Free Radicals, Mitochondrial Dysfunction and Sepsis-induced Organ Dysfunction: A Mechanistic Insight

Sepsis is a complex clinical condition and a leading cause of death worldwide. During Sepsis, there is a derailment in the host response to infection, which can progress to severe sepsis and multiple organ dysfunction or failure, which leads to death. Free radicals, including reactive oxygen species (ROS) generated predominantly in mitochondria, are one of the key players in impairing normal organ function in sepsis. ROS contributing to oxidative stress has been reported to be the main culprit in the injury of the lung, heart, liver, kidney, gastrointestinal, and other organs. Here in the present review, we describe the generation, and essential properties of various types of ROS, their effect on macromolecules, and their role in mitochondrial dysfunction. Furthermore, the mechanism involved in the ROS-mediated pathogenesis of sepsis-induced organ dysfunction has also been discussed.