scholarly journals Oxidative stress in patients on mechanical ventilation

2009 ◽  
Vol 62 (11-12) ◽  
pp. 578-581
Author(s):  
Vesna Marjanovic ◽  
Vidosava Djordjevic ◽  
Goran Marjanovic
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Head Injuries ◽  
Lipid Peroxide ◽  
Thiobarbituric Acid ◽  
Lactic Dehydrogenase ◽  
Lung Damage ◽  
Thiobarbituric Acid Reactive Substances ◽  
Acid Base Balance ◽  
Arterial Blood

Introduction. The appearance and intensity of oxidative stress were analyzed in the course of mechanical ventilation and parameters that could point toward potential lung damage. Material and methods. In three time intervals on day 1, 3 and 7 of mechanical ventilation, parameters such as: triglycerides, cholesterol, lactate, serum lactic dehydrogenase, acid-base balance and lipid peroxidation products - thiobarbituric acid reactive substances, were followed in 30 patients with head injuries. Results. A decrease in the level of partial oxygen pressure (PaO2) (p<0.01) and PaO2/FiO2 index (p<0.05) in arterial blood was recorded on day 3 of mechanical ventilation. This was accompanied with an increase in alveolar-arterial difference (AaDO2) (p<0.05), thiobarbituric acid reactive substances (p<0.001) and lactic dehydrogenase (p<0.001) comparing to day 1 of mechanical ventilation. The patients with initial PaO2>120 mmHg, had significant increase of thiobarbituric acid reactive substances and AaDO2 (p<0.05) and fall of PaO2 (p<0.001) on day 3 of mechanical ventilation. Conclusion. Oxidative stress and lipid peroxide production are increased during third day of mechanical ventilation leading to disruption of oxygen diffusion through alveolar-capillary membrane and reduction of parameters of oxygenation.

Association Between Magnesium and Oxidative Stress in Patients with Obesity

2020 ◽  
Vol 16 (5) ◽  
pp. 743-748
Author(s):  
Ana R.S. de Oliveira ◽  
Kyria J.C. Cruz ◽  
Jennifer B.S. Morais ◽  
Juliana S. Severo ◽  
Jéssica B. Beserra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Magnesium Concentration ◽  
Control Group ◽  
Compensatory Mechanism ◽  
Thiobarbituric Acid Reactive Substances ◽  
Magnesium Intake ◽  
Significant Difference ◽  
Dietary Magnesium ◽  
And Control

Background: The role of minerals in preventing the generation of oxidative stress in obese individuals has been evaluated. Magnesium is an antioxidant nutrient and a cofactor of enzymes involved in the cell membrane stabilization, attenuating the effects of oxidative stress. Objective: To evaluate the association between magnesium and concentrations of thiobarbituric acid reactive substances (TBARS) in patients with obesity and eutrophic women. Methods: A cross-sectional study was conducted with 73 women, divided into two groups: case group (patients with obesity, n=27) and control group (eutrophic women, n=46). Measurements of body mass index and waist circumference were performed. Dietary magnesium intake was assessed by the three-day food record using the NutWin software. Urinary magnesium concentration was measured by atomic absorption spectrophotometry method. Plasma concentrations of thiobarbituric acid reactive substances (TBARS) were also determined. Results: Mean values of dietary magnesium intake were 161.59 ± 60.04 and 158.73 ± 31.96 for patients with obesity and control group, respectively, with no significant difference between the groups studied (p >0.05). The value of urinary excretion of magnesium was lower than the reference values in both groups, with no significant difference between the groups studied (p >0.05). The plasma concentration of thiobarbituric acid reactive substances was significantly higher in patients with obesity compared to the control group (p <0.001). There was no correlation between levels of magnesium biomarkers and the concentration of TBARS (p >0.05). Conclusion: Patients with obesity showed a reduced dietary magnesium intake which seems to induce hypomagnesuria as a compensatory mechanism. The marker of oxidative stress evaluated in this study was not influenced by magnesium.

scholarly journals Antioxidant Activity of the Isoflavonoids from the Roots of Maackia amurensis

2013 ◽  
Vol 8 (5) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Nadezda I. Kulesh ◽  
Sergey A. Fedoreyev ◽  
Marina V. Veselova ◽  
Natalia P. Mischenko ◽  
Vladimir A. Denisenko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Glutathione Peroxidase ◽  
Column Chromatography ◽  
Thiobarbituric Acid ◽  
Formalin Injection ◽  
Thiobarbituric Acid Reactive Substances ◽  
H Nmr ◽  
Maackia Amurensis

Seven isoflavonoids, including a new glycoside, (6a R,11a R)-medicarpin-3- O-gentiobioside (6), were isolated from the roots of Maackia amurensis using repeated column chromatography on a Toyopearl HW-50F sorbent and identified by HPLC–PDA–MS, 1H NMR, 13C, 1H–1H COSY, HSQC NMR and HMBC NMR analyses as daidzin (1), genistein-7- O-gentiobioside (2), pseudobaptigenin-7- O-gentiobioside (3), formononetin-7- O-gentiobioside (4), (6a R,11a R)-maackiain-3- O-gentiobioside (5), and 5- O-methylgenistein-7- O-gentiobioside (7). In the model of oxidative stress induced by formalin injection, the isolated isoflavone and pterocarpan glucosides 1-7 were shown to reduce the formation of malondialdehyde (MDA) and other thiobarbituric acid reactive substances (TBARS), as well as glutathione peroxidase (GPO) activity in rats.

scholarly journals Lens Lipid Peroxides and Glutathione Concentrations in Diabetic Cataract

1997 ◽  
Vol 34 (2) ◽  
pp. 190-192 ◽  
Author(s):  
D Özmen ◽  
I Mutaf ◽  
B Özmen ◽  
J Mentes ◽  
O Bayindir
Keyword(s):  
G Protein ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Diabetic Cataract ◽  
Free Radical Damage ◽  
Significant Difference ◽  
Radical Damage

This study aims to explore the role of reactive oxygen radicals in the genesis of diabetic cataract. Lipid peroxide (LPO) concentrations in senile ( n = 30) and diabetic ( n = 14) cataractous lenses, were determined as thiobarbituric acid-reactive substances (TBARS) by a method modified from Satoh and Yagi, and reduced glutathione (GSH) concentrations were measured according to Beutler. Lens LPO levels (mean, SD; nmol TBARS/g protein) were significantly higher in diabetics (107·54, 18·12) than senile cataractous subjects (53·54, 15·48) ( P < 0·0001). Lens GSH levels (mean, SD; nmol/g protein) showed no significant difference between diabetics (4·29, 2·05) and senile cataractous subjects (4·68, 3·12). These results suggest that free radical damage is more effective in the genesis of diabetic cataract than in senile cataract.

Oxidative stress after human exercise: effect of N-acetylcysteine supplementation

1994 ◽  
Vol 76 (6) ◽  
pp. 2570-2577 ◽  
Author(s):  
C. K. Sen ◽  
T. Rankinen ◽  
S. Vaisanen ◽  
R. Rauramaa
Keyword(s):  
Oxidative Stress ◽  
Exercise Intensity ◽  
Radical Scavenging ◽  
Thiobarbituric Acid ◽  
Bicycle Ergometer ◽  
Thiobarbituric Acid Reactive Substances ◽  
Ergometer Exercise ◽  
Single Bout ◽  
Exercise Effect ◽  
Leukocyte Dna Damage

The association between exercise intensity and related oxidative stress was investigated in nine men who exercised for 30 min at their aerobic (AeT) and anaerobic (AnaeT) thresholds. We also tested the effect of oral N-acetylcysteine (NAC) on exercise-associated rapid blood glutathione (GSH) oxidation in subjects performing two identical maximal bicycle ergometer exercise (Max) tests. Before the second test (Max with NAC supplementation [Max(NAC)]), the men took 200 x 4 mg/day of NAC tablets for 2 days and an additional 800 mg on the test morning. Blood samples were drawn before, immediately after, and 24 h after the tests. Total and oxidized GSH levels in blood were determined. Plasma thiobarbituric acid-reactive substances and net peroxyl radical scavenging capacity (PSC) were assayed. Exercise-associated damage in leukocyte DNA was estimated by fluorometric analysis of DNA unwinding. A single bout of exercise at Max, AeT, and AnaeT resulted in a significant increase in blood GSH oxidation but did not influence net PSC of plasma. Although an association between a single bout of exercise and leukocyte DNA damage was apparent, this study suggests that the parameter may not serve as a sensitive index to assess the role of exercise intensity in the extent of exercise-associated oxidative stress. Plasma thiobarbituric acid-reactive substances did not change after either Max or Max(NAC) tests. NAC supplementation resulted in an increase in preexercise PSC, indicating a higher net antioxidant capacity of the plasma, but did not affect blood GSH.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Plasma Lipid Peroxidation as a Marker for Seminal Oxidative Stress in Stallion

2019 ◽  
Vol 11 (6) ◽  
pp. 401
Author(s):  
Patricia Wolkmer ◽  
Andressa M. G. Stumm ◽  
Luiz F. K. Borges ◽  
Eduarda P. T. Ferreira ◽  
Bruna Favaretto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Seminal Plasma ◽  
Plasma Lipid ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Semen Collection ◽  
Semen Storage ◽  
Plasma Lipid Peroxidation ◽  
Antioxidant Enzyme Catalase

This experiment aims to evaluate the correlation between lipid peroxidation levels in serum and seminal plasma in equines. Also, it investigates the lipid peroxidation in extended semen samples and its effects and sperm motility during a 72 hr refrigeration period. Blood and semen were collected from fertile Crioulo stallions. Serum and seminal plasma lipid peroxidation levels were analyzed by thiobarbituric acid reactive substances (TBARS) immediately after semen collection. After addition of extender (hour = 0), diluted semen was refrigerated and stored at 5 &deg;C. Semen analyses, TBARS and catalase activity were performed in extended semen at 0, 24, 48, and 72 hours. We noted that levels of plasma lipid peroxidation can be used as an indicative of seminal oxidative stress. Also, lipid peroxidation does not increase substantially during semen storage. Lipid peroxidation and the antioxidant enzyme catalase do not seem to be the major cause of loss and motility and consequently reduction in fertility in stallion semen during storage for 72 h at 5 &deg;C.

scholarly journals Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Christonikos Leventelis ◽  
Nikolaos Goutzourelas ◽  
Aikaterini Kortsinidou ◽  
Ypatios Spanidis ◽  
Georgia Toulia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Redox Status ◽  
Protein Carbonyls ◽  
Healthy Individuals ◽  
Thiobarbituric Acid Reactive Substances ◽  
Antioxidant Defence ◽  
Total Antioxidant ◽  
Beneficial Action ◽  
The Impact

Buprenorphine and methadone are two substances widely used in the substitution treatment of patients who are addicted to opioids. Although it is known that they partly act efficiently towards this direction, there is no evidence regarding their effects on the redox status of patients, a mechanism that could potentially improve their action. Therefore, the aim of the present investigation was to examine the impact of buprenorphine and methadone, which are administered as substitutes to heroin-dependent patients on specific redox biomarkers in the blood. From the results obtained, both the buprenorphine (n=21) and the methadone (n=21) groups exhibited oxidative stress and compromised antioxidant defence. This was evident by the decreased glutathione (GSH) concentration and catalase activity in erythrocytes and the increased concentrations of thiobarbituric acid reactive substances (TBARS) and protein carbonyls in the plasma, while there was no significant alteration of plasma total antioxidant capacity (TAC) compared to the healthy individuals (n=29). Furthermore, methadone revealed more severe oxidant action compared to buprenorphine. Based on relevant studies, the tested substitutes mitigate the detrimental effects of heroin on patient redox status; still it appears that they need to be boosted. Therefore, concomitant antioxidant administration could potentially enhance their beneficial action, and most probably, buprenorphine that did not induce oxidative stress in such a severe mode as methadone, on the regulation of blood redox status.

TP receptors regulate renal hemodynamics during angiotensin II slow pressor response

2004 ◽  
Vol 287 (4) ◽  
pp. F753-F759 ◽  
Author(s):  
Noritaka Kawada ◽  
Kathryn Dennehy ◽  
Glenn Solis ◽  
Paul Modlinger ◽  
Rebecca Hamel ◽  
...  
Keyword(s):  
Pressor Response ◽  
Thiobarbituric Acid ◽  
Ang Ii ◽  
Wild Type ◽  
Thiobarbituric Acid Reactive Substances ◽  
Filtration Fraction ◽  
Arterial Blood ◽  
Tp Receptors ◽  
Prostaglandin H ◽  
Renal Vascular

We investigated the hypothesis that thromboxane A2 (TxA2)-prostaglandin H2 receptors (TP-Rs) mediate the hemodynamic responses and increase in reactive oxygen species (ROS) to ANG II (400 ng·kg−1·min−1 sc for 14 days) using TP-R knockout (TP −/−) and wild-type (+/+) mice. TP −/− had normal basal mean arterial blood pressure (MAP) and glomerular filtration rate but reduced renal blood flow and increased filtration fraction (FF) and renal vascular resistance (RVR) and markers of ROS (thiobarbituric acid-reactive substances and 8-isoprostane PGF2α) and nitric oxide (NOx). Infusion of ANG II into TP +/+ increased ROS and thromboxane B2 (TxB2) and increased RVR and FF. ANG II infusion into TP −/− mice reduced ANG I and increased aldosterone but caused a blunted increase in MAP (TP −/−: +6 ± 2 vs. TP +/+: +15 ± 3 mmHg) and failed to increase FF, ROS, or TxB2 but increased NOx and paradoxically decreased RVR (−2.1 ± 1.7 vs. +2.6 ± 0.8 mmHg·ml−1·min−1·g−1). Blockade of AT1 receptor of TP −/− mice infused with ANG II reduced MAP (−8 mmHg) and aldosterone but did not change the RVR or ROS. In conclusion, during an ANG II slow pressor response, AT1 receptors activate TP-Rs that generate ROS and prostaglandins but inhibit NO. TP-Rs mediate all of the increase in RVR and FF, part of the increase in MAP, but are not implicated in the suppression of ANG I or increase in aldosterone. TP −/− mice have a basal increase in RVR and FF associated with ROS.

scholarly journals Gene expression in human small intestinal mucosa in vivo is mediated by iron-induced oxidative stress

2006 ◽  
Vol 25 (2) ◽  
pp. 242-249 ◽  
Author(s):  
Freddy J. Troost ◽  
Robert-Jan M. Brummer ◽  
Guido R. M. M. Haenen ◽  
Aalt Bast ◽  
Rachel I. van Haaften ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lipid Peroxidation ◽  
Small Intestine ◽  
Antioxidant Capacity ◽  
Intestinal Mucosa ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Oxidative Challenge ◽  
Gene Reporters

Iron-induced oxidative stress in the small intestine may alter gene expression in the intestinal mucosa. The present study aimed to determine which genes are mediated by an iron-induced oxidative challenge in the human small intestine. Eight healthy volunteers [22 yr(SD2)] were tested on two separate occasions in a randomized crossover design. After duodenal tissue sampling by gastroduodenoscopy, a perfusion catheter was inserted orogastrically to perfuse a 40-cm segment of the proximal small intestine with saline and, subsequently, with either 80 or 400 mg of iron as ferrous gluconate. After the intestinal perfusion, a second duodenal tissue sample was obtained. Thiobarbituric acid-reactive substances, an indicator of lipid peroxidation, in intestinal fluid samples increased significantly and dose dependently at 30 min after the start of perfusion with 80 or 400 mg of iron, respectively ( P < 0.001). During the perfusion with 400 mg of iron, the increase in thiobarbituric acid-reactive substances was accompanied by a significant, momentary rise in trolox equivalent antioxidant capacity, an indicator of total antioxidant capacity ( P < 0.05). The expression of 89 gene reporters was significantly altered by both iron interventions. Functional mapping showed that both iron dosages mediated six distinct processes. Three of those processes involved G-protein receptor coupled pathways. The other processes were associated with cell cycle, complement activation, and calcium channels. Iron administration in the small intestine induced dose-dependent lipid peroxidation and a momentary antioxidant response in the lumen, mediated the expression of at least 89 individual gene reporters, and affected at least six biological processes.

scholarly journals Patients Undergoing Myeloablative Chemotherapy and Hematopoietic Stem Cell Transplantation Exhibit Depleted Vitamin C Status in Association with Febrile Neutropenia

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1879 ◽  
Author(s):  
Anitra C. Carr ◽  
Emma Spencer ◽  
Andrew Das ◽  
Natalie Meijer ◽  
Carolyn Lauren ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Febrile Neutropenia ◽  
Vitamin C ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
C Reactive Protein ◽  
Hematopoietic Stem ◽  
Reactive Protein ◽  
Myeloablative Chemotherapy ◽  
And Oxidative Stress

Patients undergoing myeloablative chemotherapy and hematopoietic stem cell transplantation (HSCT) experience profound neutropenia and vulnerability to infection. Previous research has indicated that patients with infections have depleted vitamin C status. In this study, we recruited 38 patients with hematopoietic cancer who were undergoing conditioning chemotherapy and HSCT. Blood samples were collected prior to transplantation, at one week, two weeks and four weeks following transplantation. Vitamin C status and biomarkers of inflammation (C-reactive protein) and oxidative stress (protein carbonyls and thiobarbituric acid reactive substances) were assessed in association with febrile neutropenia. The vitamin C status of the study participants decreased from 44 ± 7 µmol/L to 29 ± 5 µmol/L by week one (p = 0.001) and 19 ± 6 µmol/L by week two (p < 0.001), by which time all of the participants had undergone a febrile episode. By week four, vitamin C status had increased to 37 ± 10 µmol/L (p = 0.1). Pre-transplantation, the cohort comprised 19% with hypovitaminosis C (i.e., <23 µmol/L) and 8% with deficiency (i.e., <11 µmol/L). At week one, those with hypovitaminosis C had increased to 38%, and at week two, 72% had hypovitaminosis C, and 34% had outright deficiency. C-reactive protein concentrations increased from 3.5 ± 1.8 mg/L to 20 ± 11 mg/L at week one (p = 0.002), and 119 ± 25 mg/L at week two (p < 0.001), corresponding to the development of febrile neutropenia in the patients. By week four, these values had dropped to 17 ± 8 mg/L (p < 0.001). There was a significant inverse correlation between C-reactive protein concentrations and vitamin C status (r = −0.424, p < 0.001). Lipid oxidation (thiobarbituric acid reactive substances (TBARS)) increased significantly from 2.0 ± 0.3 µmol/L at baseline to 3.3 ± 0.6 µmol/L by week one (p < 0.001), and remained elevated at week two (p = 0.003), returning to baseline concentrations by week four (p = 0.3). Overall, the lowest mean vitamin C values (recorded at week two) corresponded with the highest mean C-reactive protein values and lowest mean neutrophil counts. Thus, depleted vitamin C status in the HSCT patients coincides with febrile neutropenia and elevated inflammation and oxidative stress.

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