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Subacute Ingestion of Caffeine and Oolong Tea Increases Fat Oxidation without Affecting Energy Expenditure and Sleep Architecture: A Randomized, Placebo-Controlled, Double-Blinded Cross-Over Trial.
Zhang, S, Takano, J, Murayama, N, Tominaga, M, Abe, T, Park, I, Seol, J, Ishihara, A, Tanaka, Y, Yajima, K, et al
Nutrients. 2020;(12)
Abstract
Ingesting oolong tea or caffeine acutely increases energy expenditure, and oolong tea, but not caffeine, stimulates fat oxidation. The acute effects of caffeine, such as increased heart rate and interference with sleep, diminish over 1-4 days, known as caffeine tolerance. During each 14-day session of the present study, 12 non-obese males consumed oolong tea (100 mg caffeine, 21.4 mg gallic acid, 97 mg catechins and 125 mg polymerized polyphenol), caffeine (100 mg), or placebo at breakfast and lunch. On day 14 of each session, 24-h indirect calorimetry and polysomnographic sleep recording were performed. Caffeine and oolong tea increased fat oxidation by ~20% without affecting energy expenditure over 24-h. The decrease in the respiratory quotient by oolong tea was greater than that by caffeine during sleep. The effect of oolong tea on fat oxidation was salient in the post-absorptive state. These findings suggest a role of unidentified ingredients in oolong tea to stimulate fat oxidation, and this effect is partially suppressed in a postprandial state. Two weeks of caffeine or oolong tea ingestion increased fat oxidation without interfering with sleep. The effects of subacute ingestion of caffeine and oolong tea differed from the acute effects, which is a particularly important consideration regarding habitual tea consumption.
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Adjunct N-Acetylcysteine Treatment in Hospitalized Patients With HIV-Associated Tuberculosis Dampens the Oxidative Stress in Peripheral Blood: Results From the RIPENACTB Study Trial.
Safe, IP, Amaral, EP, Araújo-Pereira, M, Lacerda, MVG, Printes, VS, Souza, AB, Beraldi-Magalhães, F, Monteiro, WM, Sampaio, VS, Barreto-Duarte, B, et al
Frontiers in immunology. 2020;:602589
Abstract
Tuberculosis (TB) still causes significant morbidity and mortality worldwide, especially in persons living with human immunodeficiency virus (HIV). This disease is hallmarked by persistent oxidative stress and systemic inflammation. N-acetylcysteine (NAC), a glutathione (GSH) precursor, has been shown in experimental models to limit Mycobacterium tuberculosis infection and disease both by suppression of the host oxidative response and through direct antimicrobial activity. In a recent phase II randomized clinical trial (RIPENACTB study), use of NAC as adjunct therapy during the first two months of anti-TB treatment was safe. Whether adjunct NAC therapy of patients with TB-HIV coinfection in the context of anti-TB treatment could directly affect pro-oxidation and systemic inflammation has not been yet formally demonstrated. To test this hypothesis, we leveraged existing data and biospecimens from the RIPENACTB trial to measure a number of surrogate markers of oxidative stress and of immune activation in peripheral blood of the participants at pre-treatment and at the day 60 of anti-TB treatment. Upon initiation of therapy, we found that the group of patients undertaking NAC exhibited significant increase in GSH levels and in total antioxidant status while displaying substantial reduction in lipid peroxidation compared to the control group. Only small changes in plasma concentrations of cytokines were noted. Pharmacological improvement of the host antioxidant status appears to be a reasonable strategy to reduce TB-associated immunopathology.
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Investigating the effects of vitamins E and C on oxidative stress and hematological parameters among power plant workers: A double-blind randomized controlled clinical trial.
Hosseinabadi, MB, Khanjani, N, Norouzi, P, Mirzaii, M, Biganeh, J, Nazarkhani, F
Toxicology and industrial health. 2020;(2):99-109
Abstract
The present study aimed to determine the effect of taking antioxidant vitamins including vitamins E and C in reducing oxidative stress levels and improving blood parameters. This double-blind randomized controlled trial study was conducted among the employees working in different parts of a power plant in Semnan, Iran, in 2017. A total of 91 employees were randomly allocated to four groups including vitamin E (400 units per day), vitamin C (1000 mg per day), vitamin E + C for 90 days, and control. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (Cat), and total antioxidant capacity (TAC) in plasma, and hematological parameters were measured in the participants before and after the intervention. A significant increase was seen in the mean level of SOD, Cat, and TAC in the vitamin-treated groups as well as a significant decrease in mean MOD in vitamin C and vitamin E groups after the intervention. In the intervention groups, the number of red blood cells, hematocrit, and the level of mean corpuscular hemoglobin (MCH) and MCH concentration significantly increased. After the intervention, the mean levels of MDA, SOD, and Cat in vitamin E group were significantly lower than the control group. The mean level of TAC decreased only in the vitamin C group compared to the control group. Taking vitamins E and C as nonenzymatic scavengers of free radicals appears to decrease lipid peroxidation and increase the level of antioxidant enzymes, which can be imbalanced by exposure to extremely low-frequency electromagnetic fields in power plant employees. Furthermore, some hematological parameters can be improved by consuming these vitamins.
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4-HNE Immunohistochemistry and Image Analysis for Detection of Lipid Peroxidation in Human Liver Samples Using Vitamin E Treatment in NAFLD as a Proof of Concept.
Podszun, MC, Chung, JY, Ylaya, K, Kleiner, DE, Hewitt, SM, Rotman, Y
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society. 2020;(9):635-643
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Abstract
Lipid peroxidation is a common feature of liver diseases, especially non-alcoholic fatty liver disease (NAFLD). There are limited validated tools to study intra-hepatic lipid peroxidation, especially for small specimen. We developed a semi-quantitative, fully automated immunohistochemistry assay for the detection of 4-hydroxynoneal (4-HNE) protein adducts, a marker of lipid peroxidation, for adaptation to clinical diagnostics and research. We used Hep G2 cells treated with 4-HNE to validate specificity, sensitivity, and dynamic range of the antibody. Staining and semi-quantitative automated readout were confirmed in human needle-biopsy liver samples from subjects with NAFLD and normal liver histology. The ability to detect changes in lipid peroxidation was tested in paired liver biopsies from NAFLD subjects, obtained before and after 4 weeks of treatment with the antioxidant vitamin E (ClinicalTrials.gov NCT01792115, n=21). The cellular calibrator was linear and NAFLD patients had significantly higher levels of 4-HNE adducts compared to controls (p=0.02). Vitamin E treatment significantly decreased 4-HNE (p=0.0002). Our findings demonstrate that 4-HNE quantification by immunohistochemistry and automated image analysis is feasible and able to detect changes in hepatic lipid peroxidation in clinical trials. This method can be applied to archival and fresh samples and should be considered for use in assessing NAFLD histology.
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5.
Posttranslational Modifications in Ferroptosis.
Wei, X, Yi, X, Zhu, XH, Jiang, DS
Oxidative medicine and cellular longevity. 2020;:8832043
Abstract
Ferroptosis was first coined in 2012 to describe the form of regulated cell death (RCD) characterized by iron-dependent lipid peroxidation. To date, ferroptosis has been implicated in many diseases, such as carcinogenesis, degenerative diseases (e.g., Huntington's, Alzheimer's, and Parkinson's diseases), ischemia-reperfusion injury, and cardiovascular diseases. Previous studies have identified numerous targets involved in ferroptosis; for example, acyl-CoA synthetase long-chain family member 4 (ACSL4) and p53 induce while glutathione peroxidase 4 (GPX4) and apoptosis-inducing factor mitochondria-associated 2 (AIFM2, also known as FSP1) inhibit ferroptosis. At least three major pathways (the glutathione-GPX4, FSP1-coenzyme Q10 (CoQ10), and GTP cyclohydrolase-1- (GCH1-) tetrahydrobiopterin (BH4) pathways) have been identified to participate in ferroptosis regulation. Recent advances have also highlighted the crucial roles of posttranslational modifications (PTMs) of proteins in ferroptosis. Here, we summarize the recently discovered knowledge regarding the mechanisms underlying ferroptosis, particularly the roles of PTMs in ferroptosis regulation.
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Acute consumption of Black walnuts increases fullness and decreases lipid peroxidation in humans.
Rodrigues, LL, Cooper, JA, Paton, CM
Nutrition research (New York, N.Y.). 2019;:56-64
Abstract
Walnuts are a nutrient dense food, but most health research is on English walnuts (EW). Black walnuts (BW) contain a different antioxidant and fatty acid profile, and more protein, compared to EW. The purpose of the study was to compare postprandial responses following the consumption of 3 breakfast meals containing either butter (control), BW, or EW. We hypothesized that walnut-containing meals would mitigate post-meal increases in glucose, insulin, triglycerides, and lipid peroxidation while increasing TAC compared to the traditional meal without nuts. Furthermore, we hypothesized that the BW meal would exhibit greater TAC and subjective fullness while mitigating postprandial increases in lipid peroxidation better than the EW. This was a randomized, double-blind control crossover study in 30 healthy adults with three testing visits. At each visit, subjects consumed either the control, BW, or EW meal. Blood draws and visual analog scale appetite ratings were obtained at fasting, 30, 60, 120, and 180 min postprandially. The BW and EW meals resulted in greater suppression of appetite vs. control (P < .01 and P = .03, respectively), and the BW meal also increased fullness more than EW and control (P < .01 and P < .001, respectively). Finally, the BW meal also had a greater suppression of lipid peroxidation vs. control (P = .01). There were no other treatment differences in the other measures of appetite or for glycemia, triglycerides, or total antioxidant capacity. Substituting butter in a breakfast meal with BW or EW increased fullness; however, the BW meal was superior for suppressing overall appetite while also lowering postprandial lipid peroxidation.
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In major affective disorders, early life trauma predict increased nitro-oxidative stress, lipid peroxidation and protein oxidation and recurrence of major affective disorders, suicidal behaviors and a lowered quality of life.
Moraes, JB, Maes, M, Roomruangwong, C, Bonifacio, KL, Barbosa, DS, Vargas, HO, Anderson, G, Kubera, M, Carvalho, AF, Nunes, SOV
Metabolic brain disease. 2018;(4):1081-1096
Abstract
Early life trauma (ELT) may increase the risk towards bipolar disorder (BD) and major depression (MDD), disorders associated with activated neuro-oxidative and neuro-nitrosative stress (O&NS) pathways. It has remained elusive whether ELTs are associated with O&NS and which ELTs are associated with distinct affective disorder phenotypes. This case-control study examined patients with BD (n = 68) and MDD (n = 37) and healthy controls (n = 66). The Child Trauma Questionnaire (CTQ) was used to assess specific ELT. We measured malondialdehyde (MDA), lipid hydroperoxides (LOOH), superoxide dismutase (SOD), catalase, advanced oxidation protein products (AOPP); NO metabolites (NOx), paraoxonase 1 activity, zinc, albumin, high density lipoprotein cholesterol and -SH groups and computed z-unit weighted composite scores. Physical neglect significantly predicts higher z-unit weighted composite scores of LOOH+SOD, LOOH+SOD+NOx, LOOH+SOD+NOx + MDA and LOOH+SOD+NOx + AOPP. Sexual abuse was associated with a significantly lower composite score of zinc+albumin+SH. Emotional abuse was associated with severity of depression and anxiety, number of depressive and manic episodes, alcohol and hypnotics use, lifetime suicidal behavior and lowered quality of life. Sexual abuse was associated with an increased risk towards BD, but not MDD. ELT, especially physical neglect, may drive increased (nitro-)oxidative stress coupled with lipid and protein oxidation, which - together with emotional abuse - may play a role in severity of illness, lowered quality of life and MDD. ELTs are also associated with the onset of BD, but this link did not appear to be related to activated O&NS pathways. These novel findings deserve confirmation in prospective studies.
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Cocoa ingestion protects plasma lipids in healthy males against ex vivo oxidative conditions: A randomized clinical trial.
Barrios, M, Orozco, LC, Stashenko, EE
Clinical nutrition ESPEN. 2018;:1-7
Abstract
The effects of in vivo cocoa-based supplementation were studied as a preconditioning treatment for ex vivo acute oxidative conditions in a controlled randomized clinical trial. Subjects were 100 healthy young men at Universidad Industrial de Santander blinded to the intervention and divided into two groups: The intervention group (n = 50) receiving 30 g of cocoa powder and 50 g of dark chocolate/d for 1 week with the remaining subjects receiving placebo. Cocoa products preconditioning for 1 week resulted in modifications in the susceptibility of plasma lipids over ex vivo oxidative conditions with effects of i) a significant increase in the oxidative resistance of plasma lipids measured by dienes formation (4.2, CI: 0.18, 8.2; P = 0.04), and ii) a significant reduction in the production of toxic aldehydes as established by a decrease in the content of hexanal, quantified by gas chromatography (-0.22, CI: -0.38, -0.05; P = 0.009). The in vivo cocoa-based preconditioning demonstrated protective properties against ex vivo oxidative modifications, improving total plasma lipids resistance to oxidation and protecting plasma lipids against great acute oxidative insult in comparison with placebo. This trial was registered at clinical clinicaltrials.gov as NCT01347450.
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Effect of lithocholic acid on biologically active α,β-unsaturated aldehydes induced by H2O2 in glioma mitochondria for use in glioma treatment.
Wang, D, Bie, L, Su, Y, Xu, H, Zhang, F, Su, Y, Zhang, B
International journal of molecular medicine. 2018;(6):3195-3202
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Abstract
Lithocholic acid (LCA) is known to kill glioma cells while sparing normal neuronal cells. However, the anti-glioma mechanism of LCA is unclear at present. Although malondialdehyde (MDA) is not specific to detect tumors, biologically active α,β-unsaturated aldehydes can be used to detect the outcome of gliomas, especially the mitochondria, as a research tool. The purpose of this research was to determine the optimum conditions for a lipid peroxidation model, according to changes in the aldehydes formed from the reaction between 2-thiobarbituric acid and biologically active α,β-unsaturated aldehydes. Experimental methods and procedures were successfully established for a model of lipid peroxidation induced by H2O2 in glioma mitochondria for glioma treatment and optimum conditions for LCA treatment were determined. The optimal conditions for the model were a glioma mitochondrial concentration of 1.5 mg/ml, H2O2 concentration of 0.3 mg/ml, duration of action of 30 min, and addition of 4.0 ml of 46 mM thiobarbituric acid. The effect of LCA, as determined by changes in the UV peaks at 450, 495, and 532 nm, was optimal at a concentration of 100 µM, a duration of action of 15 min, and in an acidic microenvironment. The study concluded that a suitable concentration of LCA has anti-glioma effects as determined by the effect on changes in the UV peaks at 450, 495 and 532 nm and the mitochondrial model developed should be conducive to further in-depth research.
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Replacing carbohydrate during a glucose challenge with the egg white portion or whole eggs protects against postprandial impairments in vascular endothelial function in prediabetic men by limiting increases in glycaemia and lipid peroxidation.
McDonald, JD, Chitchumroonchokchai, C, Li, J, Mah, E, Labyk, AN, Reverri, EJ, Ballard, KD, Volek, JS, Bruno, RS
The British journal of nutrition. 2018;(3):259-270
Abstract
Eggs attenuate postprandial hyperglycaemia (PPH), which transiently impairs vascular endothelial function (VEF). We hypothesised that co-ingestion of a glucose challenge with egg-based meals would protect against glucose-induced impairments in VEF by attenuating PPH and oxidative stress. A randomised, cross-over study was conducted in prediabetic men (n 20) who ingested isoenegertic meals (1674 kJ (400 kcal)) containing 100 g glucose (GLU), or 75 g glucose with 1·5 whole eggs (EGG), seven egg whites (WHITE) or two egg yolks (YOLK). At 30 min intervals for 3 h, brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, cholecystokinin (CCK), lipids (total, LDL- and HDL-cholesterol; TAG), F2-isoprostanes normalised to arachidonic acid (F2-IsoPs/AA), and methylglyoxal were assessed. In GLU, FMD decreased at 30-60 min and returned to baseline levels by 90 min. GLU-mediated decreases in FMD were attenuated at 30-60 min in EGG and WHITE. Compared with GLU, FMDAUC was higher in EGG and WHITE only. Relative to baseline, glucose increased at 30-120 min in GLU and YOLK but only at 30-90 min in EGG and WHITE. GlucoseAUC and insulinAUC were also lower in EGG and WHITE only. However, CCKAUC was higher in EGG and WHITE compared with GLU. Compared with GLU, F2-IsoPs/AAAUC was lower in EGG and WHITE but unaffected by YOLK. Postprandial lipids and methylglyoxal did not differ between treatments. Thus, replacing a portion of a glucose challenge with whole eggs or egg whites, but not yolks, limits postprandial impairments in VEF by attenuating increases in glycaemia and lipid peroxidation.