Interaction of aging and intermittent ethanol exposure on brain cytochrome c oxidase activity levels

Jaatinen, Pia; Riikonen, Jarno; Riihioja, Päivi; Kajander, Olli A.; Hervonen, Antti

doi:10.1016/s0741-8329(03)00002-8

Cited by 26 publications

(20 citation statements)

References 55 publications

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“…Relevant to the current study, ethanol exposure oxidatively modified COX, resulting in a reduced enzyme activity [22] . In addition, COX activity was decreased by the age/EW combination in male rats but not by age per se, suggesting that COX is particularly vulnerable to EW toxicity [27]. In contrast to our findings, COX activity was not altered in the brain tissues of the ethanol-fed male rats [28].…”

contrasting

confidence: 92%

Ethanol withdrawal posttranslationally decreases the activity of cytochrome c oxidase in an estrogen reversible manner

Jung

Agarwal

Simpkins

2007

Neuroscience Letters

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Cytochrome c oxidase (COX) is a key mitochondrial enzyme that catalyzes electron transfer at the terminal stage of respiratory chain and is composed of multisubunits. We hypothesize that ethanol withdrawal (EW) impairs the activity of COX and estrogen deprivation exacerbates this problem. Five month-old ovariectomized rats with or without 17β-estradiol (E2) replacement received a control dextrin or a liquid ethanol diet (6.5%, five weeks). They were then sacrificed either during ethanol exposure or at 24 hours of EW (EW group). Mitochondria of the cerebellum and cortex were processed to measure the activities of total COX, COX subunit I, and IV. The effects of EW and E2 on the protein levels of these subunits were also assessed using an immunoblotting method. As compared to the control dextrin and ethanol exposure, EW decreased the activities of total COX, COX I, and COX IV. E2 treatment prevented the effects of EW on the activities of total COX and COX IV but not COX I. Neither EW nor E2 altered the protein levels of the subunits. These findings suggest that a counteracting relationship exists between the effects of EW and E2 on the activity of COX in a subunit specific manner. KeywordsCytochrome c oxidase; 17β-estradiol; Ethanol Withdrawal; Mitochondria Mitochondria produce cellular energy (ATP) through a series of mitochondrial enzyme complexes. Electrons are transferred across the enzyme complexes and create the electrochemical gradient between the mitochondrial membranes. Subsequently, the electrochemical gradient provides force to generate ATP. COX is a terminal enzyme complex among the series of enzymes and plays a key role in the mitochondrial function. Therefore, damage to this enzyme can cause serious clinical consequences. Indeed, the decreased activity of COX has been found in a variety of neurodegenerative illnesses such as Parkinson′s disease and Alzheimer′s disease [1][2][3].Accumulated evidence indicates that mitochondria are vulnerable to ethanol/EW toxicity. Reactive oxygen species produced during ethanol metabolism altered mitochondrial function in rodents [4,5]. The mitochondrial membrane permeability and oxidation were dramatically increased during EW [6,7], suggesting that ethanol and/or EW preferentially target mitochondria. However, most of the studies did not differentiate between ethanol exposure and *Corresponding author: Department of Pharmacology and Neuroscience, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA, Tel.: 817-735-0132, Fax: 817-735-2091, E-mail address: mjung@hsc.unt.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the cont...

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contrasting

confidence: 92%

Ethanol withdrawal posttranslationally decreases the activity of cytochrome c oxidase in an estrogen reversible manner

Jung

Agarwal

Simpkins

2007

Neuroscience Letters

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“…The AA rats acquire a high level of voluntary ethanol intake in about three weeks, when given a free access to ethanol solution with water and food freely available [24]. In earlier studies, lifelong consumption of ethanol by AA rats has been found to increase the behavioral sensitivity to ethanol over age and to produce morphological changes in peripheral sympathetic neurons and cerebellar cortex, as well as molecular alterations in brain GABA A receptor subunits [14,15,16,17,18,19,20,21,22]. …”

Section: Resultsmentioning

confidence: 99%

“…Since age-related changes in the metabolism and distribution of ethanol in the body can be a contributing factor to ethanol-induced damage, the levels of ethanol and acetaldehyde in the blood were also measured. This work is part of a project addressing the interactions of aging and lifelong ethanol consumption in the alcohol-preferring AA and the alcohol-avoiding ANA line of rats, selected for high and low ethanol consumption, respectively [14,15,16,17,18,19,20,21,22,23,24]. …”

Section: Introductionmentioning

confidence: 99%

Effects of Lifelong Ethanol Consumption on Brain Monoamine Transmitters in Alcohol-Preferring Alko Alcohol (AA) Rats

et al. 2013

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The purpose of the present study was to examine the combined effects of aging and lifelong ethanol exposure on the levels of monoamine neurotransmitters in different regions of the brain. This work is part of a project addressing interactions of aging and lifelong ethanol consumption in alcohol-preferring AA (Alko Alcohol) line of rats, selected for high voluntary consumption of ethanol. Intake of ethanol on the level of 4.5–5 g/kg/day for about 20 months induced only limited changes in the neurotransmitter levels; the concentration of noradrenaline was significantly reduced in the frontal cortex. There was also a trend towards lower levels of dopamine and 5-hydroxytryptamine (5-HT) in the frontal cortex, and towards a lower noradrenaline level in the dorsal cortex. Aging was associated with a decreased concentration of dopamine in the dorsal cortex and with a declining trend in the striatum. The levels of 5-HT in the limbic forebrain were higher in the aged than in the young animals, and in the striatum, there was a trend towards higher levels in older animals. The data suggest that a continuous intake of moderate amounts of ethanol does not enhance the age-related alterations in brain monoamine neurotransmission, while the decline in the brain level of dopamine associated with aging may be a factor contributing to age-related neurological disorders.

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“…In particular, a number of studies have shown the close association of alcoholic consumption and dementia, although the exact mechanisms are still not known (9)(10)(11)(12)(13). Studies have been shown that frequent alcohol uptake by rats can cause mitochondrial dysfunction in neurons, leading to neurodegeneration (14). Excessive alcohol consumption may contribute to structural changes in the brain as well as impairment of cognitive function (15).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic alcohol consumption on expression levels of APP and Aβ-producing enzymes

Kim¹,

Jeong²,

Yang³

et al. 2011

BMB Reports

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Chronic alcohol consumption contributes to numerous diseases, including cancers, cardiovascular diseases, and liver cirrhosis. Epidemiological studies have shown that excessive alcohol consumption is a risk factor for dementia. Along this line, Alzheimer's disease (AD) is the most common form of dementia and is caused by the accumulation of amyloid-β (Aβ plaques in neurons. In this study, we hypothesized that chronic ethanol consumption is associated with pathological processing of APP in AD. To investigate the relationship between chronic alcohol consumption and Aβ production, brain samples from rats fed an alcohol liquid diet for 5 weeks were analyzed. We show that the expression levels of APP, BACE1, and immature nicastrin were increased in the cerebellum, hippocampus, and striatum of the alcohol-fed group compared to the control group. Total nicastrin and PS1 levels were induced in the hippocampus of alcohol-fed rats. These data suggest that the altered expression of APP and Aβ-producing enzymes possibly contributes to the chronic alcohol consumption-mediated pathogenesis of AD. [BMB reports 2011; 44(2): 135-139]

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Interaction of aging and intermittent ethanol exposure on brain cytochrome c oxidase activity levels

Cited by 26 publications

References 55 publications

Ethanol withdrawal posttranslationally decreases the activity of cytochrome c oxidase in an estrogen reversible manner

Ethanol withdrawal posttranslationally decreases the activity of cytochrome c oxidase in an estrogen reversible manner

Effects of Lifelong Ethanol Consumption on Brain Monoamine Transmitters in Alcohol-Preferring Alko Alcohol (AA) Rats

Effects of chronic alcohol consumption on expression levels of APP and Aβ-producing enzymes

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