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, Zalman; Aragón, Carlos M.G.

doi:10.1007/bf00172965

Cited by 34 publications

(14 citation statements)

References 21 publications

(18 reference statements)

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“…In particular, the activity of brain catalase significantly and positively correlates with voluntary ethanol consumption in rats, 70,71 although conflicting results have been obtained in mice. 72 Rats with higher brain catalase activity generally consume more ethanol.…”

Section: Rewarding Properties Of Acetaldehyde In Animal Studiesmentioning

confidence: 99%

“…Therefore, CYP2E1 polymorphism is usually not believed to be related to alcohol abuse and alcoholism, 128 whereas there is evidence that it is associated with the susceptibility to develop alcohol liver disease. 133 Genetic polymorphism of catalase Although brain catalase activity correlates with voluntary ethanol consumption in rodents, 70,71 very few studies have investigated the effects of individual variability in the activity of human catalase. In a study with human subjects, Koechling and Amit 134 have shown that blood catalase activity significantly correlates with alcohol consumption.…”

Section: Genetic Polymorphism Of Cyp2e1mentioning

confidence: 99%

“…In a study with human subjects, Koechling and Amit 134 have shown that blood catalase activity significantly correlates with alcohol consumption. Since there is also a very significant positive correlation between blood and brain catalase activities in rats, 70 Koechling and Amit 134 have concluded that human brain catalase activity modulates the motivation to drink alcohol. This conclusion is further supported by a subsequent study showing that subjects with a familial history of alcoholism have a higher mean catalase activity than control subjects.…”

Section: Genetic Polymorphism Of Cyp2e1mentioning

confidence: 99%

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Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism

Quertemont

2004

Mol Psychiatry

152

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Acetaldehyde, the first product of ethanol metabolism, has been speculated to be involved in many pharmacological and behavioral effects of ethanol. In particular, acetaldehyde has been suggested to contribute to alcohol abuse and alcoholism. In the present paper, we review current data on the role of acetaldehyde and ethanol metabolism in alcohol consumption and abuse. Ethanol metabolism involves several enzymes. Whereas alcohol dehydrogenase metabolizes the bulk of ethanol within the liver, other enzymes, such as cytochrome P4502E1 and catalase, also contributes to the production of acetaldehyde from ethanol oxidation. In turn, acetaldehyde is metabolized by the enzyme aldehyde dehydrogenase. In animal studies, acetaldehyde is mainly reinforcing particularly when injected directly into the brain. In humans, genetic polymorphisms of the enzymes alcohol dehydrogenase and aldehyde dehydrogenase are also associated with alcohol drinking habits and the incidence of alcohol abuse. From these human genetic studies, it has been concluded that blood acetaldehyde accumulation induces unpleasant effects that prevent further alcohol drinking. It is therefore speculated that acetaldehyde exerts opposite hedonic effects depending on the localization of its accumulation. In the periphery, acetaldehyde is primarily aversive, whereas brain acetaldehyde is mainly reinforcing. However, the peripheral effects of acetaldehyde might also be dependent upon its peak blood concentrations and its rate of accumulation, with a narrow range of blood acetaldehyde concentrations being reinforcing.

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Section: Rewarding Properties Of Acetaldehyde In Animal Studiesmentioning

confidence: 99%

Section: Genetic Polymorphism Of Cyp2e1mentioning

confidence: 99%

Section: Genetic Polymorphism Of Cyp2e1mentioning

confidence: 99%

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Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism

Quertemont

2004

Mol Psychiatry

152

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“…On one hand, there is a positive correlation between brain catalase activity and the natural propensity to drink EtOH in rodents [44][45][46], which was interpreted in the inverse in that lower brain catalase activity, would be associated with less EtOH consumption. In the same way, UChA and UChB rats showed attenuated acute tolerance to motor impairment and reduced voluntary EtOH consumption when pretreated with a catalase inhibitor [47].…”

Section: Effect Of Ach Related To Addictionmentioning

confidence: 99%

Putative Role of Brain Acetaldehyde in Ethanol Addiction

Deng¹,

Deitrich²

2008

CDAR

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The putative contribution of brain acetaldehyde (AcH) to ethanol (EtOH) tolerance and dependence (addiction) is reviewed. Although the role of AcH in EtOH addiction has been controversial, there are data showing a relationship. AcH can be formed in the brain tissues through the peroxidatic activity of catalase and by oxidation via other oxidizing enzymes such as cytochrome P-4502E1. Significant formation of AcH occurs in vitro in brain tissue at concentrations of EtOH that can be achieved by voluntary consumption of EtOH by rodents. AcH itself possesses reinforcing properties, which suggests that some of the behavioral pharmacological effects attributed to EtOH may be a result of the formation of AcH, and supports the involvement of AcH in EtOH addiction. Modulation of aldehyde dehydrogenase (ALDH) and brain catalase activity can change EtOH-related addictive behaviors presumably by changing AcH levels. Moreover, some condensation reaction products of AcH may promote some actions of EtOH and its consumption. On the basis of the findings, it can be concluded that AcH may mediate some of the CNS actions of EtOH including tolerance and dependence, although further exploration the involvement of AcH in EtOH addiction is warranted.

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“…It has been postulated that central EtOH metabolism by the activity of this enzymatic complex mediates some of the psychopharmacological effects produced by this alcohol (Deng and Deitrich, 2008). Previous research has demonstrated that individual differences in the activity of brain catalase in rats of the same strain correlate positively with their voluntary EtOH intake (Amit and Aragon, 1988;Aragon et al, 1985). Moreover, it has been shown that strains of rats with higher brain catalase activity drink more EtOH than other strains with a lower activity of this enzyme in the central nervous system (CNS) (Gill et al, 1996a).…”

mentioning

confidence: 99%

Reduction in Central H₂O₂Levels Prevents Voluntary Ethanol Intake in Mice: A Role for the Brain Catalase-H₂O₂System in Alcohol Binge Drinking

Ledesma

Baliño

Aragón

2013

Alcohol Clin Exp Res

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Background: Hydrogen peroxide (H 2 O 2 ) is the cosubstrate used by the enzyme catalase to form Compound I (the catalase-H 2 O 2 system), which is the major pathway for the conversion of ethanol (EtOH) into acetaldehyde in the brain. This centrally formed acetaldehyde has been shown to be involved in some of the psychopharmacological effects induced by EtOH in rodents, including voluntary alcohol intake. It has been observed that different levels of this enzyme in the central nervous system (CNS) result in variations in the amount of EtOH consumed. This has been interpreted to mean that the brain catalase-H 2 O 2 system, by determining EtOH metabolism, mediates alcohol self-administration. To date, however, the role of H 2 O 2 in voluntary EtOH drinking has not been investigated.Methods: In the present study, we explored the consequence of a reduction in cerebral H 2 O 2 levels in volitional EtOH ingestion. With this end in mind, we injected mice of the C57BL/6J strain intraperitoneally with the H 2 O 2 scavengers alpha-lipoic acid (LA; 0 to 50 mg/kg) or ebselen (Ebs; 0 to 25 mg/kg) 15 or 60 minutes, respectively, prior to offering them an EtOH (10%) solution following a drinkingin-the-dark procedure. The same procedure was followed to assess the selectivity of these compounds in altering EtOH intake by presenting mice with a (0.1%) solution of saccharin. In addition, we indirectly tested the ability of LA and Ebs to reduce brain H 2 O 2 availability.Results: The results showed that both LA and Ebs dose-dependently reduced voluntary EtOH intake, without altering saccharin consumption. Moreover, we demonstrated that these treatments decreased the central H 2 O 2 levels available to catalase.Conclusions: Therefore, we propose that the amount of H 2 O 2 present in the CNS, by determining brain acetaldehyde formation by the catalase-H 2 O 2 system, could be a factor that determines an animal's propensity to consume EtOH.

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

Cited by 34 publications

References 21 publications

Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism

Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism

Putative Role of Brain Acetaldehyde in Ethanol Addiction

Reduction in Central H₂O₂Levels Prevents Voluntary Ethanol Intake in Mice: A Role for the Brain Catalase-H₂O₂System in Alcohol Binge Drinking

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

Cited by 34 publications

References 21 publications

Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism

Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism

Putative Role of Brain Acetaldehyde in Ethanol Addiction

Reduction in Central H2O2Levels Prevents Voluntary Ethanol Intake in Mice: A Role for the Brain Catalase-H2O2System in Alcohol Binge Drinking

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Reduction in Central H₂O₂Levels Prevents Voluntary Ethanol Intake in Mice: A Role for the Brain Catalase-H₂O₂System in Alcohol Binge Drinking