Brain catalase activity is highly correlated with ethanol-induced locomotor activity in mice.
It has been demonstrated that acute administration of lead to mice enhances brain catalase activity and ethanol-induced locomotion. These effects of lead seem to be related, since they show similar time courses and occur at similar doses. In the present study, in an attempt to further evaluate the relation between brain catalase activity and lead-induced changes in ethanol-stimulated locomotion, the interaction between lead acetate and 3-amino-1H,2,4-triazole (AT), a well-known catalase inhibitor, was assessed. In this study, lead acetate or saline was acutely injected intraperitoneally to Swiss mice at doses of 50 or 100 mg/kg 7 days before testing. On the test day, animals received an intraperitoneal injection of AT (0, 10, or 500 mg/kg). Five hours following AT treatment, ethanol (0.0 or 2.5 g/kg, ip) was injected and the animals were placed in open-field chambers, in which locomotion was measured for 10 min. Neither lead exposure nor AT administration, either alone or in combination, had any effect on spontaneous locomotor activity. AT treatment reduced ethanol-induced locomotion as well as brain catalase activity. On the other hand, ambulation and brain catalase activity were significantly increased by both doses of lead. Furthermore, AT significantly reduced the potentiation produced by lead acetate on brain catalase and on ethanol-induced locomotor activity in a dose-dependent manner. A significant correlation was found between locomotion and catalase activity across all test conditions. The results show that brain catalase activity is involved in the effects of lead acetate on ethanol-induced locomotion in mice. Thus, this study confirms the notion that brain catalase provides the molecular basis for understanding some of the mechanisms of the action of ethanol in the central nervous system.
Correa
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Area de Psicobiologia, Universitat Jaume I, Campus Crta., Borriol, Apartado 224, Castelló 12080, Spain.
Sanchis-Segura
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Aragon
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D000818:Animals; D001921:Brain / Q000201:enzymology*; D002374:Catalase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002492:Central Nervous System Depressants / Q000097:blood / Q000494:pharmacology*; D003484:Cyanamide / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D008297:Male; D051379:Mice; D009043:Motor Activity / Q000187:drug effects*; D009942:Organometallic Compounds / Q000494:pharmacology
D002492:Central Nervous System Depressants; D004791:Enzyme Inhibitors; D009942:Organometallic Compounds; D000431:Ethanol; D003484:Cyanamide; D002374:Catalase; C008261:lead acetate