In situ and real time muscle chemiluminescence determines singlet oxygen involvement in oxidative damage during endotoxemia.

Many studies have reported the occurrence of oxidative stress in different models of sepsis, but no measurements in real time and in non-invasive manner in an acute model of endotoxemia were done, being its mechanism still under debate. In the present work, we have used in situ surface chemiluminescence to evaluate the reactive oxygen species steady-state concentrations and to identify the main chemical species involved in this phenomenon. Experimental endotoxemia provoked a twofold increase in skeletal muscle chemiluminescence (control value: 31+/-4cps/cm(2)). The use of cutoff filters and D(2)O and biacetyl as specific enhancers, indicates that singlet oxygen is the main emitting species in this model. This result closely correlates with elevated TBARS levels, an index of oxidative damage to lipids. Increased NO production and NADPH oxidase activity may support the formation of ONOO(-), which in turn may originate HO, an initiator of the lipid oxidation chain. In summary, our data show for the first time that (1)O(2) is the main chemical and emitting species involved in the mechanism of oxidative stress present in an acute model of endotoxemia. This work provides new insights necessary to understand free radical mechanisms behind endotoxemic syndrome.