In sepsis, reactive oxygen species (ROS) production is increased. This process takes place mainly within the electron transport chain. ROS production is part of the pathophysiology of multiple organ failure in sepsis. Succinate yields Dihydroflavine-Adenine Dinucleotide (FADH2), which enters the chain through complex II, avoiding complex I, through which electrons are lost. The aim of this work is to determine if parenteral succinate reduces systemic ROS production and improves kidney function. Rats with cecal ligation and puncture were used as model of sepsis, and 4 groups were made: Control group; Succinate group, which only received parenteral succinate; Sepsis group; and Sepsis which received parenteral succinate. Systemic ROS are measured 24 hours after the procedure. Rats subjected to cecal puncture treated with succinate had less systemic ROS than Septic untreated rats (p = 0.007), while there were no differences in creatinine levels (p = 0.07). There was no correlation between creatinine and systemic ROS levels (p = 0.3). We concluded that parenteral succinate reduces ROS levels, but it does not reduce creatinine levels. Since there is no correlation between both levels, the processes would not be related.

Background: Oxidative stress is one of the pathophysiological processes that occur during sepsis. Reactive oxygen species (ROS) production causes lipid peroxidation and protein and DNA damage. ROS and DNA damage triggers apoptosis. Several studies have shown that organ failure in sepsis is mediated by apoptosis. The aim of this study is to investigate the levels of serum ROS and serum caspase-3 in septic patients and healthy volunteers, and their correlation.Methods: Serum samples were taken within the first 12 hours of ICU stay. The dichlorofluorescein technique was used to determine serum ROS levels, and the ELISA technique was used to quantify serum caspase-3 in septic patients and healthy volunteers.Results: There was no difference in serum ROS levels between healthy volunteers and septic patients (P = 0.26), and there was a significant difference in serum caspase-3 levels between healthy volunteers and septic patients (P < 0.001). There was no difference between patients who lived and died in the intensive care unit (ICU) in serum ROS (P = 0.089) and serum caspase-3 (P = 0.18). There was no correlation between both markers (R = -0.0013, P = 0.98). Conclusions:We conclude that there is no correlation between serum ROS and caspase-3; therefore, both processes might not be associated during the first hours of ICU stay.

We investigated the damage caused by oxidative stress using the yeast Saccharomyces cerevisiae as a model biological system. After inducing oxidative stress with menadione, we were able to evaluate the extent of cellular oxidative stress by utilizing 2',7'-dichlorofluorescein diacetate (DCFH-DA) as a marker of the presence of reactive oxygen species. Cells were grown on different carbon sources in order to compare fermentative and oxidative metabolism. Under these conditions we evaluated the effectiveness of idebenone (2,3-dimethoxy-5-methyl-6-(10- hydroxydecyl)-1,4-benzoquinone) as a molecule that could relieve menadione-induced growth inhibition in Saccharomyces cerevisiae.

We investigated the damage caused by oxidative stress using the yeast Saccharomyces cerevisiae as a model biological system. After inducing oxidative stress with menadione, we were able to evaluate the extent of cellular oxidative stress by utilizing 2',7'-dichlorofluorescein diacetate (DCFH-DA) as a marker of the presence of reactive oxygen species. Cells were grown on different carbon sources in order to compare fermentative and oxidative metabolism. Under these conditions we evaluated the effectiveness of idebenone (2,3-dimethoxy-5-methyl-6-(10- hydroxydecyl)-1,4-benzoquinone) as a molecule that could relieve menadione-induced growth inhibition in Saccharomyces cerevisiae.