• Raffaella Trentadue, Trentadue Raffaella, Flavio Fiore, Fabrizia Massaro, Massaro Fabrizia, Francesco Papa, Papa Francesco, Arcangela Iuso, Iuso Arcangela, Salvatore Scacco, Scacco Salvatore, Luigi Santacroce, Santacroce Luigi, Nicola Brienza, and Brienza Nicola.
• Department of Basic Medical Sciences, University of Bari, Italy.
• Life Sci. 2012 Sep 17;91(7-8):237-43.

AimsSepsis which is the leading cause of death in intensive care units is usually related to the number and the severity of organ failure, but the mechanisms remain to be fully established. Findings of microvascular flow abnormalities, decreased oxygen consumption and elevated tissue oxygen tensions suggest that problems may lay in cellular oxygen utilization rather than in oxygen delivery per se. Several serum factors, released during sepsis syndrome, might be involved in induction of cytopathic hypoxia and increase of cellular oxidative stress.Main MethodsHuman fibroblast cultures were incubated 12h with 10% v/v severe septic patients' sera and measurements were carried out on cellular oxygen consumption, mitochondrial respiratory enzymes activity, H(2)O(2) generation and serum levels of cytokines/chemokines by multiplex assay.Key FindingsIn fibroblast cultures a significant depression of cellular respiration and activity of mitochondrial complexes and increased H(2)O(2) production was observed after incubation with septic sera showing increased levels of TNFα, IL-1β and IL-6.SignificanceDuring sepsis syndrome some increased cytokines might target specific mitochondrial enzymes inducing an impairment of cellular energy metabolism leading to multiple organ failure.Copyright © 2012 Elsevier Inc. All rights reserved.

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