Changes in some pro-and antioxidants in rat cerebellum after chronic alcohol intake

Rouach, Hélène; Houzé, Pascal; Gentil, Monique; Orfanelli, M.-T.; Nordmann, Roger

doi:10.1016/s0006-2952(96)00770-8

Cited by 39 publications

(18 citation statements)

References 52 publications

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“…Finally, oxidative protein damage has been linked with alcohol exposure in a number of studies. Increased protein carbonyl formation, one of the most general and commonly used indicators of oxidative protein damage, has been observed in the blood, liver and intestinal mucosa following alcohol exposure [14][15][16]. Alfa lipoic acid (αLA) and its reduced form, dihydrolipoic acid (DHLA), have received attention as antioxidants with both preventive and therapeutic uses in humans and laboratory animals [17].…”

Section: Introductionmentioning

confidence: 99%

Alpha - Lipoic Acid Decreases DNA Damage and Oxidative Stress Induced by Alcohol in the Developing Hippocampus and Cerebellum of Rat

Shirpoor¹,

Minassian²,

Salami³

et al. 2008

Cell Physiol Biochem

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Background / aims: The present study was initiated in order to investigate the protective effects of α-lipoic acid upon ethanol-induced DNA damage, lipid peroxidation and protein oxidation in the developing rat hippocampus and cerebellum. Methods: Pregnant Wistar rats received ethanol with, or without lipoic acid from gestation day (GD) 7 throughout lactation. The changes in DNA damage, protein carbonyl, lipid hydroperoxide, catalase and superoxide dismutase activities were measured in the hippocampus and cerebellum of male offspring at the end of the lactation period. Results: The results indicated that DNA damage, lipid peroxidation and protein oxidation in the hippocampus and cerebellum were significantly elevated in animals that received alcohol. However, the catalase and superoxide dismutase activity results showed patterns that differed from those of DNA damage, lipid peroxidation and protein oxidation. Lipoic acid treatment significantly decreased DNA damage compared with the group that were administered alcohol alone, and restored the elevated protein carbonyl and lipid hydroperoxide levels to the levels of the control group. Conclusions: Our findings confirm that oxidative stress and DNA damage occur in the developing hippocampus and cerebellum as a result of alcohol administration, and also suggest that lipoic acid has protective effects as an antioxidant against alcohol-induced disorders in the developing hippocampus and cerebellum.

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Section: Introductionmentioning

confidence: 99%

Alpha - Lipoic Acid Decreases DNA Damage and Oxidative Stress Induced by Alcohol in the Developing Hippocampus and Cerebellum of Rat

Shirpoor¹,

Minassian²,

Salami³

et al. 2008

Cell Physiol Biochem

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“…A 4-week exposure to daily ethanol feedings increased the production of malondialdehyde, a marker of lipid peroxidation, in rat cerebellum (183). On the contrary, Rouach et al (184) found no change in the indices of lipid peroxidation in rat cerebellum after a 4-week exposure to ethanol in drinking water, although the average intake of ethanol was comparable or even higher than in the protocol of Celec et al (183). One important factor contributing to the contrasting results may be the daily phases of ethanol withdrawal in the intragastric feeding regime vs. the continuous, even exposure to ethanol in drinking water.…”

Section: Oxidative Stressmentioning

confidence: 91%

“…Several studies have suggested that ethanol withdrawal, rather than ethanol per se, subjects the CNS to oxidative damage (185)(186)(187). However, a decreased amount of a-tocopherol (vitamin E; a major lipid soluble antioxidant in the CNS) and an increased concentration of low molecular weight non-heme iron (an important pro-oxidant) were reported in the cerebellum even after the moderate, continuous ethanol exposure without any withdrawal phases (184). Compensatory increases in the cerebellar antioxidant enzymes, such as glutathione S-transferase, may, in part, counteract the ethanol/withdrawalinduced formation of reactive oxygen species (ROS) and thus protect the cerebellum from oxidative damage (184).…”

Section: Oxidative Stressmentioning

confidence: 99%

“…However, a decreased amount of a-tocopherol (vitamin E; a major lipid soluble antioxidant in the CNS) and an increased concentration of low molecular weight non-heme iron (an important pro-oxidant) were reported in the cerebellum even after the moderate, continuous ethanol exposure without any withdrawal phases (184). Compensatory increases in the cerebellar antioxidant enzymes, such as glutathione S-transferase, may, in part, counteract the ethanol/withdrawalinduced formation of reactive oxygen species (ROS) and thus protect the cerebellum from oxidative damage (184). The reduced antioxidative capacity of the aged cerebellum (188)(189)(190) and the agerelated accumulation of oxidative damage (190)(191)(192) may further increase the vulnerability of the aged cerebellum to ethanol-induced oxidative stress.…”

Section: Oxidative Stressmentioning

confidence: 99%

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Mechanisms of ethanol-induced degeneration in the developing, mature, and aging cerebellum

Jaatinen

Rintala

2008

Cerebellum

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The adverse effects of acute and chronic ethanol exposure on cerebellar functions have been acknowledged for decades, in terms of impaired control of movement and balance. In addition to the motor impairment, cerebellar degeneration has recently been shown to contribute to distinct neuropsychological deficits in chronic alcoholics, as well as in children with prenatal ethanol exposure. The basic mechanisms underlying these ethanol-induced functional alterations and the related neuropathology in the cerebellum have mostly been clarified only recently. These mechanisms include: (i) excitotoxicity; (ii) dietary factors, especially thiamine depletion; (iii) glial abnormalities; (iv) changes in growth factors; (v) apoptotic mechanisms; (vi) oxidative stress; and (vii) compromised energy production. Although these mechanisms widely apply not only to the mature cerebellum, but also to the developing and the aging cerebella, the developing and the aged cerebellum have some special characteristics, which may make them even more vulnerable to ethanol-induced degeneration. These special instances will be discussed along with the general mechanisms of ethanol-induced cerebellar degeneration.

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“…Free ionic, or incompletely sequestered iron may be essential for the appearance of ethanol-induced ROS. Several investigators have found ethanol to effect the liberation oflow molecular weight iron from bound intracellular reserves [12,20,29,30]. The superoxide anion can release iron from ferritin [31] and this may underlie such observations.…”

Section: Iron Mobilizationmentioning

confidence: 99%

Exposure of mice to tobacco smoke attenuates the toxic effect of methamphetamine on dopamine systems

2000

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SUMMARY 231The mechanisms underlying the toxicity of ethanol have been the subject of much study, but are not well understood. Unlike many selective pharmacological agents, ethanol clearly has several major loci of action. One deleterious factor in ethanol metabolism is the potential for generation of excess amounts of free radicals. The extent to which this activity accounts for the overall toxicity of ethanol is unknown. This review outlines the enzymic steps that have the capacity to generate reactive oxygen species. These steps are likely to differ in acute and extended exposures to ethanol. Acetaldehyde catabolism also has the likelihood of contributing to ethanol-related oxidative stress. The review focuses on the ethanol-induced production of excess amounts of pro-oxidant reactive species in both the liver and the central nervous system. The potential of various stages of ethanol catabolism to involve generation of free radicals is described.

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Changes in some pro-and antioxidants in rat cerebellum after chronic alcohol intake

Cited by 39 publications

References 52 publications

Alpha - Lipoic Acid Decreases DNA Damage and Oxidative Stress Induced by Alcohol in the Developing Hippocampus and Cerebellum of Rat

Alpha - Lipoic Acid Decreases DNA Damage and Oxidative Stress Induced by Alcohol in the Developing Hippocampus and Cerebellum of Rat

Mechanisms of ethanol-induced degeneration in the developing, mature, and aging cerebellum

Exposure of mice to tobacco smoke attenuates the toxic effect of methamphetamine on dopamine systems

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