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Participation of Catalase in Voluntary Ethanol Consumption in Perinatally Low‐Level Lead‐Exposed Rats
Author(s) -
Mattalloni Mara S.,
Giovanni Laura N.,
Molina Juan C.,
Cancela Liliana M.,
Virgolini Miriam B.
Publication year - 2013
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.12150
Subject(s) - catalase , acetaldehyde , saline , lactation , chemistry , ethanol , medicine , endocrinology , antioxidant , biochemistry , biology , pregnancy , genetics
Background Environmental lead ( P b) exposure and alcohol abuse pose significant public health problems for our society. One of the proposed mechanisms of action of the developmental neurotoxicant P b is related to its ability to affect antioxidant enzymes, including catalase ( CAT ). Ethanol's ( E t OH ) motivational effects are postulated to be mediated by the CAT ‐dependent acetaldehyde generated in the brain. The current study sought to investigate the role of this enzyme in the elevated EtOH intake previously reported in perinatally P b‐exposed rats. Methods Thirty‐five‐day‐old male W istar rats exposed to 220 ppm P b during gestation and lactation were offered escalating E t OH solutions (2 to 10%) or water, 2 h/d for 28 days. Once baseline 10% E t OH intake was achieved, they were injected with (i) saline ( SAL ), (ii) 3‐amino 1,2,4 triazole (aminotriazole [AT] , a CAT inhibitor, 250 mg/kg intraperitoneally [i.p.], 5 hours before the last 8 E t OH intake sessions), or (iii) 3‐nitropropionic acid (3 NPA ; a CAT activator, 20 mg/kg subcutaneously [s.c.], 45 minutes before the last 4 E t OH intake sessions). Rats were then sacrificed, blood collected, and brain regions harvested for CAT activity determination. Additional studies evaluated E t OH intake and CAT activity in response to 10 and 30 mg/kg 3 NPA . Both 3 NPA and AT were evaluated for striatal cytotoxicity. Results We observed that AT pretreatment blunted the increased E t OH intake, as well as the elevated CAT activity in blood, cerebellum, and hippocampus evidenced in the developmentally P b‐exposed rats that have consumed E t OH . Conversely, 20 mg/kg 3 NPA further increased voluntary E t OH intake in these animals as compared with controls, concomitantly with a slight elevation in CAT activity both in blood and in the striatum, associated with no changes in striatal cytotoxicity. Conclusions These results suggest a participation of CAT , and possibly acetaldehyde, in P b‐induced high E t OH intake, and open up new avenues to elucidate the mechanism that underlies the P b and E t OH interaction.