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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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Skeletal muscle lipid peroxidation and insulin resistance in humans.
Ingram, KH, Hill, H, Moellering, DR, Hill, BG, Lara-Castro, C, Newcomer, B, Brandon, LJ, Ingalls, CP, Penumetcha, M, Rupp, JC, et al
The Journal of clinical endocrinology and metabolism. 2012;(7):E1182-6
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OBJECTIVE The relationships among skeletal muscle lipid peroxidation, intramyocellular lipid content (IMCL), and insulin sensitivity were evaluated in nine insulin-sensitive (IS), 13 insulin-resistant (IR), and 10 adults with type 2 diabetes (T2DM). DESIGN Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp [glucose disposal rate (GDR)]. Lipid peroxidation was assessed by 4-hydroxynonenal (HNE)-protein adducts and general oxidative stress by protein carbonyl content. All patients were sedentary. RESULTS Protein-HNE adducts were elevated 1.6-fold in T2DM compared with IS adults, whereas IR showed intermediate levels of HNE-modified proteins. Protein-HNE adducts correlated with GDR, waist circumference, and body mass index. IMCL was increased by 4.0- and 1.9-fold in T2DM and IR patients, respectively, compared with IS, and was correlated with GDR and waist circumference but not BMI. Protein carbonyls were not different among groups and did not correlate with any of the measured variables. Correlations were detected between IMCL and protein-HNE. CONCLUSION Our data show for the first time that skeletal muscle protein-HNE adducts are related to the severity of insulin resistance in sedentary adults. These results suggest that muscle lipid peroxidation could be involved in the development of insulin resistance.
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Inhibitory effects of balsamic vinegar on LDL oxidation and lipid accumulation in THP-1 macrophages.
Iizuka, M, Tani, M, Kishimoto, Y, Saita, E, Toyozaki, M, Kondo, K
Journal of nutritional science and vitaminology. 2010;(6):421-7
Abstract
Oxidized low-density lipoprotein (LDL) is believed to contribute to atherosclerosis in part by being taken up into macrophages via scavenger receptors, thus accounting for foam cells. Balsamic vinegar is made from grapes and generally consumed in the Mediterranean region. In this study, we investigated the preventive effects of balsamic vinegar on LDL oxidation and foam cell formation. Balsamic vinegar had stronger 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging abilities and higher polyphenol concentrations than rice vinegar. Balsamic vinegar dramatically inhibited LDL oxidation by azoradicals and endothelial cell-mediated oxidation in vitro. Further, we assessed the anti-oxidative effect against LDL after balsamic vinegar consumption in human subjects. Balsamic vinegar prolonged the LDL oxidation lag time and decreased lipid peroxide (LPO) and lyso-phosphatidylcholine (LPC) in LDL particles. We next examined the effect of balsamic vinegar on foam cell formation. Oil red O staining showed that balsamic vinegar inhibited oxidized LDL-induced foam cell formation in THP-1 macrophages. The concentrations of intracellular triglycerides and total cholesterols were reduced in the presence of balsamic vinegar. In addition, balsamic vinegar decreased the mRNA and protein expression level of scavenger receptors in THP-1 macrophages. These results showed that balsamic vinegar contained abundant polyphenols and inhibited LDL oxidation and oxidized LDL-induced foam cell formation by decreasing the expression of scavenger receptors.
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Effect of antioxidant vitamin treatment on the time course of hematological and hemorheological alterations after an exhausting exercise episode in human subjects.
Senturk, UK, Yalcin, O, Gunduz, F, Kuru, O, Meiselman, HJ, Baskurt, OK
Journal of applied physiology (Bethesda, Md. : 1985). 2005;(4):1272-9
Abstract
This study examined the effects of a 2-mo antioxidant vitamin treatment on acute hematological and hemorheological alterations induced by exhausting exercise; both sedentary and trained individuals were employed. Eighteen young male, human subjects (9 sedentary, 9 trained by regular exercise) participated in the study and performed an initial maximal aerobic cycle ergometer exercise with frequent blood sampling over a 24-h period and analysis of hematological and hemorheological parameters. All subjects were treated with an antioxidant vitamin A, C, and E regimen, supplemented orally for 2 mo, and then subjected to a second exercise test and blood sampling at the end of this period. In the sedentary group during the first testing period (before vitamin treatment), white blood cell counts and granulocyte percentages were increased at 2 h after the exercise test and remained elevated for 4-12 h. Red blood cell (RBC) deformability and aggregation were also altered by exercise in the sedentary group before vitamin treatment. However, none of these parameters in the sedentary group were altered by exercise after the 2-mo period of antioxidant vitamin treatment. With the exception of a transient rise in granulocyte percentage, these parameters were also not affected in the trained subjects before the vitamin treatment. Significant increases of RBC lipid peroxidation observed 12 h after the exercise test in both sedentary and trained subjects were also totally prevented by vitamin treatment. Our results indicate that antioxidant vitamin treatment is effective in preventing the inflammation-like response and coincident adverse hemorheological changes after an episode of exhausting exercise, and suggest that such changes may be related to exercise-induced death events.
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Supplementation of a diet low in carotenoids with tomato or carrot juice does not affect lipid peroxidation in plasma and feces of healthy men.
Briviba, K, Schnäbele, K, Rechkemmer, G, Bub, A
The Journal of nutrition. 2004;(5):1081-3
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Antioxidant properties of carotenoids are thought to be at least partly responsible for the protective effects of fruits and vegetables rich in carotenoids against colon cancer. There are large amounts of in vitro data supporting this hypothesis. But there is little known about the antioxidant effects of carotenoid-rich food in vivo particularly in the gastrointestinal tract. In a randomized, crossover trial, healthy men (n = 22) who were consuming a low-carotenoid diet drank 330 mL/d tomato juice or carrot juice for 2 wk. Antioxidant capacity was assessed by the "lag time" of ex vivo LDL oxidation induced by copper and lipid peroxidation as determined by measurements of malondialdehyde (MDA) in plasma and feces using HPLC with fluorescence detection. Although consumption of both carotenoid-rich juices for 2 wk increased the carotenoid level in plasma and feces (P < 0.001), the antioxidant capacity of LDL tended to be increased by only approximately 4.5% (P = 0.08), and lipid peroxidation in the men's plasma and feces was not affected. Thus, processes other than lipid peroxidation could be responsible for the preventive effects of tomatoes and carrots against colon cancer.
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Effects of cis-9,trans-11 conjugated linoleic acid supplementation on insulin sensitivity, lipid peroxidation, and proinflammatory markers in obese men.
Risérus, U, Vessby, B, Arnlöv, J, Basu, S
The American journal of clinical nutrition. 2004;(2):279-83
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BACKGROUND We recently showed that trans-10,cis-12 (t10,c12) conjugated linoleic acid (CLA) causes insulin resistance in obese men. However, metabolic effects of the c9,t11 CLA isomer are still unknown in obese men. Because c9,t11 CLA is the predominant CLA isomer in foods and is included in dietary weight-loss products, it is important to conduct randomized controlled studies that use c9,t11 CLA preparations. OBJECTIVE We investigated the effects of c9,t11 CLA supplementation on insulin sensitivity, body composition, and lipid peroxidation in a group at high risk for cardiovascular disease. DESIGN In a randomized, double-blind, placebo-controlled study, 25 abdominally obese men received 3 g c9,t11 CLA/d or placebo (olive oil). Before and after 3 mo of supplementation, we assessed insulin sensitivity (hyperinsulinemic euglycemic clamp), lipid metabolism, body composition, and urinary 8-iso-prostaglandin F(2alpha) (a major F(2)-isoprostane) and 15-keto-dihydro-prostaglandin F(2alpha), markers of in vivo oxidative stress and inflammation, respectively. RESULTS All subjects completed the study. Compared with placebo, c9,t11 CLA decreased insulin sensitivity by 15% (P < 0.05) and increased 8-iso-prostaglandin F(2alpha) and 15-keto-dihydro-prostaglandin F(2alpha) excretion by 50% (P < 0.01) and 15% (P < 0.05), respectively. The decreased insulin sensitivity was independent of changes in serum lipids, glycemia, body mass index, and body fat but was abolished after adjustment for changes in 8-iso-prostaglandin F(2alpha) concentrations. There were no differences between groups in body composition. CONCLUSIONS A CLA preparation containing the purified c9,t11 CLA isomer increased insulin resistance and lipid peroxidation compared with placebo in obese men. Because c9,t11 CLA occurs in commercial supplements as well as in the diet, the present results should be confirmed in larger studies that also include women.
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Conjugated linoleic acid induces lipid peroxidation in humans.
Basu, S, Smedman, A, Vessby, B
FEBS letters. 2000;(1):33-6
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Conjugated linoleic acid (CLA) is shown to have chemoprotective properties in various experimental cancer models. CLA is easily oxidised and it has been suggested that an increased lipid oxidation may contribute to the antitumorigenic effects. This report investigates the urinary levels of 8-iso-PGF(2alpha), a major isoprostane and 15-keto-dihydro-PGF(2alpha), a major metabolite of PGF(2alpha), as indicators of non-enzymatic and enzymatic lipid peroxidation after dietary supplementation of CLA in healthy human subjects for 3 months. A significant increase of both 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) in urine was observed after 3 months of daily CLA intake (4.2 g/day) as compared to the control group (P<0.0001). Conjugated linoleic acid had no effect on the serum alpha-tocopherol levels. However, gamma-tocopherol levels in the serum increased significantly (P=0. 015) in the CLA-treated group. Thus, CLA may induce both non-enzymatic and enzymatic lipid peroxidation in vivo. Further studies of the mechanism behind, and the possible consequences of, the increased lipid peroxidation after CLA supplementation are urgently needed.