Endothelium-dependent vasodilation in the brachial  artery is impaired in smokers: effect of vitamin C

Cigarette smoking has been shown to cause endothelial dysfunction. To examine the effects of vitamin C and cigarette smoking on endothelium-dependent vasodilation, we measured the lumen diameter and flow velocity of the brachial arteries at rest, during reactive hyperemia following transient arterial occlusion, and after sublingual nitroglycerin (0.3 mg) in smokers ( n = 20) and nonsmokers ( n = 20) with high-resolution ultrasound after infusion of saline or saline plus vitamin C (10 mg/min for 20 min). We also performed the same study in smokers ( n = 15) before and 10 min after cigarette smoking. In addition, we measured the serum levels of vitamin C and the plasma levels of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation. The smokers had lower vitamin C levels, higher TBARS levels, and showed impairment of flow-dependent vasodilation (5.3 ± 1.9 vs. 9.2 ± 1.5%, P < 0.0001) compared with nonsmokers. Vitamin C administration improved the impairment of flow-dependent vasodilation (5.3 ± 1.9 to 9.0 ± 3.2%, P < 0.001) and decreased TBARS in smokers but not in nonsmokers. Furthermore, cigarette smoking acutely worsened the impairment of flow-dependent vasodilation (5.4 ± 1.8 to 1.5 ± 1.3%, P < 0.01) and increased TBARS. We conclude that 1) endothelium-dependent vasodilation in the brachial arteries is impaired in smokers and this impairment is improved by vitamin C administration in association with a decrease in TBARS and 2) cigarette smoking produces acute impairment of endothelium-dependent vasodilation in smokers in association with an increase in TBARS.

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Protective Effects of Chlorogenic Acid against Carbon Tetrachloride-Induced Hepatotoxicity in Mice

Processes ◽

10.3390/pr10010031 ◽

2021 ◽

Vol 10 (1) ◽

pp. 31

Author(s):

Yu-Wen Hsu ◽

Ya-Yu Chen ◽

Chia-Fang Tsai

Keyword(s):

Lipid Peroxidation ◽

Carbon Tetrachloride ◽

Chlorogenic Acid ◽

Thiobarbituric Acid ◽

Serum Levels ◽

Protective Effects ◽

Thiobarbituric Acid Reactive Substances ◽

Liver Injuries ◽

Severe Impairment ◽

Ccl4 Administration

The protective effects of chlorogenic acid (CGA) against liver injury were evaluated by its reduction in carbon tetrachloride (CCl4)-induced hepatic damage in ICR mice. The animals were orally given CGA (60, 100, and 200 mg/kg, respectively) or silymairn (200 mg/kg) daily with 0.3% CCl4 administration (3 mL/kg, dissolved in olive oil) after medicament treatment on the 7th day. Compared with the normal group, CCl4 caused severe impairment in liver according to the evidence of significant reduction in the level of total albumin and expansion (p < 0.05) of the activities in aspartate aminotransferase (AST) and alanine aminotransferase (ALT), cholesterol, triglyceride (TG), and total albumin in serum, decreased the level of glutathione (GSH), and diminished the activities of catalase, superoxide dismutase (SOD), glutathione reductase (GSH-Rd), and glutathione peroxidase (GSH-Px) in liver while increasing the level of hepatic thiobarbituric acid-reactive substances (TBARS). However, oral administration of CGA or silymarin could significantly (p < 0.05) decrease the serum levels of AST, ALT, cholesterol, TG, and total albumin and elevated the serum total albumin and the activities of GSH, catalase, SOD, GSH-Rd, and GSH-Px while leading to decline the TBARS in liver compared with CCl4-intoxicated group. Moreover, histopathology displayed that CGA decreased the formation of lesions in liver resulted from CCl4. The outcomes indicate that CGA shows the efficiency hepatoprotective consequences for CCl4-incited liver injuries in mice by the elevation of the activities of antioxidant enzymes and hindrance of lipid peroxidation.

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LEVELS OF VITAMIN C IN CHAIN SMOKERS

International Journal of Medical and Biomedical Studies ◽

10.32553/ijmbs.v4i7.1436 ◽

2020 ◽

Vol 4 (7) ◽

Author(s):

Simerpreet Kukreja

Keyword(s):

Cigarette Smoking ◽

Vitamin C ◽

Dietary Intake ◽

Serum Vitamin ◽

Inverse Correlation ◽

Serum Levels ◽

Negative Association ◽

Alcoholic Beverages ◽

Vitamin Supplementation ◽

Dietary Vitamin

Introduction: Cigarette smoking induces many chronic illnesses, but in developed countries it is a preventable risk factor. However, by increasing the protective protection mechanism, it may be possible to alleviate the smoke-induced damage. As smoking risk is minimised by vitamin C intake, it is recommended that smokers should take more vitamin C. This inverse correlation between both vitamin C intake and serum levels and smoking was independent of age, sex, body weight, ethnicity, and consumption of alcoholic beverages. The negative association between cigarette smoking and serum vitamin C levels continued, following further adjustment for dietary vitamin C intake. The risk of severe hypovitaminosis C, especially when not accompanied by vitamin supplementation, has been increased in smokers. These data indicate that the inverse relationship between smoking and serum vitamin C levels exists independently of dietary intake, while smoking adversely affects preferences for vitamin C rich foods. Methods: A survey method was performed, with 50 smokers (S) receiving either 500 mg of vitamin C or placebo (P) daily for 4 weeks, and 50 non-smokers receiving vitamin C without supplementation. All finished the hearing. Both groups were equal and C: 14.2 + /- 1.8 pack-years was the amount of cigarettes smoked. Concentrations of plasma vitamin C increased significantly (p < 0.005) only in the vitamin C supplement community. Results: At SMHRC Hospital Nagpur, we examined the relationship between smoking and vitamin C status, dietary and serum vitamin C levels of 100 participants. Smokers of 20 cigarettes a day had the lowest dietary intake of vitamin C and serum levels, whereas smokers of 1-19 cigarettes a day had lower intake of vitamin C and serum levels (compared to respondents who had never smoked. This inverse correlation between vitamin C and smoking intake and serum levels was independent of age, sex, body weight, race, and consumption of alcoholic beverages. The negative association between cigarette smoking and serum vitamin C levels continued, following further adjustment for dietary vitamin C intake. In smokers, the risk of severe hypo-vitaminosis C, particularly when not accompanied by vitamin supplementation, has increased. Conclusion: These data indicate that the inverse relationship between smoking and serum vitamin C levels exists independently of dietary intake, while smoking adversely affects preferences for vitamin C rich foods. A balanced diet for smokers will obtain a hearty recommendation at this time, but guidelines should remain cautious about high-dose nutrition supplements. Keywords: Chain Smoker, Vitamin C, hypo-vitaminosis C and cigarette.

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Biochemical Studies on Phenylhydrazine Induced Experimental Anemic Albino Rats

Journal of Universal College of Medical Sciences ◽

10.3126/jucms.v3i1.13258 ◽

2015 ◽

Vol 3 (1) ◽

pp. 41-47

Author(s):

Nirjala Laxmi Madhikarmi ◽

Kora Rudraiah Siddalinga Murthy

Keyword(s):

Lipid Peroxidation ◽

Lipid Hydroperoxide ◽

Thiobarbituric Acid ◽

Albino Rats ◽

Enzymatic Antioxidants ◽

Medical Sciences ◽

Thiobarbituric Acid Reactive Substances ◽

Biochemical Studies ◽

Healthy Control ◽

Wistar Albino Rats

INTRODUCTION: The present study evaluated the modulatory effects of diphenylhydrazine induced experimental wistar albino rats and also to assess various biochemical parameters in whole blood and red blood cell lysate.MATERIALAND METHODS: Twenty male albino rats weighing 180-200 gm were selected for the study and divided in two groups; ten phenylhydrazine dihydrochloride (PHZ) induced anemia and ten healthy control. Thiobarbituric acid reactive substances and lipid hydroperoxide were measured as lipid peroxidation parameter. The antioxidant vitamins A, C and E and enzymatic antioxidants; catalase, glutathione peroxidase and superoxide dismutase were also assessed.RESULTS: Phenylhydrazine induced anemic rats showed a significant increase in the lipid peroxidation and decrease in the antioxidants as compared to healthy rats.CONCLUSION: The study concludes that phenylhydrazine induced experimental anemic albino rats showed increased oxidative stress than compared with healthy albino rats.Journal of Universal College of Medical Sciences Vol. 3, No. 1, 2015: 41-47

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

Journal of Agricultural Science ◽

10.5539/jas.v11n6p401 ◽

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 °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 °C.

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Oxypurinol administration fails to prevent free radical-mediated lipid peroxidation during loaded breathing

Journal of Applied Physiology ◽

10.1152/jappl.1999.87.3.1123 ◽

1999 ◽

Vol 87 (3) ◽

pp. 1123-1131 ◽

Cited By ~ 13

Author(s):

G. Supinski ◽

D. Nethery ◽

D. Stofan ◽

L. Szweda ◽

A. DiMarco

Keyword(s):

Lipid Peroxidation ◽

Free Radical ◽

Xanthine Oxidase ◽

Thiobarbituric Acid ◽

Thiobarbituric Acid Reactive Substances ◽

Xanthine Oxidase Inhibitor ◽

Air Breathing ◽

Fatigue Development ◽

Loaded Breathing

The purpose of the present study was to determine whether it is possible to alter the development of fatigue and ablate free radical-mediated lipid peroxidation of the diaphragm during loaded breathing by administering oxypurinol, a xanthine oxidase inhibitor. We studied 1) room-air-breathing decerebrate, unanesthetized rats given either saline or oxypurinol (50 mg/kg) and loaded with a large inspiratory resistance until airway pressure had fallen by 50% and 2) unloaded saline- and oxypurinol-treated room-air-breathing control animals. Additional sets of studies were performed with animals breathing 100% oxygen. Animals were killed at the conclusion of loading, and diaphragmatic samples were obtained for determination of thiobarbituric acid-reactive substances and assessment of in vitro force generation. We found that loading of saline-treated animals resulted in significant diaphragmatic fatigue and thiobarbituric acid-reactive substances formation ( P < 0.01). Oxypurinol administration, however, failed to increase load trial time, reduce fatigue development, or prevent lipid peroxidation in either room-air-breathing or oxygen-breathing animals. These data suggest that xanthine oxidase-dependent pathways do not generate physiologically significant levels of free radicals during the type of inspiratory resistive loading examined in this study.

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

Physiological Genomics ◽

10.1152/physiolgenomics.00114.2005 ◽

2006 ◽

Vol 25 (2) ◽

pp. 242-249 ◽

Cited By ~ 7

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.

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

Nutrients ◽

10.3390/nu12061879 ◽

2020 ◽

Vol 12 (6) ◽

pp. 1879 ◽

Cited By ~ 1

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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EFFECTS OF VITAMIN C SUPPLEMENTATION ON THE CHRONIC PHASE OF CHAGAS DISEASE

Revista do Instituto de Medicina Tropical de São Paulo ◽

10.1590/s0036-46652015000300011 ◽

2015 ◽

Vol 57 (3) ◽

pp. 245-250 ◽

Cited By ~ 6

Author(s):

Ricardo Guimarães MARIM ◽

Alex Silva de GUSMÃO ◽

Roberto Esteves Pires CASTANHO ◽

Rafael DEMINICE ◽

Altino Luiz Silva THEREZO ◽

...

Keyword(s):

Vitamin C ◽

Chagas Disease ◽

Chronic Phase ◽

Thiobarbituric Acid ◽

Dose Equivalent ◽

Thiobarbituric Acid Reactive Substances ◽

Vitamin C Supplementation ◽

Histopathologic Analysis ◽

Different Doses ◽

Oxidative Insult

Introduction: In order to examine the effectiveness of vitamin C (ascorbic acid) in combating the oxidative insult caused by Trypanosoma cruzi during the development of the chronic phase of Chagas disease, Swiss mice were infected intraperitoneally with 5.0 × 104 trypomastigotes of T. cruzi QM1strain. Methods: Mice were given supplements of two different doses of vitamin C for 180 days. Levels of lipid oxidation (as indicated by thiobarbituric acid reactive substances-TBARS), total peroxide, vitamin C, and reduced glutathione were measured in the plasma, TBARS, total peroxide and vitamin C were measured in the myocardium and histopathologic analysis was undertaken in heart, colon and skeletal muscle. Results: Animals that received a dose equivalent to 500 mg of vitamin C daily showed increased production of ROS in plasma and myocardium and a greater degree of inflammation and necrosis in skeletal muscles than those that received a lower dose or no vitamin C whatsoever. Conclusion: Although some research has shown the antioxidant effect of vitamin C, the results showed that animals subject to a 500 mg dose of vitamin C showed greater tissue damage in the chronic phase of Chagas disease, probably due to the paradoxical actions of the substance, which in this pathology, will have acted as a pro-oxidant or pro-inflammatory.

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Lipid Peroxidation and Cherniluminescence during Naproxen Metabolism in Rat Liver Microsomes

Human & Experimental Toxicology ◽

10.1177/096032719401301203 ◽

1994 ◽

Vol 13 (12) ◽

pp. 831-838 ◽

Cited By ~ 3

Author(s):

Hiroyuki Yokoyama ◽

Toshiharu Horie ◽

Shoji Awazu

Keyword(s):

Lipid Peroxidation ◽

Singlet Oxygen ◽

Rat Liver ◽

Liver Microsomes ◽

Thiobarbituric Acid ◽

Rat Liver Microsomes ◽

Oxygen Species ◽

Thiobarbituric Acid Reactive Substances ◽

Microsomal Suspension ◽

Weight Protein

1 Rat liver microsomal suspension containing NADPH and MgCl2 was incubated at 37°C with naproxen, a non-steroidal anti-inflammatory drug. Thiobarbituric acid reactive substances (TBA-RS), high molecular weight protein aggregates and fluorescent substances were formed in the microsomal suspension. 2 Chemiluminescence was produced from the microsomal suspension. This chemiluminescence production was well correlated to the TBA-RS formation, indicating that the chemiluminescence production was closely associated with the lipid peroxidation. 3 The addition of SKF-525A to the microsomal suspension inhibited the production of TBA-RS, chemiluminescence and 6-demethylnaproxen (6-DMN), the oxidative product of naproxen. Further, the antioxidant, α-tocopherol and singlet oxygen quenchers like histidine, dimethylfuran and 1,4-diazabicyclo[2,2,2]octane strikingly inhibited the productions of chemiluminescence and TBA-RS. 4 Neither naproxen nor 6-DMN caused lipid peroxidation in the absence of NADPH. Thus, lipid peroxidation and chemiluminescence during the oxidation of naproxen in liver microsomes was suggested to be provoked by reactive oxygen species and an origin of chemiluminescence was shown to be singlet oxygen.

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