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. 2022 Sep;21(4):54–58.

Lactobacillus fermentum ME-3: A Breakthrough in Glutathione Therapy

Ross Pelton
PMCID: PMC9542933  PMID: 36644601

Abstract

It is difficult to overstate the importance of glutathione because it performs many critical biological functions. The purpose of this article is to briefly review glutathione’s functions, explain why most people have low levels of glutathione and make the case that increasing glutathione levels is one of the most important pro-active steps people can take to improve their health and slow down the onset of age-related diseases. This article will also introduce practitioners to Lactobacillus fermentum ME-3, which is a unique strain of probiotic bacteria that synthesizes glutathione.

It is difficult to overstate the importance of glutathione because it performs many critical biological functions. The purpose of this article is to briefly review glutathione’s functions, explain why most people have low levels of glutathione and make the case that increasing glutathione levels is one of the most important pro-active steps people can take to improve their health and slow down the onset of age-related diseases. This article will also introduce practitioners to Lactobacillus fermentum ME-3, which is a unique strain of probiotic bacteria that synthesizes glutathione.

Glutathione is made in every cell in the body and consequently, it is the most prevalent antioxidant in humans, which explains why it is often referred to as the Master Antioxidant.1 In its role as an antioxidant, glutathione also helps to recycle and preserve all other antioxidants.2 Glutathione also detoxifies a wide range of environmental toxins, and it also neutralizes endogenously generated free radicals.

Glutathione is a critical regulator of the immune system,3 and it is increasingly being recognized for its antiviral activity.4 Glutathione also plays a critical role in the function and protection of mitochondria. Mitochondrial levels of glutathione (mGSH) play a critical role defending mitochondria against DNA damage and also in the repair of oxidative damage that can lead to mitochondrial dysfunction and cell death.5

Introducing Lactobacillus fermentum ME-3

Professor Marika Mikelsaar, head of the Department of Microbiology at the University of Tartu in Estonia is credited with the discovery of Lactobacillus fermentum ME-3.6 This strain of bacteria was originally isolated from the intestinal tract of a healthy 1-year old child. Upon testing, Lactobacillus fermentum ME-3 (called ME-3 for simplicity) exhibited extremely high antioxidant activity.6

After the discovering that Lactobacillus fermentum ME-3 expressed antioxidant activity, additional studies revealed that ME-3 synthesized glutathione. Because ME-3 synthesized glutathione, Professor Mikelsaar realized that it might produce a number of health benefits. Now, after being studied intensely for over 25 years, studies have shown that ME-3’s benefits fall into the following four broad categories: anti-inflammatory activity, antioxidant activity, detoxification, and immune support.

ME-3’s Antioxidant Activity

Lactobacillus fermentum ME-3 has been called a complete glutathione system.7 ME-3 can increase glutathione levels by three different mechanisms. ME-3 synthesizes glutathione, it can extract glutathione from the surrounding environment, and it recycles, or regenerates oxidized glutathione back to its reduced or active state.8 Researchers suggest that ME-3 is the only organism known to be capable of increasing glutathione levels by three different mechanisms, simultaneously.

In addition to producing glutathione, studies show that taking ME-3 also results in increased levels of important glutathione-dependent enzymes such as glutathione peroxidase, glutathione reductase, and glutathione S-transferases, which contribute to glutathione’s function and regeneration.8 As previously mentioned, ME-3 is the only substance known that functions as a “complete glutathione system” to synthesize, increase cellular uptake and recycle/regenerate glutathione.

Lactobacillus fermentum ME-3 also produces the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD).8 Mitochondria consume over 90 percent of the oxygen used by cells,9 which makes them especially vulnerable to oxidative free radical damage.10 MnSOD is an antioxidant enzyme that neutralizes the highly reactive mitochondrial superoxide radical (O2–). Consequently, MnSOD provides a critical first line of defense against cellular oxidative stress.11

Increasing Total Antioxidant Activity

Lactobacillus fermentum ME-3 provides additional antioxidant support because the additional glutathione produced enables redox recycling, which helps regenerate oxidized antioxidants such as vitamin C and vitamin E back to their active forms. Lactobacillus fermentum ME-3 has been shown to have the highest Total Antioxidant Activity (TAA) and the highest Total Antioxidant Status (TAS) of any probiotic tested to date.12

Supporting Cardiovascular Health

Lactobacillus fermentum ME-3 has been shown to improve several cardiovascular risk factors as evidenced by the results from the following 2-week double-blind, placebo-controlled human clinical. Subjects taking ME-3 had lower levels of oxidized LDL-cholesterol, triglycerides and increases in PON and HDL-cholesterol.13 During this same time, the values of these markers got slightly worse for the placebo control subjects.

Glutathione & Mitochondria Health

Under normal healthy conditions, mitochondria contain relatively high concentrations of glutathione. Consequently, mitochondrial glutathione is the primary defense against oxidative free radical damage to mitochondria.14

Improving Detoxification

Since ME-3 substantially increases glutathione levels, scientists realized it will increase glutathione’s detoxification capabilities. Glutathione plays a critical role in many important detoxification processes including toxic metals such as mercury15 and cadmium,16 reactive oxygen species (ROS),17 reactive nitrogen species (RNS),18 and a wide range of xenobiotics.19 Also, glutathione gets depleted during the process of detoxifying things that are quite common in many people’s lives such as alcohol,20 artificial sweeteners such as aspartame,21 tobacco smoke,22 and the commonly used analgesic acetaminophen.23

ME-3 Reduces Inflammation

Lactobacillus fermentum ME-3 helps lower levels of several key inflammatory markers such as high sensitivity C-reactive protein (hs-CRP) and interleukin 6 (IL-6) and it is also capable of stimulating production of the peptide adiponectin and of reducing levels of glycated hemoglobin.24 These functions are important for supporting normal inflammatory activity.

Elevates PON1/Detoxifies Organophosphates (OPs)

According to the CDC, organophosphates (OPs) are the most widely used insecticides in use today. OPs are neurotoxins that are widely applied on agricultural crops, on residential gardens and they are in many products that are commonly used household products. OPs are also commonly used as plasticizers and flame retardants in consumer products.25 These compounds are so toxic that they are also used as chemical warfare nerve agents.26

Human paraoxonase 1 (PON1) is a multi-tasking enzyme that metabolizes and detoxifies organophosphates.27 PON1 is exclusively synthesized in the liver and bound to high-density lipoproteins (HDLs).28 The PON1 enzyme also expresses anti-inflammatory, antioxidant, antidiabetic, and antimicrobial activity.27

According to a 2004 report, “Almost every person is, or has been exposed to organophosphate insecticides in their home, work, or environment.29 Also, a U.S. government-funded study titled Forth National Report on Human Exposure to Environmental Chemicals reported that 93% of tested children had measurable metabolites of organophosphates.30 Childhood exposure and exposure during pregnancy to OPs is associated with higher incidence of ADHD,31 and autism.32 Thus, products containing Lactobacillus fermemtum ME-3 may help reduce the risk of health problems due to organophosphate exposure.

Survivability

To be effective, a probiotic must be able to survive exposure to the strong acidic conditions in the stomach and exposure to the digestive bile acids present in the small intestine.

In in vitro studies, Lactobacillus fermentum ME-3 was capable of surviving at pH values ranging from to 2.5 to 4.0 without a loss in viable cell count. Even at pH 2.0, ME-3 bacteria survived for up to 6 hours. When exposed to bile acids, ME-3 survived for 24 hours without significant loss of live bacteria.33 Thus, in vitro testing suggests that Lactobacillus fermentum ME-3 can tolerate exposure to harsh acidity in the stomach as well as exposure to bile acids in the small intestine. Hence, Lactobacillus fermentum ME-3 thrives and survives in conditions that simulate the harsh environments that exist in the human gastrointestinal tract.

Published Studies on ME-3

There are 12 published scientific studies on Lactobacillus fermentum ME-3 listed in PubMed. I’m just going to summarize several of these studies in this article, which document and report some of ME-3’s benefits.

ME-3 & Type 2 Diabetes Complications

Type 2 diabetes is an escalating epidemic in the United States and worldwide. Individuals with type 2 diabetes have a much greater risk of developing health problems such as diabetic ulcers, peripheral neuropathy, kidney and liver damage, blindness, and amputations.34 A process named glycation is one of the underlying causes of these secondary health problems.35

Glycation occurs when sugars, primarily glucose or fructose, bind with proteins to form advanced glycation end products or AGEs (fructose has approximately 10 times greater glycation activity than glucose).36 The process of glycation is irreversible and renders proteins (and enzymes) non-functional. The accumulation of these altered proteins (AGEs) is reported to be the most common molecular symptom of aging.37

The following study used two genotypes of mice that are bred to develop type 2 diabetes early in life. They develop elevated insulin levels at about 10-14 days, elevated blood sugar when they are between 4 to 8 weeks old, become obese by about 3 to 4 weeks of age.

In this study, each strain was administered a daily gavage of either water or the Lactobacillus fermentum ME-3 strain of probiotic bacteria (1010 CFU) for 12 weeks. After 12 weeks, the diabetic mice that received the ME-3 treatment, gained less weight, and exhibited improved glucose tolerance. Treatment with ME-3 also reduced median levels of two reliable glycation markers from 12 to 30%. Reduced hepatic steatosis (fatty liver) and improved plasma lipid profiles were also observed in both genotypes.38

The results from this study suggest that Lactobacillus fermentum ME-3 may help lower the formation and accumulation of glycation end products (AGEs) and reduce the incidence of some common diabetes-related problems.

Results from Human ME-3 Clinical Trials

  1. Lowering Cardiovascular Risks: 21 volunteers were assigned to two treatment groups. The control group ingested goats’ milk group and the test group ingested goats’ milk with Lactobacillus fermentum ME-3 for 21 days. Consumption of fermented goats’ milk improved anti-atherogenicity in healthy subjects as shown by the following results:39

    • 16% reduction in oxidized LDL-cholesterol

    • 20% decrease is 8-isoprostanes

    • 49% increase in the ratio of GHS/GSSG

    • 26% increase in total antioxidant activity

  2. Improved Stroke Recovery: 21 elderly patients who survived a recent stroke (6-18 days earlier) were randomly divided into two groups. In addition to physician-prescribed medications, the patients consumed either 3 capsules containing ME-3 or a placebo twice daily for 3 weeks. The patients consuming ME-3 exhibited significant improvements in the Scandinavian Stroke Scale (from 33 up to 42) and the Functional Independence Measure inventory (from 21 up to 40). Stroke patients also experienced impressive improvements in the following blood markers: oxidized LDL-cholesterol, glutathione levels & ratio of reduced to oxidized glutathione, total antioxidant capacity, paraoxonase enzyme activity as well as reductions in markers of inflammation and free radical damage.40

Glutathione and Immune Function

Glutathione is essential for the function and activity of T-lymphocytes, B-lymphocytes41 and NK cells.42 Hence, glutathione is a critical regulator of the human immune system.

Glutathione’s Antiviral Activity

Humanity is just beginning to recover from a global pandemic that was caused by SARS-CoV-2 virus. Because glutathione provides antioxidant, antiviral, and immune-regulating activity, studies were conducted looking for a relationship between glutathione levels and COVID19. It has been reported that glutathione levels play a role in suppressing the inflammatory cytokine storm that is one of the manifestations of severe cases of COVID-19.43 One study proposed that low levels of glutathione are the most likely cause of serious manifestations and death in COVID-19 patients.44

The Glutathione Deficiency Hypothesis

In 1987, Drs. John Richie and Calvin Lang proposed the Glutathione Deficiency Hypothesis based on the results of their studies on glutathione and aging. In one study, they gave adult mosquitoes a glutathione precursor in their drinking water. Compared to controls, glutathione levels in the test mosquitoes increased from 50-100%, which resulted in 30-38% increase in the lifespan.45 In their conclusion, they stated the following: “These findings confirm the GSH deficiency hypothesis and demonstrate a specific biochemical mechanism of aging that can be nutritionally modified.”

Widespread Glutathione Deficiency

Many things contribute to glutathione depletion such as poor diets, alcohol, smoking and the ingestion of OTC, recreational and prescription drugs. In addition to these concerns, there are tens of thousands of confirmed toxic substances in the environment. Toxins are in the air, water, land and in the food we eat. A study titled Body Burden: The Pollution in Newborns revealed that some infants are exposed to hundreds of chemicals while still in the womb.46

The National Institutes of Health (NIH) published a report based on a review of over 108 000 articles on glutathione in the National Library of Medicine’s NIH database. The title of this report is: Diseases Associated With Low Glutahtione & Some Clinical Applications Of Raising Glutathione Levels.47

This NIH review, covering of over 108 000 PubMed citations on diseases associated with low glutathione, reveals that virtually all diseases are associated with low glutathione levels.

The Importance of Boosting Glutathione Levels

When glutathione neutralizes a free radical, or when it binds and eliminates toxins, glutathione levels decline. It is also known that glutathione synthesis in humans declines with age.48 Thus, boosting glutathione levels is an important pro-active step that will help many people improve their health and slow down the onset of age-related diseases.

A study conducted by the University of Michigan School of Public Health and the University of Louisville School of Medicine compared glutathione levels in elderly individuals with various diseases such as arthritis, hypertension, heart disease, circulatory problems, diabetes, intestinal problems and UTIs. The results revealed that, in a sample of independently living elderly people, an individual’s glutathione levels was the largest factor in the incidence of disease.49

Results from animal and human clinical trials indicate that boosting glutathione levels helps to improve many age-associated diseases such as mitochondrial function, inflammation, insulin resistance, endothelial dysfunction, muscle strength, exercise capacity and cognitive function.50 Consequently, glutathione is now recognized as a reliable biomarker of aging.51

Oral glutathione supplements are quickly degraded before they can be absorbed. Although newer liposomal delivery systems have been shown increase plasma glutathione levels, no glutathione-enhancing product has ever achieved the 49% increase in the ratio of reduced to oxidized glutathione that has been documented in human clinical trials with the oral ingestion of Lactobacillus fermentum ME-3.

Boosting Glutathione Levels with Lactobacillus fermentum ME-3

The studies reviewed in this article confirm that oral ingestion of Lactobacillus fermentum ME-3 is a very effective method of boosting glutathione levels in humans. Because Lactobacillus fermentum ME-3 was discovered by Professor Marika Mikelsaar at the University of Tartu in Estonia, the University of Tartu holds the patent rights for Lactobacillus fermentum ME-3. Products containing Lactobacillus fermentum ME-3 can easily be found by doing an internet search for Lactobacillus fermentum ME-3.

Biography

Ross Pelton, RPh, PhD, CCN, is a pharmacist, a certified clinical nutritionist (CCN) and he is currently the Scientific Director for Essential Formulas. Ross “brands” himself as The Natural Pharmacist and he is the author of The Drug-Induced Nutrient Depletion Handbook. IMCJ readers can use the following link to get a FREE copy of Ross’ Quick Reference Guide to Drug-Induced Nutrient Depletions: naturalpharmacist.net/dind Join Ross in the Life Extension Revolution. To be on Ross’ mailing list and receive periodic updates on cutting edge health information, click on the Subscribe link on his website: naturalpharmacist.net

References

  • 1.Dhivya H. Glutathione—a master antioxidant and an immune system modulator. J Bio Inf Sci. 2012;1(3):28-30. [Google Scholar]
  • 2.Adeoye O, Olawumi J, Opeyemi A, Christiania O. Review on the role of glutathione on oxidative stress and infertility. JBRA Assist Reprod. 2018;22(1):61-66. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Ferreira AV, Koeken VACM, Matzaraki V, et al. Glutathione Metabolism Contributes to the Induction of Trained Immunity. Cells. 2021;10(5):971. doi:10.3390/cells10050971 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Bartolini D, Stabile AM, Bastianelli S, et al. SARS-CoV2 infection impairs the metabolism and redox function of cellular glutathione. Redox Biol. 2021;45:102041. doi:10.1016/j.redox.2021.102041 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Mari M, et al. Mitochondrial Glutathioone, a Key Survival Antioxidant. Antiox Redox Signal. 2009. Nov. 11 (11:2685-2700. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Mikelsaar M, Zilmer M. Lactobacillus fermentum ME-3 - an antimicrobial and antioxidative probiotic. Microb Ecol Health Dis. 2009;21(1):1-27. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Kullisar T, et al. Complete glutathione system in probiotic Lactobacillus fermentum ME-3. Appl Biochem Microbiol. 2010;46(5):481-486. doi:10.1134/S0003683810050030 [PubMed] [Google Scholar]
  • 8.Kullisaar T, Songisepp E, Aunapuu M, et al. Complete glutathione system in probiotic Lactobacillus fermentum ME-3. Prikl Biokhim Mikrobiol. 2010;46(5):527-531. [PubMed] [Google Scholar]
  • 9.Rolfe DF, Brown GC. Cellular energy utilization and molecular origin of standard metabolic rate in mammals. Physiol Rev. 1997;77(3):731-758. doi:10.1152/physrev.1997.77.3.731 [DOI] [PubMed] [Google Scholar]
  • 10.Fariss MW, Chan CB, Patel M, Van Houten B, Orrenius S. Role of mitochondria in toxic oxidative stress. Mol Interv. 2005;5(2):94-111. doi:10.1124/mi.5.2.7 [DOI] [PubMed] [Google Scholar]
  • 11.Ansenberger-Fricano K, Ganini D, Mao M, et al. The peroxidase activity of mitochondrial superoxide dismutase. Free Radic Biol Med. 2013;54:116-124. doi:10.1016/j.freeradbiomed.2012.08.573 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Hütt P, Shchepetova J, Lõivukene K, Kullisaar T, Mikelsaar M. Antagonistic activity of probiotic lactobacilli and bifidobacteria against entero- and uropathogens. J Appl Microbiol. 2006;100(6):1324-1332. doi:10.1111/j.1365-2672.2006.02857.x [DOI] [PubMed] [Google Scholar]
  • 13.Kullisaar T, Shepetova J, Zilmer K, et al. An antioxidant probiotic reduces postprandial lipemia and oxidative stress. Cent Eur J Biol. 2011;6(1):32-40. [Google Scholar]
  • 14.Ribas V, García-Ruiz C, Fernández-Checa JC. Glutathione and mitochondria. Front Pharmacol. 2014;5:151. doi:10.3389/fphar.2014.00151 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Kromidas L, Trombetta LD, Jamall IS. The protective effects of glutathione against methylmercury cytotoxicity. Toxicol Lett. 1990;51(1):67-80. doi:10.1016/0378-4274(90)90226-C [DOI] [PubMed] [Google Scholar]
  • 16.Singhal RK, Anderson ME, Meister A. Glutathione, a first line of defense against cadmium toxicity. FASEB J. 1987;1(3):220-223. doi:10.1096/fasebj.1.3.2887478 [DOI] [PubMed] [Google Scholar]
  • 17.Mailloux RJ, McBride SL, Harper ME. Unearthing the secrets of mitochondrial ROS and glutathione in bioenergetics. Trends Biochem Sci. 2013;38(12):592-602. doi:10.1016/j.tibs.2013.09.001 [DOI] [PubMed] [Google Scholar]
  • 18.Heales SJ, Bolaños JP. Impairment of brain mitochondrial function by reactive nitrogen species: the role of glutathione in dictating susceptibility. Neurochem Int. 2002;40(6):469-474. doi:10.1016/S0197-0186(01)00117-6 [DOI] [PubMed] [Google Scholar]
  • 19.Koob M, Dekant W. Bioactivation of xenobiotics by formation of toxic glutathione conjugates. Chem Biol Interact. 1991;77(2):107-136. doi:10.1016/0009-2797(91)90068-I [DOI] [PubMed] [Google Scholar]
  • 20.Yeh MY, Burnham EL, Moss M, Brown LA. Chronic alcoholism alters systemic and pulmonary glutathione redox status. Am J Respir Crit Care Med. 2007;176(3):270-276. doi:10.1164/rccm.200611-1722OC [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Abhilash M, Paul MV, Varghese MV, Nair RH, Nair H. Effect of long term intake of aspartame on antioxidant defense status in liver. Food Chem Toxicol. 2011;49(6):1203-1207. doi:10.1016/j.fct.2011.02.019 [DOI] [PubMed] [Google Scholar]
  • 22.van der Toorn M, Smit-de Vries MP, Slebos DJ, et al. Cigarette smoke irreversibly modifies glutathione in airway epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2007;293(5):L1156-L1162. doi:10.1152/ajplung.00081.2007 [DOI] [PubMed] [Google Scholar]
  • 23.Hinson JA, Roberts DW, James LP. Mechanisms of acetaminophen-induced liver necrosis. Handb Exp Pharmacol. 2010;196:369-405. doi:10.1007/978-3-642-00663-0_12 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24.US Patent WO 2014102692 A1: Method of treatment using Lactobacillus fermentum me-3. http://www.google.com/patents/WO2014102692A1?cl=en
  • 25.Doherty BT, Hoffman K, Keil AP, et al. Prenatal exposure to organophosphate esters and behavioral development in young children in the Pregnancy, Infection, and Nutrition Study. Neurotoxicology. 2019;73:150-160. doi:10.1016/j.neuro.2019.03.007 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 26.Ruark CD, Hack CE, Robinson PJ, Anderson PE, Gearhart JM. Quantitative structure-activity relationships for organophosphates binding to acetylcholinesterase. Arch Toxicol. 2013;87(2):281-289. doi:10.1007/s00204-012-0934-z [DOI] [PubMed] [Google Scholar]
  • 27.Bajaj P, Tripathy RK, Aggarwal G, Pande AH. Human paraoxonase 1 as a pharmacologic agent: limitations and perspectives. ScientificWorldJournal. 2014;2014:854391. doi:10.1155/2014/854391 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Aviram M. Does paraoxonase play a role in susceptibility to cardiovascular disease? Mol Med Today. 1999;5(9):381-386. doi:10.1016/S1357-4310(99)01546-4 [DOI] [PubMed] [Google Scholar]
  • 29.Casida JE, Quistad GB. Organophosphate toxicology: safety aspects of nonacetylcholinesterase secondary targets. Chem Res Toxicol. 2004;17(8):983-998. doi:10.1021/tx0499259 [DOI] [PubMed] [Google Scholar]
  • 30.CDC. Fourth National Report on Human Exposure to Environmental Chemicals. Available at http://www.cdc.gov/exposurereport/pdf/FourthReport.pdf. [PubMed]
  • 31.Bouchard MF, Bellinger DC, Wright RO, Weisskopf MG. Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides. Pediatrics. 2010;125(6):e1270-e1277. doi:10.1542/peds.2009-3058 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32.Shelton JF, Geraghty EM, Tancredi DJ, et al. Neurodevelopmental disorders and prenatal residential proximity to agricultural pesticides: the CHARGE study. Environ Health Perspect. 2014;122(10):1103-1109. doi:10.1289/ehp.1307044 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33.Songisepp E. Evaluation of technological and functional properties of the new probiotic Lactobacillus fermentum ME-3. Doctoral Thesis: University of Tartu; 2005. [Google Scholar]
  • 34.Trikkalinou A, Papazafiropoulou AK, Melidonis A. Type 2 diabetes and quality of life. World J Diabetes. 2017;8(4):120-129. doi:10.4239/wjd.v8.i4.120 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.Monnier VM, Taniguchi N. Advanced glycation in diabetes, aging and age-related diseases: editorial and dedication. Glycoconj J. 2016;33(4):483-486. doi:10.1007/s10719-016-9704-0 [DOI] [PubMed] [Google Scholar]
  • 36.McPherson JD, Shilton BH, Walton DJ. Role of fructose in glycation and cross-linking of proteins. Biochemistry. 1988;27(6):1901-1907. doi:10.1021/bi00406a016 [DOI] [PubMed] [Google Scholar]
  • 37.Hipkiss AR. Accumulation of altered proteins and ageing: causes and effects. Exp Gerontol. 2006;41(5):464-473. doi:10.1016/j.exger.2006.03.004 [DOI] [PubMed] [Google Scholar]
  • 38.Guilbaud A, Howsam M, Niquet-Léridon C, et al. The Effect of Lactobacillus fermentum ME-3 Treatment on Glycation and Diabetes Complications. Mol Nutr Food Res. 2020;64(6):e1901018. doi:10.1002/mnfr.201901018 [DOI] [PubMed] [Google Scholar]
  • 39.Kullisaar T, Songisepp E, Mikelsaar M, Zilmer K, Vihalemm T, Zilmer M. Antioxidative probiotic fermented goats’ milk decreases oxidative stress-mediated atherogenicity in human subjects. Br J Nutr. 2003;90(2):449-456. doi:10.1079/BJN2003896 [DOI] [PubMed] [Google Scholar]
  • 40.Kullisaar T, Mikelsaar M, Kaur S, et al. Probiotics, Oxidative Stress, Inflammation and Diseases. 4th Central European Congress on Food. May 15-17, Caveat, Croatia. [Google Scholar]
  • 41.Silber R, Farber CM, Papadopoulos E, et al. Glutathione depletion in chronic lymphocytic leukemia B lymphocytes. Blood. 1992;80(8):2038-2043. doi:10.1182/blood.V80.8.2038.2038 [PubMed] [Google Scholar]
  • 42.Millman AC, Salman M, Dayaram YK, Connell ND, Venketaraman V. Natural killer cells, glutathione, cytokines, and innate immunity against Mycobacterium tuberculosis. J Interferon Cytokine Res. 2008;28(3):153-165. doi:10.1089/jir.2007.0095 [DOI] [PubMed] [Google Scholar]
  • 43.Silvagno F, Vernone A, Pescarmona GP. The Role of Glutathione in Protecting against the Severe Inflammatory Response Triggered by COVID-19. Antioxidants. 2020;9(7):624. doi:10.3390/antiox9070624 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Polonikov A. Endogenous Deficiency of Glutathione as the Most Likely Cause of Serious Manifestations and Death in COVID-19 Patients. ACS Infect Dis. 2020;6(7):1558-1562. doi:10.1021/acsinfecdis.0c00288 [DOI] [PubMed] [Google Scholar]
  • 45.Richie JP, Jr, Mills BJ, Lang CA. Correction of a glutathione deficiency in the aging mosquito increases its longevity. Proc Soc Exp Biol Med. 1987; 184(1): 113-117. doi:10.3181/00379727-184-42454 [DOI] [PubMed] [Google Scholar]
  • 46.Environmental Working Group (EWG). 2005. Jul 14. A Benchmark Investigation Of Industrial Chemicals, Pollutants And Pesticides In Umbilical Cord Blood. https://canvas.uw.edu/courses/1220635/files/50877519.
  • 47.Diseases Associated With Low Glutahtione & Some Clinical Applications Of Raising Glutathione Levels. National Library of Medicine/National Institutes of Health database. 2013. https://www.slideshare.net/Dapoalimi/clinical-applications-of-raising-glutathione-levels?from_action=save
  • 48.Sekhar RV, Patel SG, Guthikonda AP, et al. Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation. Am J Clin Nutr. 2011;94(3):847-853. doi:10.3945/ajcn.110.003483 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 49.Julius M, Lang CA, Gleiberman L, Harburg E, DiFranceisco W, Schork A. Glutathione and morbidity in a community-based sample of elderly. J Clin Epidemiol. 1994;47(9):1021-1026. doi:10.1016/0895-4356(94)90117-1 [DOI] [PubMed] [Google Scholar]
  • 50.Sekhar RV. GlyNAC Supplementation Improves Glutathione Deficiency, Oxidative Stress, Mitochondrial Dysfunction, Inflammation, Aging Hallmarks, Metabolic Defects, Muscle Strength, Cognitive Decline, and Body Composition: Implications for Healthy Aging. J Nutr. 2021;151(12):3606-3616. doi:10.1093/jn/nxab309 [DOI] [PubMed] [Google Scholar]
  • 51.Singh RJ. Glutathione: A marker and antioxidant for aging. doi:10.1067/mlc.2002.129505 [DOI] [PubMed] [Google Scholar]

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