It is known that peroxides, which are increased during Se deficiency because of reduced glutathione peroxidase (GSH-Px) activity, can influence the prostacyclin I2/thromboxane A2 (PGI2/TXA2) ratio. In this study we analyzed the PGI2 and TXA2 formation of aortas of long-term Se-deficient rats. Despite low GSH-Px activity in the Se-deficient group, the basal PGI2 and TXA2 formation was not different versus control animals (PGI2: 2295+/-1134 pg/mg vs 2940+/-1134 pg/mg; TXA2: 3.83+/-1.06 pg/mg vs 5.67+/-2.99 pg/mg). However, we checked the capacity of the aortas of Se-deficient rats to compensate for a suddenly increased peroxide concentration. After peroxide stimulation, the PGI2 release was significantly lower in the Se-deficient group compared to the control group (PGI2: 3507+/-1829 pg/mg vs 7986+/-2636 pg/mg). Again, the TXA2 release did not show any differences. The release ratio of PGI2/TXA2 decreased under peroxide stress in Se-deficient animals. Although long-term Se deficiency showed a relatively well-balanced metabolism under resting conditions, sudden stress, accompanied by an excessive radical production, cannot be compensated.