dysregulated inflammatory res- ponse and oxidative stress. One postulated mechanism is a set of changes in mitochondrial function with an inhibition or a dysfunction of the mitochondrial respira- tory chain and a decrease of oxygen use [2]. A large body of evidence supports a key role of excessive production of reactive oxygen species in mitochondrial dysfunction and cellular injury during the various phases of sepsis (early- and late-phase MOF) [3,4]. Understanding the precise effect of sepsis on the mitochondrial function and the involvement of mitochondria in the development of MOF is fundamental. CoQ 10 , also known as ubiquinone, plays a crucial role in the mitochondrial respiratory chain for ATP production. CoQ 10 is a lipophilic mobile electron carrier that is located in the inner mitochondrial membrane. CoQ 10 receives electrons from complex I (NADH dehydroge- nase) and complex II (succinate dehydrogenase) (reduc- tion of ubiquinone to ubiquinol). Complex III (coenzyme Q-cytochrome c reductase) accepts electrons from ubiquinol and passes them to cytochrome c. CoQ 10 has been reported to have the ability to act as an effective antioxidant. Ubiquinone prevents peroxidation damage to cell membranes, regenerates α-tocopherol, and main- tains thiol levels. CoQ 10 is also a cofactor for uncoupling proteins. Finally, CoQ 10 plays a role in the control of mitochondrial transition pore opening, which is involved in apoptosis. Several studies suggest an important role of CoQ 10 deficiency in neurodegenerative conditions such as Par- kinson disease, Friedreich ataxia, and Huntington chorea and a benefit of oral supplementation [5]. In addition, CoQ 10 deficiency could play a role in the pathogenesis of heart failure. Recently, McMurray and colleagues [6] reported that a low serum CoQ 10 concentration was associated with worse outcomes in heart failure. It is important to note that, in that study, CoQ 10 was a marker of more advanced disease but that low plasma coenzyme CoQ 10 was not an independent predictor of prognosis. So if there is a deficit in CoQ 10 during sepsis, the drug could be used in the prevention and treatment of sepsis- associated MOF to boost mitochondrial function and to mitigate cellular damage caused by oxidative stress. Until now, only animal models have been used to test the impact of CoQ 10 on the consequences of sepsis. Injection of CoQ 10 into the rostral ventrolateral medulla (medullary origin of sympathetic vasomotor tone) of rats diminished mortality and lipopolysaccharide-induced hypotension during exposure to lipopolysaccharide [7]. Lowes and colleagues [8] reported that MitoQ, an antioxidant this is selectively targeted to mitochondria and that comprises the lipophilic triphenylphosphonium cation covalently bound to ubiqui- nol, was able to limit oxidative stress, maintain the mito- chondrial membrane potential, and prevent mitochondrial damage (endothelial cell model of sepsis) and acute liver and renal dysfunction (rat model of sepsis). In rat and mouse models of sepsis induced by endotoxin injected intraperitoneally, Supinski and colleagues [9] demon- strated that MitoQ prevented endotoxin-induced reduc- tions in cardiac pressure-generating capacity, systolic Abstract Donnino and colleagues provide new insights into the feld of oxidative stress and mitochondrial dysfunction during septic shock. These authors suggest a coenzyme Q 10 (CoQ 10 ) defciency in patients with septic shock. Larger prospective observational trials measuring CoQ 10 in patients with septic shock are required to confrm the possibility of CoQ 10 depletion. This study is a new step toward a study testing CoQ 10 as a potential therapeutic agent for patients with septic shock. © 2010 BioMed Central Ltd Coenzyme Q 10 defciency in septic shock patients Laurent Dupic 1 , Olivier Huet 2,3 and Jacques Duranteau* 3 See related research by Donnino et al., http://ccforum.com/content/15/4/R189 COMMENTARY *Correspondence: jacques.duranteau@bct.aphp.fr 3 Assistance Publique - Hôpitaux de Paris, Hôpital Bicêtre, Département d’Anesthésie-Réanimation, EA 3509 Université Paris Sud XI, France F-94275, Le Kremlin-Bicêtre, France Full list of author information is available at the end of the article Dupic et al. Critical Care 2011, 15:194 http://ccforum.com/content/15/5/194 © 2011 BioMed Central Ltd