OXIDATIVE STRESS IN MUSCLE AND LIVER OF RATS WITH SEPTIC SYNDROME

Sepsis, as infection associated to systemic manifestations, was produc ed in rats by cecal ligation and double perforation. Sham-operated rat s were used as controls. The spontaneous chemiluminescence of rat addu ctor muscle and liver were measured at 6, 12, 24, and 30 h after the s urgical procedure. Muscle chemiluminesce showed a maximal increase of about twofold (control emission 10 +/- 1 cps/cm(2)) after 6-12 h of se psis, while liver chemiluminescence increased by about 80% (control em ission: 11 +/- 1 cps/cm(2)) after 24 h of sepsis. The activities of mu scle antioxidant enzymes were found maximally diminished after 12 h of sepsis: 46% decrease for Mn-superoxide dismutase, 83% decrease for ca talase, and 55% decrease for glutathione peroxidase. In liver, only ca talase activity showed a 52% decrease after 24 h of sepsis. State 3 ox ygen uptake of muscle mitochondria with either malate-glutamate or suc cinate as substrates was 40% decreased after 12 h of sepsis in both ca ses. State 4 oxygen uptake of muscle mitochondria was not affected. Th e rate of H2O2 production of muscle mitochondria after 12 h of sepsis with either malate-glutamate or succinate as substrates was increased about 2.5 times but was not affected when assayed in the presence of a s rotenone and antimycin. The oxygen uptake of liver mitochondria isol ated from septic rats did not show differences as compared with those of control rats after 6 to 24 h of sepsis. Oxidative stress appears to occur in skeletal muscle early at the onset of the septic syndrome, w ith inhibition of active mitochondrial respiration and inactivation of antioxidant enzymes. The liver undergoes a milder oxidative stress la ter in the development of the septic syndrome, without mitochondrial d amage and with slight catalase inactivation.