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Brain Catalase Inhibition Blocks Ethanol‐Related Decrease of Blood Luteinizing Hormone Levels in Mice
Author(s) -
SanchisSegura Carles,
Aragon Carlos M. G.
Publication year - 2002
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/j.1530-0277.2002.tb02667.x
Subject(s) - catalase , ethanol , endorphins , luteinizing hormone , chemistry , endocrinology , medicine , hypothalamus , hormone , pharmacology , enzyme , biochemistry
Background It has been demonstrated that ethanol decreases blood luteinizing hormone (LH) levels in rodents. This effect seems to be produced by the capacity of ethanol to release β‐endorphins from the hypothalamic arcuate nucleus and, in a second step, by a μ‐receptor–mediated inhibitory effect of these peptides on hypothalamic LH‐releasing hormone‐synthesizing neurons. However, it has been reported that, in primary hypothalamic cultures, the ethanol‐produced β‐endorphin release is mediated by the enzyme catalase. Therefore, the aim of this study was to assess whether catalase inhibition modifies ethanol effects on blood LH levels. Methods Swiss albino mice were pretreated with the catalase inhibitor 3‐amino‐1,2,4‐triazole (AT; 0.0–0.5 g/kg) and, 3.5 hr later, saline, ethanol (2.5 g/kg), or morphine (30 mg/kg) was administered. Blood samples were collected 2 hr after ethanol administration, and LH levels were immunoenzymatically assayed. Results The catalase inhibitor AT dose‐dependently blocked the ethanol‐produced decrease in blood LH levels without altering those observed after saline or morphine administration. This effect was highly correlated with the decrease in brain catalase activity produced by AT. Conclusions These results show an antagonistic effect between AT and ethanol on blood LH levels and suggest a role of brain catalase activity on this effect of ethanol. Data are discussed in terms of a possible functional relationship between brain catalase and β‐endorphins in the mediation of some of the psychopharmacological consequences observed after ethanol administration.