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Homogenates of perfused rat brains incubated in the presence of ethanol (50-100 mM) and glucose (10 mM) were found to oxidize ethanol to acetaldehyde. The addition of glucose oxidase, a known hydrogen peroxide generator, to the incubation medium, significantly (P less than 0.05) increased the generation of acetaldehyde. The presence in the incubation medium of metyrapone, an inhibitor of cytochrome P450, or pyrazole, an alcohol dehydrogenase inhibitor, did not affect the levels of acetaldehyde obtained. Conversely, the presence of 3-amino-1,2,4-triazole, a known catalase inhibitor, induced a concentration-dependent reduction of the amount of acetaldehyde generated after incubation, even in the presence of glucose oxidase. Homogenates of perfused brains of rats treated with 3-amino-1,2,4-triazole or cyanamide (another H2O2-dependent catalase blocker) also showed a dose-dependent reduction of the acetaldehyde obtained. These findings support the notion that a catalase-mediated oxidation of ethanol is present in rat brain homogenates. It is suggested that this local oxidation of ethanol may have important biological implications. The data of both studies increase support for the notion that acetaldehyde is produced directly in the brain and that it may be the agent mediating some of the psychopharmacological properties of ethanol and be one of the factors determining the propensity of an animal to voluntarily consume ethanol.

Whole brain dopamine (DA) and norepinephrine (NE) levels were measured in sexually maturing (2 years +) male and female rainbow trout, Oncorhynchus mykiss, following exposure to 0.01 mg/L hydrogen cyanide (HCN). Following a 12 day exposure period in July and August 1988, whole brain DA levels of HCN exposed fish were significantly higher (p less than 0.05), relative to control fish, as measured by high performance liquid chromatography (HPLC). Brain NE levels were unaffected by HCN exposure. Whole brain DA and NE levels showed a strong correlation in control fish (r = +0.81), but not in HCN exposed fish (r = +0.28), likely due to altered DA levels in the latter group. No significant differences were found in brain DA and NE levels between males and females. Mean diameters of oocyte from ovaries of the vitellogenic females were significantly (p less than 0.01) reduced from 226 to 183 microns in control and HCN exposed fish respectively. Testes from males revealed significantly (p less than 0.001) higher numbers of spermatogonial cysts in HCN exposed fish. Evidence is given that chronic exposure to sublethal levels of HCN significantly alters brain DA levels in both sexes of rainbow trout, reduces growth in vitellogenic oocytes of the ovary in females and interferes with the passage of spermatogonia to the spermatocyte stage in sexually maturing males. Collectively, these results suggest that sublethal HCN affects the reproductive mechanisms via the hypophyseal-gonad axis in sexually maturing rainbow trout.