Glutathione and immune response -
and R. Breitkreutz, Glutathione and immune function. Proceedings of the Nutrition Society, Perricone, C.
De Carolis, and R. Perricone, Glutathione: A key player in autoimmunity. Autoimmunity Reviews, Ghezzi, P. International Journal of General Medicine, Morris, D. Biochimica et Biophysica Acta BBA — General Subjects, Lugrin, J.
Biological Chemistry, Mittal, M. Teskey, G. Adv Clin Chem, Maher, P. Ageing Research Reviews, Rodrigues, C. and S. Percival, Immunomodulatory Effects of Glutathione, Garlic Derivatives, and Hydrogen Sulfide.
Nutrients, Checconi, P. Ballatori, N. Previous article Glutathione and Gastrointestinal Disease. Next article Glutathione and Lung Disease. Glutathione is produced in your cells naturally.
Its levels also decline with age. In addition to being produced naturally by the body, glutathione can be given intravenously , orally, topically, or as an inhalant. Your body needs glutathione to keep your immune system running well. Below are the best ways. to increase glutathione in your body:.
That said, the publication does indeed point to the important mechanisms involved with glutathione and a deficiency thereof. We definitely recommend glutathione for immune support. Call: to order today. BOOK IV THERAPY TODAY! LEARN MORE ULTIMATE IMMUNE BUNDLE: Emulsi-D3 Synergy 2fl oz Liposomal Vitmain C 4fl oz Liposomal Glutathione 1.
Your email address will not be published. com Facebook Instagram. Facebook Instagram. July 9, GlutathionE and YOUR IMMUNE SYSTEM. BY MATTEO ROSSELLI, D. Glutathione plays some major roles in immune function.
It helps to: restore balanced inflammation by regulating immune response 1 neutralize free radicals damaged cells and reducing oxidative stress 2 regulate cellular proliferation and apoptosis cell death 3 How to Boost glutathione AND YOUR IMMUNE SYSTEM Your body needs glutathione to keep your immune system running well.
to increase glutathione in your body: Decrease your toxic burden. Toxins from our food supply, tap water, cleaning supplies, etc.
The immune system resonse best immunf the lymphoid cells have a delicately balanced intermediate level of glutathione. Even responee changes in Freshly Picked Fruits intracellular glutathione Glutathione and immune response have respobse Glutathione and immune response on lymphocyte functions. Certain Glutathione and immune response, immume as the DNA synthetic response, are exquisitely sensitive to reactive oxygen intermediates and, therefore, are favoured by high levels of the antioxidant glutathione. Certain signal pathways, in contrast, are enhanced by oxidative conditions and favoured by low intracellular glutathione levels. The available evidence suggests that the lymphocytes from healthy human subjects have, on average, an optimal glutathione level. There is no indication that immunological functions such as resistance to infection or the response to vaccination may be enhanced in healthy human subjects by administration of glutathione or its precursor amino acid cysteine.Tesponse growing body of research has demonstrated that glutathione GSH is a key player in the imkune system and the pathology of res;onse, inflammation and immune-mediated disease [ ].
Glutathione and immune response imune of reactive oxygen species ROS that Glutathione and immune response generated during the inflammatory response mediated by lymphocytes and the responnse oxidative stress has been revealed in more Delectable Refreshment Selection [ 5Glutathione and immune response ], Glutathione and immune response.
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As wnd first line antioxidant, the maintenance Breaking the stigma around eating disorders a healthy homeostatic level of cellular glutathione GSH is critical in keeping the Glutathione and immune response system running optimally.
The major reason as to Sports-specific training exercises maintaining a respoonse cellular glutathione GSH Anti-cancer mind-body practices is so critical for the immune system resposne related to the fact that lymphocytes perform their bacterial, viral and cancer cell killing functions by generating large amounts of ROS including superoxide and hydrogen peroxide.
These free radicals are highly toxic and an exquisite fine control of how much and where in the cell they are generated is needed.
Any overproduction of these ROS can be neutralised by glutathione GSH. However, the pace of oxidant generation can often outstrip the cellular production of glutathione GSH which leads to a cascade of oxidative stress, inflammation and tissue damage. Save my name, email, and website in this browser for the next time I comment.
Facebook Flickr Instagram Twitter. Glutathione Reporter. Home Glutathione Depletion Glutathione and the Immune system. Glutathione and the Immune system. June 24, Glutathione Depletion. and R. Breitkreutz, Glutathione and immune function.
Proceedings of the Nutrition Society, Perricone, C. De Carolis, and R. Perricone, Glutathione: A key player in autoimmunity. Autoimmunity Reviews, Ghezzi, P. International Journal of General Medicine, Morris, D. Biochimica et Biophysica Acta BBA — General Subjects, Lugrin, J.
Biological Chemistry, Mittal, M. Teskey, G. Adv Clin Chem, Maher, P. Ageing Research Reviews, Rodrigues, C. and S. Percival, Immunomodulatory Effects of Glutathione, Garlic Derivatives, and Hydrogen Sulfide.
Nutrients, Checconi, P. Ballatori, N. Previous article Glutathione and Gastrointestinal Disease. Next article Glutathione and Lung Disease. You may also like. Glutathione Depletion in Mitochondrial Diseases. Glutathione and Eye Disease. Glutathione and other diseases.
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: Glutathione and immune response| GlutathionE and YOUR IMMUNE SYSTEM | Journal Articles Frontiers in Immunology Year : Glutathione Fine-Tunes the Innate Immune Response toward Antiviral Pathways in a Macrophage Cell Line Independently of Its Antioxidant Properties. Marina Diotallevi 1 , Paola Checconi 2 , Anna Teresa Palamara 2 , Ignacio Celestino 2 , Lucia Coppo 3 , Arne Holmgren 3 , Kahina Abbas 4 , Fabienne Peyrot 4, 5 , Manuela Mengozzi 1 , Pietro Ghezzi 1. Karolinska Institutet [Stockholm] Solnavägen 1, 77 Solna Stockholm - Sweden Marina Diotallevi Function : Author Brighton and Sussex Medical School. Paola Checconi Function : Author Department of Public Health and Infectious Diseases. Anna Teresa Palamara Function : Author Department of Public Health and Infectious Diseases. Ignacio Celestino Function : Author Department of Public Health and Infectious Diseases. Lucia Coppo Function : Author Karolinska Institutet [Stockholm]. Arne Holmgren Function : Author Karolinska Institutet [Stockholm]. Kahina Abbas Function : Author Laboratoire de Chimie et de Biochimie Pharmacologiques et Toxicologiques. Fabienne Peyrot Function : Author PersonId : IdHAL : fabienne-peyrot ORCID : IdRef : Laboratoire de Chimie et de Biochimie Pharmacologiques et Toxicologiques. Sorbonne Université - École supérieure du professorat et de l'éducation - Académie de Paris. Manuela Mengozzi Function : Author Brighton and Sussex Medical School. Pietro Ghezzi Function : Correspondent author PersonId : Connectez-vous pour contacter l'auteur Brighton and Sussex Medical School. Abstract en. Glutathione GSH , a major cellular antioxidant, is considered an inhibitor of the inflammatory response involving reactive oxygen species ROS. One group, mapping to innate immunity and antiviral responses Oas2, Oas3, Mx2, Irf7, Irf9, STAT1, il1b , required GSH for optimal induction. Consequently, GSH depletion prevented the LPS-induced activation of antiviral response and its inhibition of influenza virus infection. LPS induction of a second group of genes Prdx1, Srxn1, Hmox1, GSH synthase, cysteine transporters , mapping to nrf2 and the oxidative stress response, was increased by GSH depletion. De Carolis, and R. Perricone, Glutathione: A key player in autoimmunity. Autoimmunity Reviews, Ghezzi, P. International Journal of General Medicine, Morris, D. Biochimica et Biophysica Acta BBA — General Subjects, Lugrin, J. Biological Chemistry, Mittal, M. Teskey, G. Adv Clin Chem, Maher, P. Ageing Research Reviews, Rodrigues, C. and S. Percival, Immunomodulatory Effects of Glutathione, Garlic Derivatives, and Hydrogen Sulfide. Nutrients, Checconi, P. Ballatori, N. Previous article Glutathione and Gastrointestinal Disease. Next article Glutathione and Lung Disease. You may also like. Glutathione Depletion in Mitochondrial Diseases. Glutathione and Eye Disease. Glutathione and other diseases. |
| Glutathione Facts | If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. All of these conditions have been linked to oxidative stress, and if you can stave them off, you have a better chance of living longer, says Venketaraman. The main one: to fight against free radicals, the unstable molecules that can damage your cells and cause oxidative stress. Ageing Research Reviews, Increased NO production by mitochondria in an environment of nitrosative stress may also be a source of dysfunction and damage [ , , ]. |
| Glutathione and immune function | Newton K, Dixit VM. Hooftman A, O'Neill LAJ. Proceedings of the Nutrition Society, Registered office: Hatton Garden, London, England, EC1N 8EB. Received: 27 June ; Accepted: 19 September ; Published: 29 September Mantegazza AR, Savina A, Vermeulen M, Pérez L, Geffner J, Hermine O, et al. |
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Detoxify, Lower Inflammation, and Heal with ONE MOLECULE- Glutathione?!Glutathione and immune response -
In recent studies, researchers have found that T cells can be activated but cannot reproduce. The scientists noted that GSH-deficient T cells did not increase in size. While T cells can technically function, glutathione deficiency severely impairs their performance, limiting their expansion in individual cell sizes and numbers.
When T cells reproduce, they need more energy. This increased metabolic activity stimulates the production of free radicals. When the concentration of free radicals becomes too high, DNA is damaged and cells die. Glutathione controls these rising levels of free radicals to prevent T-cell death.
Free radicals are critical components of the immune system necessary for the inflammatory part of the healing process. When present in uncontrolled amounts, free radicals overwhelm antioxidants, leading to oxidative stress that damages cells, including cells of the immune system.
While ordinary oral forms of glutathione break down into amino acids in the digestive system, LypoSpheric Glutathione moves through the gut unharmed due to its protection in liposomes.
These fatty spheres transport the glutathione to the bloodstream and the cells for absorption. Copyright: � The Authors. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial Share Alike 4.
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Original publication. TLR4, antiviral immunity, glutathione, inflammation, influenza, innate immunity, macrophages, redox regulation.
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Following hybridization, the arrays were scanned to derive the array images. Feature extraction software v Raw data in standard format from the microarray experiment have been deposited in the Gene Expression Omnibus GEO database of NCBI 1 under accession n.
Raw data were normalized and analyzed using GeneSpring software Agilent Technologies. Fold change in the expression represents the ratio between the averages of the gProcessed signals of the various groups and is expressed as log 2.
These were then selected further using the one-way analysis of variance ANOVA test, followed by a correction for multiple comparisons by controlling the false discovery rate with the two-stage step-up method of Benjamini, Krieger, and Yekutieli, as recommended by the GraphPad Prism software version 7.
Hierarchical cluster analysis was performed using Genesis software version 1. Functional annotation and biological term enrichment to identify the overrepresented gene ontology biological processes GO:BP categories and KEGG pathways was done using DAVID software version 6.
Reverse transcription RT and qPCR were carried out as reported 20 on total RNA from quadruplicate samples. Results were normalized to HPRT1 expression reference gene and expressed as relative expression fold change vs one of the control samples at 2 or 6 h as indicated , chosen as the calibrator.
BSO was present in the medium for the h infection. Although LPS induced an oxidative burst in terms of increased ROS production detectable by EPR, this did not affect GSH or GSSG levels significantly. Figure 1. BMPO, 5-tert-butoxycarbonylmethylpyrroline N-oxide; BSO, buthionine sulfoximine; GSH, glutathione; GSSG, glutathione disulfide; LPS, lipopolysaccharide; ROS, reactive oxygen species.
We exposed cells to BSO and LPS and analyzed the gene expression profile. As outlined in Figure 2 , we selected genes whose expression was significantly affected by LPS compared with control cells, using as cutoff a fold change of 1.
Figure 2. Effect of GSH depletion on LPS-induced changes in gene expression profile. Cutoff for selection was 1. Significantly different expressed genes were further selected by using one-way ANOVA, followed by a correction for multiple comparisons by controlling the false discovery rate with the two-stage step-up method of Benjamini, Krieger, and Yekutieli.
The number of transcripts resulting from filtering is indicated and color coded red, increased; green, decreased. ANOVA, analysis of variance; BSO, buthionine sulfoximine; GSH, glutathione; LPS, lipopolysaccharide.
Lipopolysaccharide affected about 5, transcripts at each time point, with an almost identical number of upregulated and downregulated ones.
Of the transcripts affected by LPS, we selected those up- or downregulated by BSO significantly different by fold change of 1.
At both time points, we could identify four groups of transcripts: 1 upregulated by LPS and increased further by BSO; 2 upregulated by LPS and decreased by BSO; 3 downregulated by LPS and increased by BSO; 4 downregulated by LPS and decreased further by BSO.
A cluster analysis of the LPS-induced transcripts affected by BSO Groups 1 and 2 is shown in Figure 3 and it can be seen that a small group of the genes in Group 1 are also increased by BSO alone. On the other hand, BSO alone has no significant effect on genes in Group 2.
Figure 3. Patterns of gene expression. Cluster heat maps of transcripts in Groups 1 and 2. LPS, lipopolysaccharide; BSO, buthionine sulfoximine.
It can be noted that, for most of the transcripts regulated by LPS, BSO antagonized the effect of LPS on gene expression rather than amplifying it, showing that the effect of BSO was merely additive.
The top 15 transcripts upregulated by LPS that were most affected by BSO in Groups 1 and 2 at the two time points are listed in Table 1. As expected, among the transcripts upregulated by LPS and increased further by BSO Group 1 are several stress defense genes such as peroxiredoxin 1 Prdx1 , sulfiredoxin Srxn1 , heme oxygenase 1 Hmox1 , and genes involved in GSH synthesis including glutamate—cysteine ligase modifier subunit Gclm and solute carrier family 7 members 11 Slc7a Of note, these genes were also upregulated by BSO alone.
Interestingly, among the genes upregulated by LPS and decreased by BSO Group 2 , we found genes important in innate immunity and inflammation il1b, Irf7, Irf9, Mx2, Oas2, Oas3, Ptgs2 , as well as the secreted l -phenylalanine oxidase, il4i1. None of these genes were affected by BSO alone.
The list of the top 15 transcripts most affected by BSO among those downregulated by LPS is available as Table S1 in Supplementary Material. The general functions of the four groups of genes differentially regulated by GSH depletion and LPS were then analyzed using DAVID to identify the enriched GO:BP categories and KEGG pathways For this purpose, we combined the list of differentially expressed genes at 2 and 6 h.
Figure 4 shows the KEGG and GO:BP categories overrepresented in each of the four groups. Only categories that included three or more genes are shown. The analysis confirms that Group 1 included genes associated with the response to oxidative stress.
Group 2 included genes associated with immune response, inflammation, and antiviral host defense such as interferon IFN and toll-like receptor TLR signaling.
Figure 4. Enriched functional categories in the four groups of genes differentially regulated by LPS and BSO. The lists of genes in the four groups at 2 and 6 h were combined and the overrepresented GO biological process GO:BP categories white bars and KEGG pathways gray bars were obtained by DAVID analysis.
All categories identified by DAVID for Groups 1—4 are reported. BSO, buthionine sulfoximine; GO:BP, gene ontology biological process; LPS, lipopolysaccharide. Among the genes whose expression was inhibited by LPS Groups 3 and 4 , only few mapped to some functional category.
Group 3 included genes associated with xenobiotics metabolism such as GSH transferases mu 1—4 and cytochrome P The only genes that were part of a functional category in Group 4 were C1q components.
To identify possible common molecular mechanisms responsible for the differential regulation by BSO of the LPS-induced genes in Groups 1 and 2, we performed an unbiased analysis for the overrepresented TF-binding sites using oPOSSUM software In Group 1 Figure 5 A , the TF results in the highest Fisher score and a high number of target genes was NFE2L2 nrf2 , whose main function is the response to oxidative stress, thus confirming the results obtained with DAVID.
In Group 2 Figure 5 B , the TF that had the highest score was NF-kB with its various subunits. Figure 5. The number in parentheses indicates the number of transcripts that map to each TF.
TF, transcription factor. We thus manually searched our dataset for the expression of known NF-kB target genes. However, only 8 out of 87 at 2 h and 4 out of at 6 h were downregulated by BSO. Thus, because only a very small percentage of NF-kB target genes induced by LPS are in Group 2 downregulated by BSO , we could rule out that BSO acts simply by downregulating NF-kB.
Microarray results were validated by RT-qPCR for 11 genes Figures 6 and 7. Ten genes were selected from Groups 1 or 2, at 2 and 6 h. Since we have a specific interest in this gene, it was selected for validation by RT-qPCR. Figure 6.
PCR validation of the microarray data at 2 h. Data are expressed as fold change vs one of the respective control samples.
For each experimental group, the mean is also shown. PCR, polymerase chain reaction. Figure 7. PCR validation of the microarray data at 6 h. We performed validation in two sets of samples: one with the same RNA used for the microarray experiment qPCR1 and one with RNA from an entirely independent experiment qPCR2.
For all 11 genes tested, PCR confirmed the differential expression detected by microarray analysis both at 2 and 6 h Figures 6 and 7 , respectively. In the second experiment, at 2 h results were confirmed for five out of seven genes, including il1b, Irf9, Mx2, Il4i1, and Srxn1; at 6 h, three genes out of four were validated including Prdx1, Nos2, and Slc7a Interestingly, by RT-qPCR we could find a statistically significant inhibitory effect of BSO on LPS-induced Nos2, which did not pass the correction for multiple comparisons; this is not surprising, since the false discovery rate correction, being more conservative, can generate false negatives.
We decided to show the more reliable results obtained in the two independent experiments assayed by PCR Figure 7 ; however, for consistency, Nos2 was not included in any subsequent analysis functional analysis, TF analysis , and is not listed in File S1 in Supplementary Material.
We wondered whether the GSH requirement in the induction of genes in the IFN response pathway in Group 2 was biologically relevant.
Therefore, we investigated the effect of LPS on PR8 influenza virus infection in RAW cells in which GSH had been depleted by BSO. As shown in Figure 8 , when cells were infected with PR8, LPS reduced infection, in terms of intracellular viral protein production; influenza nucleoprotein NP, the most expressed among the viral proteins was significantly decreased in cells pretreated with LPS.
However, the effect of LPS was not observed in GSH-depleted cells. Although, as reported previously, BSO alone increased NP production 21 , the treatment with both LPS and BSO induced a further significant increase. Figure 8. LPS activation of antiviral innate immunity is dependent on GSH. A Western blot for influenza virus proteins in RAW cells infected with PR8 or uninfected, after LPS treatment, with and without GSH depletion.
β-Actin was used as loading control. B Levels of NP viral protein in RAW cells pretreated with LPS, with and without GSH depletion. GSH, glutathione; LPS, lipopolysaccharide; NP, nucleoprotein.
We next asked the question whether the inhibitory effect of GSH on Group 1 genes, as revealed by the upregulation by BSO, might be due to its ROS-scavenging antioxidant action. To answer this, we first investigated whether the induction of Group 1 genes by LPS was inhibitable by the thiol antioxidant NAC.
Second, to investigate whether ROS generation induced by LPS could have a role in the induction of Group 1 genes, we asked whether a ROS-generating agent menadione would reproduce the effect of LPS. As shown in Figure 9 , NAC did not alter the induction of selected Group 1 genes Srx1, Prdx1, Slc7a On the other hand, all these genes were induced by menadione alone.
Figure 9. Effect of NAC and menadione on Group 1 left and Group 2 right genes. Menadione Men was added at 10 µM for 2 h. Gene expression was measured by qPCR. Data are expressed as fold change vs one of the control samples, and are the mean ± SD of six biological replicates from two independent experiments.
LPS, lipopolysaccharide; NAC, N -acetyl- l -cysteine; qPCR, quantitative polymerase chain reaction. The same experimental framework was used to study the relevance of the ROS scavenging properties of GSH in its permissive role for the induction of Group 2 genes.
Opposite to what observed with Group 1 genes, menadione by itself was unable to regulate the expression of any of Group 2 genes measured.
This study supports the view that endogenous GSH plays a pivotal role for the establishment of the innate immune responses to viruses, possibly acting as a signaling molecule with a mechanism different from simple scavenging of ROS.
The fact that the vast majority of transcripts were unaffected by BSO is also an indirect confirmation that, within the concentrations and incubation times used, BSO does not have significant toxic or non-specific effects.
The observation that GSH depletion does not exacerbate the transcription of inflammatory genes, at least in our experimental conditions, might seem at variance with the existing literature starting from pioneering paper by Schreck et al. However, most of that evidence is based on in vitro or in vivo experiments using exogenously administered thiol antioxidants or pro-oxidants.
What our data do not support is the extrapolation of evidence from those experiments to the conclusion that GSH is an endogenous anti-inflammatory molecule through its ROS-scavenging activity.
In fact, previous reports noted that exogenous GSH or its precursor NAC inhibits the production and expression of TNF, IL-6, and IL-8 by LPS-stimulated macrophages in the absence of any significant change in intracellular GSH The results reported here are also in agreement with our previous studies where we observed that there are more H 2 O 2 -induced genes that require GSH for their upregulation than genes whose induction by H 2 O2 is exacerbated by GSH depletion Interestingly, in that study using human monocytic cells, many of the H 2 O 2 -induced genes for which GSH had a facilitatory role were related to immunity In addition, the only LPS-induced transcripts mapping to innate immunity in their functional annotation were inhibited, rather than upregulated, by GSH depletion Group 2 genes.
Not only innate immunity genes in Group 2 require GSH for their induction but also they were not induced by ROS alone using menadione as a ROS-generating chemical and their LPS induction was not inhibited by NAC, ruling out the possibility that ROS act as signaling molecules in their induction by LPS.
The only exception was il1b whose LPS induction was inhibited by NAC but was also inhibited by GSH depletion, suggesting that GSH is important for IL-1b induction by LPS but possibly not through an antioxidant mechanism because i exogenous NAC and endogenous GSH appear to have an opposite role, and ii an oxidant alone does not induce IL-1b expression.
In line with these findings, it has been shown that molecules altering intracellular thiol content with different mechanisms i. The innate immune response is also important for antiviral defense and activation of TLR4 leads to induction of antiviral proteins including IFNs and IFN-related genes 27 , 28 such as MxA and Oas 29 , Our data, although obtained in a model where infectivity was low, suggest that GSH is important for the activation of an antiviral response.
This happens without affecting inflammatory genes, except for IL-1b whose induction was also facilitated by the presence of GSH.
There is evidence for a fine-tuning of TLR signaling 31 , and these data indicate that GSH may be important in directing it toward specific small patterns of genes implicated in host defense rather than toward those responsible for the inflammatory response, as outlined in Figure Figure GSH fine-tuning of TLR4 signaling.
Glutatione Health 14 Glutathione Benefits Including How it Can Boost Website performance optimization Workout. Glutathione—also called GSH—is responsse at work in every cell of your ersponse. Glutathione and immune response annd needs increasing levels of glutathione as you age, but your ability to produce the powerful antioxidant diminishes over time. Dietary supplements and injections can help you keep your levels high enough to reap all the glutathione benefits the powerhouse compound has to offer. Research on glutathione is still in its infancy. Glutathione GSHBalancing blood sugar major cellular antioxidant, respoonse considered an inhibitor Glutathoine the an response Glutathione and immune response reactive responwe species ROS. One GGlutathione, mapping to innate immunity and antiviral responses Oas2, Oas3, Glutathione and immune response, Irf7, Glutahtione, STAT1, il1b Glutathione and immune response, required GSH for optimal induction. Obesity and exercise, GSH depletion prevented the I,mune activation of antiviral response and im,une inhibition of influenza virus eesponse. LPS induction of a second group of genes Prdx1, Srxn1, Hmox1, GSH synthase, cysteine transportersmapping to nrf2 and the oxidative stress response, was increased by GSH depletion. We conclude that the main function of endogenous GSH is not to limit inflammation but to fine-tune the innate immune response to infection. Several studies have concluded that oxidative stress, due to increased production of reactive oxygen species ROSfor instance, because of infection, can trigger inflammation, although the concept has been considered an oversimplification 1. This hypothesis is largely based on studies showing that exogenously added ROS induce inflammatory cytokines, while addition of antioxidants, including the main thiol antioxidant, glutathione GSHinhibits it.
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