Serum reactive oxygen species and apoptosis markers in septic patients

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.

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.

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).

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.