in the previous issue of critical care , donnino and colleagues   suggest a coenzyme q10 ( coq10 ) deficiency in patients with septic shock . this study provides new insights into the field of oxidative stress and mitochondrial dysfunction during septic shock . though extensively studied , the pathophysiology of sepsis - associated multi - organ failure ( mof ) remains unknown . one postulated mechanism is a set of changes in mitochondrial function with an inhibition or a dysfunction of the mitochondrial respiratory chain and a decrease of oxygen use . 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 ) . understanding the precise effect of sepsis on the mitochondrial function and the involvement of mitochondria in the development of mof is fundamental . coq10 , also known as ubiquinone , plays a crucial role in the mitochondrial respiratory chain for atp production . coq10 is a lipophilic mobile electron carrier that is located in the inner mitochondrial membrane . coq10 receives electrons from complex i ( nadh dehydrogenase ) and complex ii ( succinate dehydrogenase ) ( reduction of ubiquinone to ubiquinol ) . complex iii ( coenzyme q - cytochrome c reductase ) accepts electrons from ubiquinol and passes them to cytochrome c. coq10 has been reported to have the ability to act as an effective antioxidant . ubiquinone prevents peroxidation damage to cell membranes , regenerates -tocopherol , and maintains thiol levels . finally , coq10 plays a role in the control of mitochondrial transition pore opening , which is involved in apoptosis . several studies suggest an important role of coq10 deficiency in neurodegenerative conditions such as parkinson disease , friedreich ataxia , and huntington chorea and a benefit of oral supplementation . in addition , coq10 deficiency could play a role in the pathogenesis of heart failure . recently , mcmurray and colleagues   reported that a low serum coq10 concentration was associated with worse outcomes in heart failure . it is important to note that , in that study , coq10 was a marker of more advanced disease but that low plasma coenzyme coq10 was not an independent predictor of prognosis . so if there is a deficit in coq10 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 coq10 on the consequences of sepsis . injection of coq10 into the rostral ventrolateral medulla ( medullary origin of sympathetic vasomotor tone ) of rats diminished mortality and lipopolysaccharide - induced hypotension during exposure to lipopolysaccharide . lowes and colleagues   reported that mitoq , an antioxidant this is selectively targeted to mitochondria and that comprises the lipophilic triphenylphosphonium cation covalently bound to ubiquinol , was able to limit oxidative stress , maintain the mitochondrial 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   demonstrated that mitoq prevented endotoxin - induced reductions in cardiac pressure - generating capacity , systolic pressure - diastolic relationship , and mitochondrial respiration rates . these authors found that mitoq prevented the endotoxin - induced increase of cardiac levels of active caspases 9 and 3 . in this context , donnino and they report that coq10 levels of patients with septic shock are significantly lower than those of healthy controls . this result is interesting because it is the first report of low coq10 levels in patients with septic shock . a major point to be considered in the interpretation of these low coq10 levels is the set of changes in its major carriers , the low- and high - density lipoproteins , because the levels of these carriers can be affected by sepsis . the main limitation of this study is that it is a post hoc analysis of a prospective randomized trial of simvastatin versus placebo in patients with septic shock . as several studies have reported that patients treated with statins showed significant decreases in plasma / serum coq10 , it could be argued that the observed low coq10 levels are due to the simvastatin group . however , as mentioned by the authors , the sample size for this study is small and larger prospective observational trials measuring coq10 in patients with septic shock are required . but while we share the enthusiasm for coq10 supplementation and mitochondria - targeted coq10 as putative therapies in sepsis , low coq10 levels could be associated with greater disease severity without playing an important mechanistic role in the pathophysiology of sepsis . this question can be definitively answered only by appropriately designed clinical trials testing the therapeutic efficacy of coq10 supplementation or mitochondria - targeted coq10 . in conclusion , donnino and colleagues this is an exciting hypothesis in the field of oxidative stress and mitochondrial dysfunction during septic shock . this study is a new step toward a study testing coq10 as a potential therapeutic agent for patients with septic shock .
donnino and colleagues provide new insights into the field of oxidative stress and mitochondrial dysfunction during septic shock . 
 these authors suggest a coenzyme q10 ( coq10 ) deficiency in patients with septic shock . 
 larger prospective observational trials measuring coq10 in patients with septic shock are required to confirm the possibility of coq10 depletion . 
 this study is a new step toward a study testing coq10 as a potential therapeutic agent for patients with septic shock .