The impact of oxidative stress in thiamine deficiency: A multifactorial targeting issue

Hazell, Alan S.; Faim, Samantha; Wertheimer, Guilherme Soares de Oliveira; Silva, Vinícius Rodrigues; Marques, Cleiton S.

doi:10.1016/j.neuint.2013.01.009

Cited by 48 publications

(45 citation statements)

References 95 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another possible mechanism is neuroinflammation which may contribute TD-induced CNS damage. TD significantly increases pro-inflammatory cytokines, chemokines, interferons, as well as many transcription factors known to control inflammatory gene expression are upregulated in TD animals [33]. The neuroinflammation may alter mitochondrial membrane potential and thus its function, resulting in an increase in ROS [84].…”

Section: Mechanisms Underlying Td-mediated Neurodegenerationmentioning

confidence: 99%

“…Therapeutic effects of thiamine supplementation have been observed in some neurodegenerative diseases and alcohol-induced dementia [28-30]. In addition, accumulating evidence has been documented that TD is able to cause regionally specific neuronal death in animal and human brains which is accompanied with a mild chronic impairment of oxidative metabolism [31-33]. TD also causes the activation of microglia, astrocytes and endothelial cells [34] as well as abnormalities of cerebral glucose metabolism [35].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

2016

View full text Add to dashboard Cite

Thiamine (Vitamin B1) is an essential nutrient and indispensable for normal growth and development of the organism due to its multilateral participation in key biochemical and physiological processes. Humans must obtain thiamine from their diet since it is synthesized only in bacteria, fungi and plants. Thiamine deficiency (TD) can result from inadequate intake, increased requirement, excessive deletion and chronic alcohol consumption. TD affects multiple organ systems, including the cardiovascular, muscular, gastrointestinal, and central and peripheral nervous systems. In the brain, TD causes a cascade of events including mild impairment of oxidative metabolism, neuroinflammation and neurodegeneration, which are commonly observed in neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Thiamine metabolites may serve as promising biomarkers for neurodegenerative diseases and thiamine supplementations exhibit therapeutic potential for patients of some neurodegenerative diseases. Experimental TD has been used to model aging-related neurodegenerative diseases. However, to date, the cellular and molecular mechanisms underlying TD-induced neurodegeneration are not clear. Recent research evidence indicates that TD causes oxidative stress, endoplasmic reticulum (ER) stress and autophagy in the brain, which are known to contribute to the pathogenesis of various neurodegenerative diseases. In this review, we discuss the role of oxidative stress, ER stress and autophagy in TD-mediated neurodegeneration. We propose that it is the interplay of oxidative stress, ER stress and autophagy that contributes to TD-mediated neurodegeneration.

show abstract

Section: Mechanisms Underlying Td-mediated Neurodegenerationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

2016

View full text Add to dashboard Cite

show abstract

“…Benfotiamine diminishes superoxide and hydroxyl radical levels in diabetic and aging hearts by regenerating the antioxidant NADPH, secondary to the activation of the pentose phosphate shunt. By preventing advanced glycation end products accumulation, benfotiamine prevents myocardial interstitial fibrosis [21,22,23].…”

Section: Resultsmentioning

confidence: 99%

Benfothiamine Administration in Patients with Dilated Cardiomyopathy and Advanced Heart Failure with Chronic Diuretic Treatment

Iluțiu-Varvara¹,

Rădulescu²,

Donca³

2017

Studia UBB Chemia

View full text Add to dashboard Cite

ABSTRACT.It is well known that long term administration of high dose loop diuretics in patients with heart failure, may in some cases aggravate the cardiac failure symptoms. Part of this effect may be due to thiamine depletion secondary to diuretics use. The aim of our present study was to assess whether administration of benfothiamine in patients with advanced congestive cardiac failure treated on long term with high dose loop diuretics, can prevent the alteration of heart failure.

show abstract

“…Thiamine deficiency is associated with excitotoxic-mediated neuronal cell death. [102] Furthermore, thiamine deficiency is associated with increased production of ROS as well as increased expression of heme oxygenase (HO-1) and eNOS. [102][103][104] Thiamine can reverse oxidative stress that is not related to thiamine deficiency, suggesting that thiamine may act as a site-directed antioxidant.…”

Section: Thiaminementioning

confidence: 99%

Hydrocortisone, Ascorbic acid and Thiamine (HAT Therapy) for the Treatment of Sepsis. Focus on Ascorbic Acid

Marik¹

2018

Preprint

View full text Add to dashboard Cite

Sepsis is a devastating disease that carries an enormous toll in terms of human suffering and lives lost. Over 100 novel pharmacologic agents which targeted specific molecules or pathways have failed to improve the outcome of sepsis. Preliminary data suggests that the combination of Hydrocortisone, Ascorbic Acid and Thiamine (HAT therapy) may reduce organ failure and mortality in patients with sepsis and septic shock. HAT therapy is based on the concept that a combination of readily available, safe and cheap agents which target multiple components of the host’s response to an infectious agent will synergistically restore the dysregulated immune response and thereby prevent organ failure and death. This paper reviews the rationale for HAT therapy with a focus on vitamin C.

show abstract

The impact of oxidative stress in thiamine deficiency: A multifactorial targeting issue

Cited by 48 publications

References 95 publications

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

Benfothiamine Administration in Patients with Dilated Cardiomyopathy and Advanced Heart Failure with Chronic Diuretic Treatment

Hydrocortisone, Ascorbic acid and Thiamine (HAT Therapy) for the Treatment of Sepsis. Focus on Ascorbic Acid

Contact Info

Product

Resources

About