Antioxidant Vitamins and Brain Dysfunction in Alcoholics

González‐Reimers, Emilio; Fernández-Rodríguez, Camino; Martín-González, M. Candelaria; Hernández-Betancor, Iván; Abreu-González, Pedro; Vega-Prieto, Marı́a José de la; Elvira-Cabrera, Oswaldo; Santolaria-Fernández, Francisco

doi:10.1093/alcalc/agt150

Cited by 21 publications

(7 citation statements)

References 33 publications

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“…Recently, it has been reported that serum retinol concentrations are lower in alcoholics 44) and smokers. 45) The decrease in serum retinol concentrations may be one reason why the risk of carcinogenesis is high in people who often smoke and drink.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pre- and Post-Administration of Vitamin A on the Growth of Refractory Cancers in Xenograft Mice

Imai

Yamasaki

et al. 2017

Biological & Pharmaceutical Bulletin

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Vitamin A is an essential nutrient that is obtained from the daily diet. The major forms of vitamin A in the body consist of retinol, retinal, retinoic acid (RA), and retinyl esters. Retinal is fundamental for vision and RA is used in clinical therapy of human acute promyelocytic leukemia. The actions of retinol and retinyl palmitate (RP) are not known well. Recently, we found that retinol is a potent anti-proliferative agent against human refractory cancers, including gallbladder cancer, being more effective than RA, while RP was inactive. In the current study, we determined serum retinol concentrations in xenograft mice bearing tumors derived from four refractory cancer cell lines. We also examined the effects of vitamin A on proliferation of human gallbladder cancer cells in vivo. Serum retinol concentrations were significantly lower in xenograft mice with tumors derived from various refractory cancer cell lines as compared with control mice. The growth of tumors was inhibited with increasing serum retinol concentrations obtained post-administration of RP. In addition, pre-administration of RP increased serum retinol concentrations and suppressed tumor growth. These results indicate that administration of RP can maintain retinol concentrations in the body and that this might suppress cancer cell growth and attachment. The regulation of vitamin A concentration in the body, which is critical biomarker of health, could be beneficial for cancer prevention and therapy.

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Section: Discussionmentioning

confidence: 99%

Effects of Pre- and Post-Administration of Vitamin A on the Growth of Refractory Cancers in Xenograft Mice

Imai

Yamasaki

et al. 2017

Biological & Pharmaceutical Bulletin

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“…Overexpression of SOD reduces the neurotoxicity by amyloid precursor protein and prevents memory deficits by reducing the activity of hippocampal superoxide. The most important exogenous antioxidants in the CNS are vitamin E, C, Omega 3 fatty acids, and selenium but both vitamin E and C levels in the CNS fall after alcohol exposure by ROS activity [121] , [122] .…”

Section: The Potential Therapeutic Approach To Prevent Neurodegenerationmentioning

confidence: 99%

Effect of alcohol on the central nervous system to develop neurological disorder: pathophysiological and lifestyle modulation can be potential therapeutic options for alcohol-induced neurotoxication

Pervin

Stephen

2021

AIMS Neuroscience

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The central nervous system (CNS) is the major target for adverse effects of alcohol and extensively promotes the development of a significant number of neurological diseases such as stroke, brain tumor, multiple sclerosis (MS), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS). Excessive alcohol consumption causes severe neuro-immunological changes in the internal organs including irreversible brain injury and it also reacts with the defense mechanism of the blood-brain barrier (BBB) which in turn leads to changes in the configuration of the tight junction of endothelial cells and white matter thickness of the brain. Neuronal injury associated with malnutrition and oxidative stress-related BBB dysfunction may cause neuronal degeneration and demyelination in patients with alcohol use disorder (AUD); however, the underlying mechanism still remains unknown. To address this question, studies need to be performed on the contributing mechanisms of alcohol on pathological relationships of neurodegeneration that cause permanent neuronal damage. Moreover, alcohol-induced molecular changes of white matter with conduction disturbance in neurotransmission are a likely cause of myelin defect or axonal loss which correlates with cognitive dysfunctions in AUD. To extend our current knowledge in developing a neuroprotective environment, we need to explore the pathophysiology of ethanol (EtOH) metabolism and its effect on the CNS. Recent epidemiological studies and experimental animal research have revealed the association between excessive alcohol consumption and neurodegeneration. This review supports an interdisciplinary treatment protocol to protect the nervous system and to improve the cognitive outcomes of patients who suffer from alcohol-related neurodegeneration as well as clarify the pathological involvement of alcohol in causing other major neurological disorders.

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“…Repeated microtrauma associated with the bizarre style of life of many alcoholics, prone to aggression and violence may also contribute ( Harris et al, 2019 ). Altered nutritional status ( Romero-Acevedo et al, 2019 ), or several micronutrient deficiencies also probably play a role ( González-Reimers et al, 2014 ), especially thiamine deficiency ( Topiwala and Ebmeier, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Sclerostin, vascular risk factors, and brain atrophy in excessive drinkers

Martín-González

Godoy-Reyes²,

Abreu-González³

et al. 2023

Front. Hum. Neurosci.

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ObjectiveHeavy alcohol consumption causes several organic complications, including vessel wall calcification. Vascular damage may be involved in the development of brain atrophy and cognitive impairment. Recently, sclerostin (whose levels may be altered in alcoholics) has emerged as a major vascular risk factor. The objective of the present study is to analyze the prevalence of vascular calcifications in alcoholics, and the relationships of these lesions with brain atrophy, as well as the role of sclerostin on these alterations.Patients and methodsA total of 299 heavy drinkers and 32 controls were included. Patients underwent cranial computed tomography, and several indices related to brain atrophy were calculated. In addition, patients and controls underwent plain radiography and were evaluated for the presence or absence of vascular calcium deposits, cardiovascular risk factors, liver function, alcohol intake, serum sclerostin, and routine laboratory variables.ResultsA total of 145 (48.47%) patients showed vascular calcium deposits, a proportion significantly higher than that observed in controls (χ2 = 16.31; p < 0.001). Vascular calcium deposits were associated with age (t = 6.57; p < 0.001), hypertension (t = 5.49; p < 0.001), daily ethanol ingestion (Z = 2.18; p = 0.029), duration of alcohol consumption (Z = 3.03; p = 0.002), obesity (χ2 = 4.65; p = 0.031), total cholesterol (Z = 2.04; p = 0.041), triglycerides (Z = 2.05; p = 0.04), and sclerostin levels (Z = 2.64; p = 0.008). Calcium deposits were significantly related to Bifrontal index (Z = 2.20; p = 0.028) and Evans index (Z = 2.25; p = 0.025). Serum sclerostin levels were related to subcortical brain atrophy, assessed by cella media index (Z = 2.43; p = 0.015) and Huckmann index (ρ = 0.204; p = 0.024). Logistic regression analyses disclosed that sclerostin was the only variable independently related to brain atrophy assessed by altered cella media index. Sclerostin was also related to the presence of vascular calcifications, although this relationship was displaced by age if this variable was also included.ConclusionPrevalence of vascular calcification in alcoholics is very high. Vascular calcium deposits are related to brain atrophy. Serum sclerostin is strongly related to brain shrinkage and also shows a significant relationship with vascular calcifications, only displaced by advanced age.

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Antioxidant Vitamins and Brain Dysfunction in Alcoholics

Cited by 21 publications

References 33 publications

Effects of Pre- and Post-Administration of Vitamin A on the Growth of Refractory Cancers in Xenograft Mice

Effects of Pre- and Post-Administration of Vitamin A on the Growth of Refractory Cancers in Xenograft Mice

Effect of alcohol on the central nervous system to develop neurological disorder: pathophysiological and lifestyle modulation can be potential therapeutic options for alcohol-induced neurotoxication

Sclerostin, vascular risk factors, and brain atrophy in excessive drinkers

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