Lipid peroxidation in the rat brain after CO inhalation is temperature dependent

We reported previously that 7-hydroperoxycholesterols, 7α- and 7β-hydroperoxycholest-5-en-3β-ol (7α-OOH and 7β-OOH), indicated lipid peroxidation [1]. In the present study, we measured not only 7-hydroperoxycholesterols but also oxysterols (7α- and 7β-hydroxycholesterol, 7α-OH, and 7β-OH) and 3β-hydroxycholest-5-en-7-one (7-keto) in the brains of rats that underwent either a sham operation (control), hypoxia, or CO inhalation (1005 ppm) at 37°C for 90 min followed by 48 h of recovery. The levels of 7-hydroperoxycholesterols, 7β-OH, and 7-keto were low in the hypoxia group, while the levels were unaltered in the CO group compared with the controls. Among the three groups of CO inhalation, these levels were high in the hyperthermia group (39°C), and the 7-hydroperoxycholesterols were low in the hypothermia group (32°C), compared with the control group. The blood O2 saturation was almost normal in the hypothermia group, while it was similarly low in the hyperthermia and normothermia groups. The temperature-dependent lipid peroxidation in the brain after CO inhalation and recovery can not be explained by hypoxia due to CO-hemoglobin formation, but may contribute to the delayed neuronal death following CO inhalation. Hypothermia may be applicable to treat patients after CO inhalation.