The catalase inhibitor sodium azide reduces ethanol-induced locomotor activity.

The involvement of brain catalase in modulating the psychopharmacological effects of ethanol was investigated by examining ethanol-induced locomotor activity in sodium azide-treated mice. Mice were pretreated with i.p. injections of the catalase inhibitor sodium azide (5, 10, or 15 mg/kg) or saline. Following this treatment, animals received i.p. injections of ethanol (0.0, 1.6, 2.4, or 3.2 g/kg). Ten minutes after ethanol administration, locomotor activity was recorded during a 10-min testing period in open-field chambers. The time effect between the two treatments (0, 30, 60, or 90 min) was also evaluated. Results indicated that sodium azide alone did not change spontaneous locomotor activity. However, this catalase inhibitor significantly reduced ethanol-induced locomotor activity when it was injected simultaneously or 30 min before ethanol injections. Moreover, perfused brain homogenates of mice treated with sodium azide also showed a significant reduction of catalase activity. No differences in blood ethanol levels were observed between sodium azide and saline pretreated animals. Results of an additional experiment showed that sodium azide (10 mg/kg, at 30 min) did not produce an effect on d-amphetamine- (2 mg/kg) or tert-butanol- (0.5 g/kg) induced locomotor activities. A specific interaction between ethanol and sodium azide at the level of the central nervous system is suggested. These results provide further support for the involvement of brain catalase in ethanol-induced behavioral effects. They also support the notion that acetaldehyde may be produced directly in the brain by catalase and that it may be an important regulator of ethanol's locomotor effects.