Higher correlation of ethanol consumption with brain than liver aldehyde dehydrogenase in three strains of rats

Socaransky, S.M.; Aragón, Carlos M.G.; Amit, Zalman; Blander, Adina

doi:10.1007/bf00427454

Cited by 31 publications

(9 citation statements)

References 24 publications

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“…Similarly, brain ALDH activity has been modulated to increase the locomotor-stimulating effects of ethanol in rats (Spivak et al, 1987; Martí-Prats et al, 2013). Moreover, a positive correlation between voluntary ethanol consumption and brain ALDH activity (Sinclair and Lindros, 1981; Socaransky et al, 1984) has been described, also, by means of a lentiviral vector encoding for ALDH and enhancing acetaldehyde metabolism (Karahanian et al, 2015). Besides the evidence gathered by behavioral studies, the involvement of local acetaldehyde formation in the central effects of ethanol was also provided by an in vitro electrophysiological approach showing that local catalase inhibition, through 3-AT administration, prevents the effect of ethanol on pVTA DA neurons (Melis et al, 2007).…”

Section: Role Of Brain Ethanol-derived Acetaldehyde In the Effects Ofmentioning

confidence: 99%

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Peana

Sánchez-Catalán

Hipólito

et al. 2017

Front. Behav. Neurosci.

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After decades of uncertainties and drawbacks, the study on the role and significance of acetaldehyde in the effects of ethanol seemed to have found its main paths. Accordingly, the effects of acetaldehyde, after its systemic or central administration and as obtained following ethanol metabolism, looked as they were extensively characterized. However, almost 5 years after this research appeared at its highest momentum, the investigations on this topic have been revitalized on at least three main directions: (1) the role and the behavioral significance of acetaldehyde in different phases of ethanol self-administration and in voluntary ethanol consumption; (2) the distinction, in the central effects of ethanol, between those arising from its non-metabolized fraction and those attributable to ethanol-derived acetaldehyde; and (3) the role of the acetaldehyde-dopamine condensation product, salsolinol. The present review article aims at presenting and discussing prospectively the most recent data accumulated following these three research pathways on this never-ending story in order to offer the most up-to-date synoptic critical view on such still unresolved and exciting topic.

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Section: Role Of Brain Ethanol-derived Acetaldehyde In the Effects Ofmentioning

confidence: 99%

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Peana

Sánchez-Catalán

Hipólito

et al. 2017

Front. Behav. Neurosci.

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“…As such, these enzymes may be acting as a biological marker system mediating voluntary ethanol consumption. The major difficulty with the interpretation of the data described above lies in the fact that the determinations of enzyme activity were performed after a relatively prolonged period of ethanol intake (25 days) (Socaransky et al 1984;Aragon et al 1985c). Consequently, one could not rule out some chronic effect of ethanol ingestion on the activity of the enzymes, even when an ethanol-free interval was imposed between the ethanol intake period and enzyme determinations (Aragon et al 1985c).…”

mentioning

confidence: 99%

Catalase activity measured in rats naive to ethanol correlates with later voluntary ethanol consumption: possible evidence for a biological marker system of ethanol intake

Amit

Aragón

1988

Psychopharmacology

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Catalase activity in blood collected from young rats naive to ethanol (65 days) was significantly and positively correlated with later voluntary consumption of ethanol. Catalase activity levels were also correlated with catalase activity in brain and blood sampled after exposure to ethanol. The results obtained in the present study extend and confirm earlier findings (Aragon et al. 1985c) that brain catalase activity and voluntary ethanol intake are unidirectionally and causally related. The results also suggest that brain catalase activity may be part of an enzymatic system controlling the production and elimination of acetaldehyde in brain. This system may be a biological marker system mediating the affinity of organisms to ingest ethanol.

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“…Altered central DA function has been implicated as influencing the propensity for ethanol consumption in humans [42]. Enhanced 5-HT 2A receptor status in the hypothalamus and corpus striatum of ethanol treated rats was reported [43].…”

Section: Discussionmentioning

confidence: 99%

Enhanced dopamine D2 receptor function in hypothalamus and corpus striatum: their role in liver, plasma and in vitro hepatocyte ALDH regulation in ethahol treated rats

et al. 2008

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Dopamine D 2 receptors are involved in ethanol self-administration behavior and also suggested to mediate the onset and offset of ethanol drinking. In the present study, we investigated dopamine (DA) content and Dopamine D 2 (DA D 2 ) receptors in the hypothalamus and corpus striatum of ethanol treated rats and aldehyde dehydrogenase (ALDH) activity in the liver and plasma of ethanol treated rats and in vitro hepatocyte cultures. Hypothalamic and corpus striatal DA content decreased significantly (P \ 0.05, P \ 0.001 respectively) and homovanillic acid/ dopamine (HVA/DA) ratio increased significantly (P \ 0.001) in ethanol treated rats when compared to control. Scatchard analysis of [ 3 H] YM-09151-2 binding to DA D 2 receptors in hypothalamus showed a significant increase (P \ 0.001) in B max without any change in K d in ethanol treated rats compared to control. The K d of DA D 2 receptors significantly decreased (P \ 0.05) in the corpus striatum of ethanol treated rats when compared to control. DA D 2 receptor affinity in the hypothalamus and corpus striatum of control and ethanol treated rats fitted to a single site model with unity as Hill slope value. The in vitro studies on hepatocyte cultures showed that 10 -5 M and 10 -7 M DA can reverse the increased ALDH activity in 10% ethanol treated cells to near control level. Sulpiride, an antagonist of DA D 2 , reversed the effect of dopamine on 10% ethanol induced ALDH activity in hepatocytes. Our results showed a decreased dopamine concentration with enhanced DA D 2 receptors in the hypothalamus and corpus striatum of ethanol treated rats. Also, increased ALDH was observed in the plasma and liver of ethanol treated rats and in vitro hepatocyte cultures with 10% ethanol as a compensatory mechanism for increased aldehyde production due to increased dopamine metabolism. A decrease in dopamine concentration in major brain regions is coupled with an increase in ALDH activity in liver and plasma, which contributes to the tendency for alcoholism. Since the administration of 10 -5 M and 10 -7 M DA can reverse the increased ALDH activity in ethanol treated cells to near control level, this has therapeutic application to correct ethanol addicts from addiction due to allergic reaction observed in aldehyde accumulation.

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Higher correlation of ethanol consumption with brain than liver aldehyde dehydrogenase in three strains of rats

Cited by 31 publications

References 24 publications

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Catalase activity measured in rats naive to ethanol correlates with later voluntary ethanol consumption: possible evidence for a biological marker system of ethanol intake

Enhanced dopamine D2 receptor function in hypothalamus and corpus striatum: their role in liver, plasma and in vitro hepatocyte ALDH regulation in ethahol treated rats

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