Induction of brain CYP2E1 by chronic ethanol treatment and related oxidative stress in hippocampus, cerebellum, and brainstem

Zhong, Yanjun; Dong, Guicheng; Luo, Haiguang; Cao, Jie J; Wang, Chang; Wu, Jianyuan; Feng, Yu‐Qi; Yue, Jiang

doi:10.1016/j.tox.2012.08.009

Cited by 56 publications

(36 citation statements)

References 49 publications

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“…This is likely due to differences in GSH consumption and de novo synthesis based on oxidative stress states (Dringen, 2000;Dringen and Hirrlinger, 2003). Whereby higher levels of alcohol and/or tobacco consumption promote the production of ROS (Nordmann et al, 1990;Zhong et al, 2012;Zhang et al, 2007), leading to higher GSH consumption (Janaky et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

A longitudinal proton magnetic resonance spectroscopy study investigating oxidative stress as a result of alcohol and tobacco use in youth with bipolar disorder

Chitty

Lagopoulos

Hickie

et al. 2015

Journal of Affective Disorders

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Alcohol and tobacco have been suggested to be "aggravating factors" for neuroprogression in bipolar disorder (BD), however the impact of these substances on the underlying neurobiology is limited. Oxidative stress is a key target for research into neuroprogression in BD and in accordance with this model, our previous cross-sectional studies have found that risky alcohol and tobacco use in BD is associated with increased oxidative stress, investigated via in vivo glutathione (GSH) measured by proton magnetic resonance spectroscopy( 1 H-MRS) in the anterior cingulate cortex (ACC). What remains unknown is whether the negative impact on GSH levels can be modified as a result of limiting alcohol and tobacco use.Thirty BD patients were included in the study. 1 H-MRS and tobacco and alcohol measures were conducted at baseline and follow-up assessments (15.5 +/-4.6 months apart).Pearson's correlations were performed between percentage change in ACC-GSH and changes in alcohol/tobacco use. Regression analyses were then conducted to further explore the significant correlations. An increase in GSH was associated with a decrease in alcohol consumption (r = -0.381, p < 0.05) and frequency of tobacco use (-0.367, p = 0.05). Change in alcohol consumption, tobacco use and age were significant predictors of change in ACC-GSH (F (3, 26) = 3.69, p < 0.05). Due to the high comorbidity of alcohol and tobacco use in the sample, the individual effects of these substances on GSH levels could not be determined.This study offers longitudinal evidence that changing risky drinking patterns and tobacco use early in the course of BD is associated with improvements in antioxidant capacity, and therefore may be specific targets for early intervention and prevention of neuroprogression in BD.3

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Section: Discussionmentioning

confidence: 99%

A longitudinal proton magnetic resonance spectroscopy study investigating oxidative stress as a result of alcohol and tobacco use in youth with bipolar disorder

Chitty

Lagopoulos

Hickie

et al. 2015

Journal of Affective Disorders

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show abstract

“…In the context of alcohol, this may be related to the 'wear and tear' of neural compensatory upregulation of the NMDA receptor that occurs as a result of chronic alcohol use (see section 2.1.2). Alternatively, the direct effects of alcohol and its substrates on the brain could also be identified as a source of aggravation, as a xenobiotic substance known to promote oxidative stress (Tsai et al, 1998;Zhong et al, 2012).…”

Section: Memantinementioning

confidence: 99%

“…Certainly this concept would extend to identifying the neurobiology of the BD-alcohol comorbidity, with the potential to dampen, cease or even reverse the effects of alcohol on the brain. An ideal neurobiological target for investigation is neural oxidative stress, as a system that is implicated in the effects of alcohol on the brain (Nordmann et al, 1990;Tsai et al, 1998;Zhong et al, 2012) and is a key target for research into BD neuroprogression (Berk et al, 2011).…”

Section: Memantinementioning

confidence: 99%

“…The mechanisms by which alcohol promotes oxidative stress in the brain are largely unknown, although it has been posited that they may be attributable to the production of ROS and lipid peroxidation associated with its metabolism (Tsai et al, 1998;Zhong et al, 2012).…”

Section: Oxidative Stressmentioning

confidence: 99%

“…The second BDalcohol neurobiological 'intersection' we selected for enquiry was neural oxidative stress. Oxidative stress is believed to contribute to the neuroprogression of BD (Berk et al, 2011) which may be a consequence of the effects of xenobiotic substances in the brain, such as alcohol (Tsai et al, 1998;Zhong et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Alcohol use in bipolar disorder: A neurobiological model to help predict susceptibility, select treatments and attenuate cortical insult

Chitty

Lagopoulos

Hickie

et al. 2015

Neuroscience & Biobehavioral Reviews

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In a series of neurophysiological and neuroimaging studies we investigated the neurobiology related to alcohol use in young people with bipolar disorder. Impairments were identified across frontal and temporal representations of event-related potential and proton magnetic resonance spectroscopy markers; mismatch negativity and in vivo glutathione, respectively. We propose these findings reflect impairments in the Nmethyl-D-aspartate receptor and antioxidant capacity. This review seeks to place these findings within the broader literature in the context of two propositions:

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Interactions of ethanol and caffeine on apoptosis in the rat cerebellum (voluntary ethanol consumers)

Martinez

Rossetto

Neto

et al. 2018

Cell Biology International

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Ethanol alters motricity, learning, cognition, and cellular metabolism in the cerebellum. The combination of ethanol with caffeine by consuming "energy drinks" is becoming increasingly popular among young people. We analyzed the use of ethanol and caffeine on apoptosis in the cerebellum of UChB rats. The adult rats were divided into three groups (n = 14/group): UChB group: rats fed with 1:10 (v/v) ethanol ad libitum (free choice for water or ethanol) drinking from >1.9 mL of ethanol/kg body weight/day, Control group and UChB/caffeine group (free choice for water or ethanol + caffeine 300 mg/L). The treatments occurred from Day 100 till Day 150, totalizing 50 days of ethanol/caffeine ingestion. Cerebellar sections were subjected to immunohistochemistry and gene expression for Real Time-PCR (RT-PCR) for Caspase-3, XIAP, and insulin-like growth factor 1-receptor (IGF-1R). The results showed a significant increase in the gene expression of Caspase-3 and XIAP in UChB group. On the other hand, the animals of the UChB/caffeine group showed similar results to the Controls. Regarding IGFR-1, there was greater expression in the UChB groups with strong labeling in Purkinje cells. Ethanol produces neuronal and glial neurodegeneration on the cerebellum of UChB rats. The simultaneous ingestion of ethanol and caffeine reversed the ethanol damages acting caffeine with a neuroprotective effect.

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Induction of brain CYP2E1 by chronic ethanol treatment and related oxidative stress in hippocampus, cerebellum, and brainstem

Cited by 56 publications

References 49 publications

A longitudinal proton magnetic resonance spectroscopy study investigating oxidative stress as a result of alcohol and tobacco use in youth with bipolar disorder

A longitudinal proton magnetic resonance spectroscopy study investigating oxidative stress as a result of alcohol and tobacco use in youth with bipolar disorder

Alcohol use in bipolar disorder: A neurobiological model to help predict susceptibility, select treatments and attenuate cortical insult

Interactions of ethanol and caffeine on apoptosis in the rat cerebellum (voluntary ethanol consumers)

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