The Status of Oxidative Stress in Patients with Alcohol Dependence: A Meta-Analysis

Mi, Yang; Zhou, Xiaofei; Tan, Xi; Huang, Xincheng; Liu, Yuan; Zhang, Zipeng; Yang, Yan; Xu, Min; Wang, Ying; Li, Zezhi

doi:10.3390/antiox11101919

Cited by 10 publications

(6 citation statements)

References 130 publications

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“…Early detection and monitoring of molecular mechanisms leading to alcohol impairment of cognitive functions remain a major challenge for predictive diagnosis and prognosis in clinical practice. In this regards, oxidative stress and inflammation are key underlying mechanisms in the brain that can be explored to identify stress biomarkers capable of predicting cognitive dysfunctions in patients with AUD [ 9 , 10 , 11 , 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…The underlying mechanisms by which alcohol activate innate immune signaling and oxidative stress affecting cognitive functions are partially understood, despite the remarkable ability of alcohol to activate the Toll-like receptor (TLR) 4 directly [ 9 , 10 , 11 , 12 ]. Alcohol toxicity-induced oxidative stress and inflammation in the brain lead to neuronal cell death (intracellular damage and apoptosis) and impaired neuronal function (e.g., mitochondrial dysfunction), caused by the release of neuroimmune signaling, such as high-mobility group box 1 (HMGB1), as well as the accumulation of reactive oxygen and nitrogen species (ROS/RNS) and toxic protein aggregates, including advanced glycation end-products (AGEs) [ 13 , 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Plasma Concentrations of High Mobility Group Box 1 Proteins and Soluble Receptors for Advanced Glycation End-Products Are Relevant Biomarkers of Cognitive Impairment in Alcohol Use Disorder: A Pilot Study

Rodríguez de Fonseca,

Medina-Paz,

Sapozhnikov

et al. 2024

Toxics

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Alcohol use disorder (AUD) is a major component in the etiology of cognitive decline and dementia. Underlying mechanisms by which long-term alcohol abuse causes cognitive dysfunction include excessive oxidative stress and inflammation in the brain, activated by increased reactive oxygen/nitrogen species (ROS/RNS), advanced glycation end-products (AGEs) and high-mobility group box 1 protein (HMGB1). In a pilot study, we examine the potential clinical value of circulating biomarkers of oxidative stress including ROS/RNS, HMGB1, the soluble receptor for AGE (sRAGE), the brain biomarker of aging apolipoprotein D (ApoD), and the antioxidant regulator nuclear factor erythroid 2-related factor 2 (NRF2) as predictive indices for cognitive impairment (CI) in abstinent patients with AUD (n = 25) compared to patients with established Alzheimer’s disease (AD, n = 26) and control subjects (n = 25). Plasma concentrations of sRAGE were evaluated with immunoblotting; ROS/RNS with a fluorometric kit; and HMGB1, ApoD, and NRF2 by ELISA. Abstinent AUD patients had higher sRAGE, ROS/RNS (p < 0.05), and ApoD (p < 0.01) concentrations, similar to those of AD patients, and lower NRF2 (p < 0.01) concentrations, compared to controls. These changes were remarkable in AUD patients with CI. HMGB1, and sRAGE correlated positively with duration of alcohol use (rho = 0.398, p = 0.022; rho = 0.404, p = 0.018), whereas sRAGE correlated negatively with periods of alcohol abstinence (rho = −0.340, p = 0.045). A predictive model including ROS/RNS, HMGB1, sRAGE, alcohol use duration, and alcohol abstinence periods was able to differentiate AUD patients with CI (92.3% of correct predictions, ROC-AUC= 0.90) from those without CI. In conclusion, we propose ROS/RNS, HMGB1, and sRAGE as stress biomarkers capable of predicting cognitive impairment in AUD patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma Concentrations of High Mobility Group Box 1 Proteins and Soluble Receptors for Advanced Glycation End-Products Are Relevant Biomarkers of Cognitive Impairment in Alcohol Use Disorder: A Pilot Study

Rodríguez de Fonseca,

Medina-Paz,

Sapozhnikov

et al. 2024

Toxics

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“…The exact teratogenic mechanism of alcohol on fetal development is still unclear. EtOH contributes to the malfunctioning of the neurological system in children exposed in utero by decreasing glutathione peroxidase action, with an increase in the production of ROS [ 30 , 31 , 61 ]. It causes oxidative stress and the oxidation of polyunsaturated fatty acids with the formation of aldehyde toxicants [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…Upon admission to the hospital, we performed an ultrasound exam with evidence of reduced amniotic fluid (amniotic fluid index—AFI: 73 mm) and an estimated fetal weight of 1559 g, equal to the first percentile (z-score −3.303) for gestational age [ 29 , 30 , 31 ]. Fetal Doppler showed an umbilical artery pulsatility index (PI) of 1.23, equal to the 96th percentile (z-score 1.697), middle cerebral artery PI of 1.62, equal to the 16th percentile (z-score −0.995), with the cerebroplacental ratio of 1.32, equal to the 3rd percentile (z-score −2.004) for gestational age.…”

Section: Case Reportmentioning

confidence: 99%

Oxidative Stress in a Mother Consuming Alcohol during Pregnancy and in Her Newborn: A Case Report

Derme,

Piccioni,

Brunelli

et al. 2023

Antioxidants

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Fetal alcohol spectrum disorder (FASD) is a set of conditions resulting from prenatal alcohol exposure (PAE). FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe. The exact teratogenic mechanism of alcohol on fetal development is still unclear. Ethanol (EtOH) contributes to the malfunctioning of the neurological system in children exposed in utero by decreasing glutathione peroxidase action, with an increase in the production of reactive oxygen species (ROS), which causes oxidative stress. We report a case of a mother with declared alcohol abuse and cigarette smoking during pregnancy. By analyzing the ethyl glucuronide (EtG, a metabolite of alcohol) and the nicotine/cotinine in the mother’s hair and meconium, we confirmed the alcohol and smoking abuse magnitude. We also found that the mother during pregnancy was a cocaine abuser. As a result, her newborn was diagnosed with fetal alcohol syndrome (FAS). At the time of the delivery, the mother, but not the newborn, had an elevation in oxidative stress. However, the infant, a few days later, displayed marked potentiation in oxidative stress. The clinical complexity of the events involving the infant was presented and discussed, underlining also the importance that for cases of FASD, it is crucial to have more intensive hospital monitoring and controls during the initial days.

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“…emphasized the crucial roles of aberrant histone deacetylase 2-mediated histone modifications and synaptic plasticity within the AMY in the pathogenesis of AUD [114]. It has been widely reported that biological processes such as oxidative stress, GABAergic neurotransmission and neuroimmune were strongly related to the onset and progression of AUD [115][116][117]. Nevertheless, there is still a lack of research on the relationships between ncRNAs and genetic and epigenetic mechanisms, as well as the possible involvement of ncRNAs-mediated cellular functions and biological processes in the course of AUD.…”

Section: Conclusion and Future Perspectivementioning

confidence: 99%

Functional roles, regulatory mechanisms and theranostics applications of ncRNAs in alcohol use disorder

Wang¹,

Liu²,

Xia³

et al. 2023

Int. J. Biol. Sci.

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Alcohol use disorder (AUD) is one of the most prevalent neuropsychological disorders worldwide, and its pathogenesis is convoluted and poorly understood. There is considerable evidence demonstrating significant associations between multiple heritable factors and the onset and progression of AUD. In recent years, a substantial body of research conducted by emerging biotechnologies has increasingly highlighted the crucial roles of noncoding RNAs (ncRNAs) in the pathophysiology of mental diseases. As in-depth understanding of ncRNAs and their mechanisms of action, they have emerged as prospective diagnostic indicators and preclinical therapeutic targets for a variety of psychiatric illness, including AUD. Of note, dysregulated expression of ncRNAs such as circRNAs, lncRNAs and miRNAs was routinely found in AUD individuals, and besides, exogenous regulation of partial ncRNAs has also been shown to be effective in ameliorating alcohol preference and excessive alcohol consumption. However, the exact molecular mechanism still remains elusive. Herein, we systematically summarized current knowledge regarding alterations in the expression of certain ncRNAs as well as their-mediated regulatory mechanisms in individuals with AUD. And finally, we detailedly reviewed the potential theranostics applications of gene therapy agents targeting ncRNAs in AUD mice. Overall, a deeper comprehension of functional roles and biological mechanisms of ncRNAs may make significant contributions to the accurate diagnosis and effective treatment of AUD.

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The Status of Oxidative Stress in Patients with Alcohol Dependence: A Meta-Analysis

Cited by 10 publications

References 130 publications

Plasma Concentrations of High Mobility Group Box 1 Proteins and Soluble Receptors for Advanced Glycation End-Products Are Relevant Biomarkers of Cognitive Impairment in Alcohol Use Disorder: A Pilot Study

Plasma Concentrations of High Mobility Group Box 1 Proteins and Soluble Receptors for Advanced Glycation End-Products Are Relevant Biomarkers of Cognitive Impairment in Alcohol Use Disorder: A Pilot Study

Oxidative Stress in a Mother Consuming Alcohol during Pregnancy and in Her Newborn: A Case Report

Functional roles, regulatory mechanisms and theranostics applications of ncRNAs in alcohol use disorder

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