uglevod
Senior Member
- Messages
- 220
Probably we are all chronically(sublinically) septic:
Fluctuation of serum vitamin E (α-tocopherol) concentrations during exacerbation and remission phases in patients with chronic fatigue syndrome
https://link.springer.com/article/10.1007/s00380-009-1206-6
The etiology of chronic fatigue syndrome remains unknown. Oxidative stress may be involved in its pathogenesis. Vitamin E is a major endogenous lipid-soluble antioxidative substance, and is consumed during the lipid peroxidation process. We studied a population comprising 27 patients with chronic fatigue syndrome (10 men and 17 women, 29 ± 6 years of age) and 27 age- and sex-matched control subjects. Serum vitamin E (α-tocopherol) concentrations were determined and expressed as mg/g total lipids (total cholesterol and triglyceride) to evaluate oxidative stress. Serum α-tocopherol concentrations (mg/g lipids) were significantly (P < 0.001) lower in the patients with chronic fatigue syndrome (2.81 ± 0.73) than in the control subjects (3.88 ± 0.65). The patients with chronic fatigue syndrome were re-examined during a follow-up interval. After 8 ± 2 months, 16 patients exhibited a status that warranted re-examination during remission of the symptoms at a regular visit to our hospital (Group 1), while the remaining 11 did not (Group 2). The serum α-tocopherol levels were significantly elevated during remission as compared with those at baseline in Group 1 (2.71 ± 0.62 → 3.24 ± 0.83, P < 0.001). The levels did not significantly change after the interval in Group 2 (2.97 ± 0.86 → 2.85 ± 0.73, not significant). In conclusion, serum α-tocopherol concentrations were significantly lower in the patients with chronic fatigue syndrome as compared with the control subjects, suggesting increased oxidative stress in the former. The low level of serum α-tocopherol was ameliorated during the remission phase as compared with the exacerbation phase in the patients with chronic fatigue syndrome, suggesting that increased oxidative stress may be involved in the pathogenesis of chronic fatigue syndrome and might also be directly related to the severity of the symptoms of chronic fatigue syndrome.
The Role of Vitamin E in Immunity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6266234/
Antioxidants attenuate endotoxin-induced activation of alveolar macrophages
https://www.surgjournal.com/article/S0039-6060(05)80353-8/pdf
Background. Endotoxin (lipopolysaccharide [LPS]) stimulation of tissue-fixed macrophages induces the generation of toxic oxidants. However, recent studies also implicate redox changes in both the signal transduction pathways for cytokine genes and the generation of physiologically active arachidonic acid metabolites. Because cytokines and arachidonic acid metabolites initiate and perpetuate deleterious systemic inflammatory reponses, we tested whether macrophage activation could be modulated by antioxidants.
Methods. Rabbit alveolar macrophages were obtained by bronchoalveolar lavage, isolated, treated with the antioxidants vitamin E or N-acetylcysteine (NAC), and stimulated with an optimal dose of LPS (10 ng/ml). Assays were performed for tumor necrosis factor (TNF), procoagulant activity, and prostaglandin E2. Total cellular RNA was extracted for Northern blot analysis of TNF messenger RNA.
Results. Exposure of the macrophage to the antioxidants vitamin E and NAC inhibited TNF production, accumulation of TNF messenger RNA, procoagulant activity expression, and prostaglandin E2 production.
Conclusions. Macrophage signal transduction of LPS is dependent on the generation of reactive oxygen intermediates that can be blocked both at the level of the lipid membrane (vitamin E) and at the intracellular level (NAC).
This suggests a potential therapeutic role for antioxidants in disease states such as adult respiratory distress syndrome and multiple organ failure syndrome, which are characterized by excessive macrophage activation.
https://ods.od.nih.gov/factsheets/VitaminE-HealthProfessional/
Numerous foods provide vitamin E. Nuts, seeds, and vegetable oils are among the best sources of alpha-tocopherol, and significant amounts are available in green leafy vegetables and fortified cereals (see Table 2 for a more detailed list). Most vitamin E in American diets is in the form of gamma-tocopherol from soybean, canola, corn, and other vegetable oils and food products.
Vitamin E (α- and γ-Tocopherol) Levels in the Community: Distribution, Clinical and Biochemical Correlates, and Association with Dietary Patterns
https://www.mdpi.com/2072-6643/10/1/3/htm
the half-life of α-tocopherol in plasma is 48h, and the ingested α-tocopherol appears in plasma within 2–4h and peaks in 5–14h
Attenuation of lipopolysaccharide (LPS)-induced cytotoxicity by tocopherols and tocotrienols
https://pubmed.ncbi.nlm.nih.gov/24024142/
Protective effect of vitamin E in an animal model of LPS-induced inflammation
https://pubmed.ncbi.nlm.nih.gov/15663600/
The association between vitamin E deficiency and critically ill children with sepsis and septic shock
https://ma.x-mol.com/paper/1395481143459430400
Background: Literature is scarce on the assessment of vitamin E status in septic children. We aim to investigate the prevalence of vitamin E deficiency in critically ill children with sepsis and septic shock and its association with clinical features and outcomes. Methods: We compared serum vitamin E status between the confirmed or suspected infection and no infection groups, the sepsis shock and no sepsis shock groups upon pediatric intensive care unit admission. Clinical characteristics were compared in subgroup patients with and without vitamin E deficiency. The association between vitamin E deficiency and septic shock were evaluated using univariate and multivariable methods. Results: 182 critically ill children with confirmed or suspected infection and 114 without infection were enrolled. The incidence of vitamin E deficiency was 30.2% in the infection group and 61.9% in the septic shock subgroup (P < 0.001). 30-days mortality in critically ill children with vitamin E deficiency was significantly higher than that without vitamin E deficiency (27.3%, vs. 14.2%, P < 0.05). Vitamin E levels were inversely associated with higher pediatric risk of mortality (r = − 0.238, P = 0.001) and cardiovascular sequential organ failure assessment (r= -0.249, p<0.001) scores in critically ill children with infection. In multivariable logistic regression, vitamin E deficiency showed an independent effect on septic shock (adjusted OR：6.749, 95%CI: 2.449-18.60, P<0.001). Conclusion: Vitamin E deficiency is highly prevalent in critically ill children with sepsis and contributed to the septic shock.
Usefulness of Antioxidants as Adjuvant Therapy for Septic Shock: A Randomized Clinical Trial
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698534/
Western diet regulates immune status and the response to LPS-driven sepsis independent of diet-associated microbiome
https://www.pnas.org/content/116/9/3688
The Western diet (WD) is high in fats and sucrose and low in fiber and is the most prevalent diet in westernized countries. We find that in our model of sepsis, mice fed WD had increased sepsis severity and poorer outcomes. WD-fed mice had higher baseline inflammation, increased sepsis-associated immunoparalysis, and altered neutrophil populations in the blood. The WD-dependent increase in sepsis severity and mortality was independent of the diet-associated microbiome, suggesting that diet may be directly regulating innate immunity. We used our identified disease factors and found WD-fed mice occupy a unique path in sepsis disease progression. Our data provide insight into diet-dependent reprogramming of the immune response and will be important in treating and diagnosing a WD-fed population.
...
Before LPS treatment, healthy mice fed WD had an increased frequency of monocytes and neutrophils in the blood compared with SC[standard fiber-rich chow] mice. However, WD-fed mice exhibited increased neutrophil populations and decreased activated monocytes in the blood during sepsis compared with SC mice.
Chronic muscle weakness and mitochondrial dysfunction in the absence of sustained atrophy in a preclinical sepsis model
https://elifesciences.org/articles/49920
Fluctuation of serum vitamin E (α-tocopherol) concentrations during exacerbation and remission phases in patients with chronic fatigue syndrome
https://link.springer.com/article/10.1007/s00380-009-1206-6
The etiology of chronic fatigue syndrome remains unknown. Oxidative stress may be involved in its pathogenesis. Vitamin E is a major endogenous lipid-soluble antioxidative substance, and is consumed during the lipid peroxidation process. We studied a population comprising 27 patients with chronic fatigue syndrome (10 men and 17 women, 29 ± 6 years of age) and 27 age- and sex-matched control subjects. Serum vitamin E (α-tocopherol) concentrations were determined and expressed as mg/g total lipids (total cholesterol and triglyceride) to evaluate oxidative stress. Serum α-tocopherol concentrations (mg/g lipids) were significantly (P < 0.001) lower in the patients with chronic fatigue syndrome (2.81 ± 0.73) than in the control subjects (3.88 ± 0.65). The patients with chronic fatigue syndrome were re-examined during a follow-up interval. After 8 ± 2 months, 16 patients exhibited a status that warranted re-examination during remission of the symptoms at a regular visit to our hospital (Group 1), while the remaining 11 did not (Group 2). The serum α-tocopherol levels were significantly elevated during remission as compared with those at baseline in Group 1 (2.71 ± 0.62 → 3.24 ± 0.83, P < 0.001). The levels did not significantly change after the interval in Group 2 (2.97 ± 0.86 → 2.85 ± 0.73, not significant). In conclusion, serum α-tocopherol concentrations were significantly lower in the patients with chronic fatigue syndrome as compared with the control subjects, suggesting increased oxidative stress in the former. The low level of serum α-tocopherol was ameliorated during the remission phase as compared with the exacerbation phase in the patients with chronic fatigue syndrome, suggesting that increased oxidative stress may be involved in the pathogenesis of chronic fatigue syndrome and might also be directly related to the severity of the symptoms of chronic fatigue syndrome.
The Role of Vitamin E in Immunity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6266234/
Antioxidants attenuate endotoxin-induced activation of alveolar macrophages
https://www.surgjournal.com/article/S0039-6060(05)80353-8/pdf
Background. Endotoxin (lipopolysaccharide [LPS]) stimulation of tissue-fixed macrophages induces the generation of toxic oxidants. However, recent studies also implicate redox changes in both the signal transduction pathways for cytokine genes and the generation of physiologically active arachidonic acid metabolites. Because cytokines and arachidonic acid metabolites initiate and perpetuate deleterious systemic inflammatory reponses, we tested whether macrophage activation could be modulated by antioxidants.
Methods. Rabbit alveolar macrophages were obtained by bronchoalveolar lavage, isolated, treated with the antioxidants vitamin E or N-acetylcysteine (NAC), and stimulated with an optimal dose of LPS (10 ng/ml). Assays were performed for tumor necrosis factor (TNF), procoagulant activity, and prostaglandin E2. Total cellular RNA was extracted for Northern blot analysis of TNF messenger RNA.
Results. Exposure of the macrophage to the antioxidants vitamin E and NAC inhibited TNF production, accumulation of TNF messenger RNA, procoagulant activity expression, and prostaglandin E2 production.
Conclusions. Macrophage signal transduction of LPS is dependent on the generation of reactive oxygen intermediates that can be blocked both at the level of the lipid membrane (vitamin E) and at the intracellular level (NAC).
This suggests a potential therapeutic role for antioxidants in disease states such as adult respiratory distress syndrome and multiple organ failure syndrome, which are characterized by excessive macrophage activation.
https://ods.od.nih.gov/factsheets/VitaminE-HealthProfessional/
Numerous foods provide vitamin E. Nuts, seeds, and vegetable oils are among the best sources of alpha-tocopherol, and significant amounts are available in green leafy vegetables and fortified cereals (see Table 2 for a more detailed list). Most vitamin E in American diets is in the form of gamma-tocopherol from soybean, canola, corn, and other vegetable oils and food products.
Vitamin E (α- and γ-Tocopherol) Levels in the Community: Distribution, Clinical and Biochemical Correlates, and Association with Dietary Patterns
https://www.mdpi.com/2072-6643/10/1/3/htm
the half-life of α-tocopherol in plasma is 48h, and the ingested α-tocopherol appears in plasma within 2–4h and peaks in 5–14h
Attenuation of lipopolysaccharide (LPS)-induced cytotoxicity by tocopherols and tocotrienols
https://pubmed.ncbi.nlm.nih.gov/24024142/
Protective effect of vitamin E in an animal model of LPS-induced inflammation
https://pubmed.ncbi.nlm.nih.gov/15663600/
The association between vitamin E deficiency and critically ill children with sepsis and septic shock
https://ma.x-mol.com/paper/1395481143459430400
Background: Literature is scarce on the assessment of vitamin E status in septic children. We aim to investigate the prevalence of vitamin E deficiency in critically ill children with sepsis and septic shock and its association with clinical features and outcomes. Methods: We compared serum vitamin E status between the confirmed or suspected infection and no infection groups, the sepsis shock and no sepsis shock groups upon pediatric intensive care unit admission. Clinical characteristics were compared in subgroup patients with and without vitamin E deficiency. The association between vitamin E deficiency and septic shock were evaluated using univariate and multivariable methods. Results: 182 critically ill children with confirmed or suspected infection and 114 without infection were enrolled. The incidence of vitamin E deficiency was 30.2% in the infection group and 61.9% in the septic shock subgroup (P < 0.001). 30-days mortality in critically ill children with vitamin E deficiency was significantly higher than that without vitamin E deficiency (27.3%, vs. 14.2%, P < 0.05). Vitamin E levels were inversely associated with higher pediatric risk of mortality (r = − 0.238, P = 0.001) and cardiovascular sequential organ failure assessment (r= -0.249, p<0.001) scores in critically ill children with infection. In multivariable logistic regression, vitamin E deficiency showed an independent effect on septic shock (adjusted OR：6.749, 95%CI: 2.449-18.60, P<0.001). Conclusion: Vitamin E deficiency is highly prevalent in critically ill children with sepsis and contributed to the septic shock.
Usefulness of Antioxidants as Adjuvant Therapy for Septic Shock: A Randomized Clinical Trial
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698534/
Western diet regulates immune status and the response to LPS-driven sepsis independent of diet-associated microbiome
https://www.pnas.org/content/116/9/3688
The Western diet (WD) is high in fats and sucrose and low in fiber and is the most prevalent diet in westernized countries. We find that in our model of sepsis, mice fed WD had increased sepsis severity and poorer outcomes. WD-fed mice had higher baseline inflammation, increased sepsis-associated immunoparalysis, and altered neutrophil populations in the blood. The WD-dependent increase in sepsis severity and mortality was independent of the diet-associated microbiome, suggesting that diet may be directly regulating innate immunity. We used our identified disease factors and found WD-fed mice occupy a unique path in sepsis disease progression. Our data provide insight into diet-dependent reprogramming of the immune response and will be important in treating and diagnosing a WD-fed population.
...
Before LPS treatment, healthy mice fed WD had an increased frequency of monocytes and neutrophils in the blood compared with SC[standard fiber-rich chow] mice. However, WD-fed mice exhibited increased neutrophil populations and decreased activated monocytes in the blood during sepsis compared with SC mice.
Chronic muscle weakness and mitochondrial dysfunction in the absence of sustained atrophy in a preclinical sepsis model
https://elifesciences.org/articles/49920
