Restoration of Blood Total Glutathione Status and Lymphocyte Function Following<i>α</i>-Lipoic Acid Supplementation in Patients with HIV Infection

Jariwalla, Raxit J.; Lalezari, Jacob; Cenko, Diane; Mansour, Sam E.; Kumar, Abha; Gangapurkar, Bhakti; Nakamura, Daniel

doi:10.1089/acm.2006.6397

Cited by 47 publications

(34 citation statements)

References 28 publications

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“…4 Furthermore, reduced glutathione concentration and/or a disproportionate ratio of GSH:GSSG has been associated with a number of diseases, including cancer, human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS), hepatitis, type 2 diabetes, Parkinson's disease, and cystic fibrosis. 2,[8][9][10][11][12][13][14] Although no experimental research to date has demonstrated disease prevention from GSH supplementation or other strategies to specifically increase GSH, observational research suggests increased dietary glutathione intake has been associated with reduced risk for oral cancer.…”

Section: Introductionmentioning

confidence: 99%

Effects of Oral Glutathione Supplementation on Systemic Oxidative Stress Biomarkers in Human Volunteers

Allen

Bradley

2011

The Journal of Alternative and Complementary Medicine

135

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Background: The tripeptide glutathione (GSH) is the most abundant free radical scavenger synthesized endogenously in humans. Increasing mechanistic, clinical, and epidemiological evidence demonstrates that GSH status is significant in acute and chronic diseases. Despite ease of delivery, little controlled clinical research data exist evaluating the effects of oral GSH supplementation. Objectives: The study objectives were to determine the effect of oral GSH supplementation on biomarkers of systemic oxidative stress in human volunteers. Design: This was a randomized, double-blind, placebo-controlled clinical trial. Setting/location: The study was conducted at Bastyr University Research Institute, Kenmore, WA and the Bastyr Center for Natural Health, Seattle, WA. Subjects: Forty (40) adult volunteers without acute or chronic disease participated in this study. Intervention: Oral GSH supplementation (500 mg twice daily) was given to the volunteers for 4 weeks. Outcome measures: Primary outcome measures included change in creatinine-standardized, urinary F2-isoprostanes (F2-isoP) and urinary 8-hydroxy-2¢-deoxyguanosine (8-OHdG). Changes in erythrocyte GSH concentrations, including total reduced glutathione (GSH), oxidized glutathione (GSSG), and their ratio (GSH:GSSG) were also measured by tandem liquid chromatography/mass spectrometry. Analysis of variance was used to evaluate differences between groups. Results: There were no differences in oxidative stress biomarkers between treatment groups at baseline. Thirtynine (39) participants completed the study per protocol. Changes in creatinine standardized F2-isoP (ng/mg creatinine) (0.0 -0.1 versus 0.0 -0.1, p = 0.38) and 8-OHdG (lg/g creatinine) (-0.2 -3.3 versus 1.0 -3.2, p = 0.27) were nonsignificant between groups at week 4. Total reduced, oxidized, and ratio measures of GSH status were also unchanged. Conclusions: No significant changes were observed in biomarkers of oxidative stress, including glutathione status, in this clinical trial of oral glutathione supplementation in healthy adults.

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Section: Introductionmentioning

confidence: 99%

Effects of Oral Glutathione Supplementation on Systemic Oxidative Stress Biomarkers in Human Volunteers

Allen

Bradley

2011

The Journal of Alternative and Complementary Medicine

135

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“…However, the use of the ALA is hampered by its instability and its rapid metabolism, suggesting that formulations containing ALA, in a form ensuring its stability and improving its bioavailability, can have important applications as medicines, nutritional supplements or cosmeceuticals [76] . Also, ALA as a mitochondrial cofactor termed 'mitochondrial nutrient' has been tested in a number of clinical trials such as alcohol-related liver disease [77] , diabetes-associated neuropathy [78] , heart disease [79] , HIV-1-related lipoatrophy [80] and mitochondrial diseases disease [81] . Also, there are only two clinical trial papers.…”

Section: Discussionmentioning

confidence: 99%

Chemopreventive Effects of Alpha Lipoic Acid on Obesity-Related Cancers

Moon

2016

Ann Nutr Metab

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Background: It has been generally accepted that being overweight or obese is a risk factor for several types of cancers, including breast, thyroid, colon, pancreatic and liver. In fact, people who are obese have more fat tissues that can produce hormones, such as insulin or estrogen, which may cause cancer cells to grow. Alpha lipoic acid (ALA) is anorganosulfur compound derived from octanoic acid, which is produced in animals normally, and is essential for aerobic metabolism. Summary: Studies in both in vitro cells and in vivo animal models have shown that ALA inhibits the initiation and promotion stages of carcinogenesis, suggesting that ALA has considerable attention as a chemopreventive agent. This brief review collects the scattered data available in the literature concerning ALA and highlights its anti-cancer properties, intermediary metabolism and exploratory implications. Key Messages: Based on scientific evidences so far, ALA might be useful agents in the management or chemoprevention of obesity-related cancers.

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“…A number of studies support its use in the ancillary treatment of many diseases, such as diabetes, cardiovascular, neurodegenerative, autoimmune diseases, cancer and AIDS (Khalili et al 2014;Shinto et al 2014;Sancheti et al 2013a;Gębka et al 2014;Padmalayam 2012;Yamasaki et al 2014;Jariwalla et al 2008;Gorąca et al 2011) . In addition to its anti-oxidative role, LA supplementation in diet modulates the inflammatory response by inhibiting IL-6 and TNF-α expression (Li et al 2014) . LA significantly inhibited LPS-induced production of nitric oxide and TNF-α via an attenuated activation of NF-κB and activator protein-1 (Kiemer et al 2002) .…”

Section: Discussionmentioning

confidence: 99%

Lipoic acid protects dopaminergic neurons in LPS-induced Parkinson’s disease model

et al. 2015

Metab Brain Dis

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Parkinson's disease (PD) is a chronic neurodegenerative disease of the central nervous system (CNS), characterized by a loss of dopaminergic neurons, which is thought to be caused by both genetic and environmental factors. Recent findings suggest that neuroinflammation may be a pathogenic factor in the onset and progression of sporadic PD. Here we explore the potential therapeutic effect of lipoic acid (LA) on a lipolysaccharide (LPS)-induced inflammatory PD model. Our results for the first time showed that LA administration improved motor dysfunction, protected dopaminergic neurons loss, and decreased α-synuclein accumulation in the substantia nigra (SN) area of brain. Further, LA inhibited the activation of nuclear factor-κB (NF-κB) and expression of pro-inflammatory molecules in M1 microglia. Taken together, these results suggest that LA may exert a profound neuroprotective effect and is thus a promising anti-neuroinflammatory and anti-oxidative agent for halting the progression of PD. Interventions aimed at either blocking microglia-derived inflammatory mediators or modulating the polarization of microglia may be potentially useful therapies that are worth further investigation.

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Restoration of Blood Total Glutathione Status and Lymphocyte Function Followingα-Lipoic Acid Supplementation in Patients with HIV Infection

Abstract: Supplementation with alpha-lipoic acid may positively impact patients with HIV and acquired immune deficiency syndrome by restoring blood total glutathione level and improving functional reactivity of lymphocytes to T-cell mitogens.

Cited by 47 publications

References 28 publications

Effects of Oral Glutathione Supplementation on Systemic Oxidative Stress Biomarkers in Human Volunteers

Effects of Oral Glutathione Supplementation on Systemic Oxidative Stress Biomarkers in Human Volunteers

Chemopreventive Effects of Alpha Lipoic Acid on Obesity-Related Cancers

Lipoic acid protects dopaminergic neurons in LPS-induced Parkinson’s disease model

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