Improving the thiobarbituric acid-reactive-substances assay for estimating lipid peroxidation in plant tissues containing anthocyanin and other interfering compounds

Planta ◽  
1999 ◽  
Vol 207 (4) ◽  
pp. 604-611 ◽  
Author(s):  
D. Mark Hodges ◽  
John M. DeLong ◽  
Charles F. Forney ◽  
Robert K. Prange
Keyword(s):  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Plant Tissues ◽  
Thiobarbituric Acid Reactive Substances

scholarly journals Biochemical Studies on Phenylhydrazine Induced Experimental Anemic Albino Rats

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 

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 °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.

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

1999 ◽  
Vol 87 (3) ◽  
pp. 1123-1131 ◽  
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.

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.

Lipid Peroxidation and Cherniluminescence during Naproxen Metabolism in Rat Liver Microsomes

1994 ◽  
Vol 13 (12) ◽  
pp. 831-838 ◽  
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.

Dehydroepiandrosterone administration prevents the oxidative damage induced by acute hyperglycemia in rats

1997 ◽  
Vol 155 (2) ◽  
pp. 233-240 ◽  
Author(s):  
M Aragno ◽  
E Brignardello ◽  
E Tamagno ◽  
V Gatto ◽  
O Danni ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
Thiobarbituric Acid Reactive Substances ◽  
Acute Hyperglycemia ◽  
Tissue Resistance ◽  
In Vivo Administration ◽  
Different Doses

Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. Dehydroepiandrosterone, which has recently been found to have antioxidant properties, was administered i.p. to rats at different doses (10, 50 or 100 mg/kg body weight) 3 h before treatment with dextrose (5 g/kg). Lipid peroxidation was evaluated on liver, brain and kidney homogenates, measuring both steady-state concentrations of thiobarbituric acid reactive substances, and fluorescent chromolipids, evaluated as hydroxynonenal adducts. Formation of thiobarbituric acid reactive substances was significantly higher in hyperglycemic than in normoglycemic animals. Three hours (but not 1 h) dehydroepiandrosterone-pretreatment protected tissues against lipid peroxidation induced by dextrose; both thiobarbituric acid reactive substances and hydroxynonenal adducts in liver, kidney and brain homogenates were significantly lower in dehydroepiandrosterone-pretreated animals. Dehydroepiandrosterone did not modify the cytosolic level of antioxidants, such as alpha-tocopherol or glutathione, nor the activities of glutathione peroxidase, reductase or transferase. The results of this study indicate that the 'in vivo' administration of dehydroepiandrosterone increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia.

scholarly journals Damage to DNA concurrent with lipid peroxidation in rat liver slices

1988 ◽  
Vol 252 (3) ◽  
pp. 893-896 ◽  
Author(s):  
C G Fraga ◽  
A L Tappel
Keyword(s):  
Lipid Peroxidation ◽  
Dna Damage ◽  
Rat Liver ◽  
Incubation Time ◽  
Ferrous Iron ◽  
Thiobarbituric Acid ◽  
Butylated Hydroxytoluene ◽  
Thiobarbituric Acid Reactive Substances ◽  
Butyl Hydroperoxide ◽  
Liver Slices

Lipid peroxidation and DNA damage were evaluated in liver slices incubated for 2 h at 37 degrees C with 1 mM-t-butyl hydroperoxide (t-BOOH), 1 mM-BrCCl3 or 50 microM-ferrous iron. t-BOOH induced the greatest amount of damage to DNA and increased the production of thiobarbituric acid-reactive substances (TBARS). Both phenomena depended on the incubation time. Ferrous iron induced both DNA damage and TBARS production, and BrCCl3 did not induce significant DNA damage and was the weakest TBARS inducer. Butylated hydroxytoluene at 1 mM inhibited both DNA damage and TBARS production. DNA damage and lipid peroxidation in liver slices were correlated, indicating that these events were concurrent.

scholarly journals CHARACTERISTICS CHANGES IN PRO-OXIDANT-ANTIOXIDANT STATUS IN PATIENTS WITH ACUTE LEUKEMIA DURING CHEMOTHERAPY

2020 ◽  
Vol 20 (1) ◽  
pp. 23-28
Author(s):  
H.S. Maslova ◽  
I.M. Skrypnyk ◽  
O.F. Hopko
Keyword(s):  
Lipid Peroxidation ◽  
Acute Myeloid Leukemia ◽  
Acute Lymphoblastic Leukemia ◽  
Acute Leukemia ◽  
Catalase Activity ◽  
Myeloid Leukemia ◽  
Lymphoblastic Leukemia ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Acute Myeloid

Changes in the processes of lipid peroxidation and antioxidant system activity are involved in the pathogenesis of carcinogenesis and can affect tumor resistance to chemotherapy. The aim of this study to investigate the nature of changes in pro-oxidant-antioxidant status in patients with acute leukemia during remission induction chemotherapy.  Materials and methods. The study involved 42 patients with newly diagnosed acute leukemia, 22 of them were diagnosed to have acute myeloid leukemia and 20 patients had acute lymphoblastic leukemia. The age range was 18-58 years, there were 19 women (45.2%) and 23 men (54.8%). The patients were divided into two groups: I (n=22) included patients with acute myeloid leukemia, who had chemotherapy modes "7+3" and "5+2" for variants M0-2 and "7+3+etoposide" or "5+2+etoposide" for M4-5 variants; II (n=20) group included patients with acute lymphoblastic leukemia, who received chemotherapy according to D. Hoelzer protocol. Hemogram parameters (red blood cells, hemoglobin, white blood cells, platelets) were evaluated at baseline and on the 28th day of chemotherapy. The concentration of thiobarbituric acid reactive substances and catalase activity in the blood serum were assessed as well. Examination of acute myeloid leukemia patients was performed before the chemotherapy, on the 4th and 28th days since chemotherapy started; acute lymphoblastic leukemia patients were examined before chemotherapy, on the 23rd and 28th days. The group of healthy individuals consisted of 20 persons, including 9 (45%) women and 11 (55%) men, aged 22-26 years. Results. The detailed clinical picture of acute leukemia was accompanied by typical changes in hemogram in the patients of both test groups, and namely, by the development of leukocytosis, anemia, thrombocytopenia. At the same time, the patients with acute myeloid leukemia and acute lymphoblastic leukemia demonstrated an increased concentration of thiobarbituric acid reactive substances in 1.8 and 1.89 times, respectively (p<0.05) that was accompanied by an increased serum catalase activity in 1.96 and 1.8 times, respectively (p<0.05) compared to healthy individuals. During "7+3" chemotherapy, acute myeloid leukemia patients were found to show thiobarbituric acid reactive substances increased in 1.9 times on the 4th day of treatment and decreased on the 28th day.The patients with acute lymphoblastic leukemia managed according to the D. Hoelzer protocol demonstrated an increased concentration of thiobarbituric acid reactive substances in the blood serum in 1.33 times on the 23rd day of treatment (p<0.05), maintaining this level up to the 28th day. The catalase activity in the patients of the comparison groups did not change. Conclusion. The debut of acute leukemia is accompanied by activation of lipid peroxidation and antioxidant system enzymes. Сhemotherapy promotes the shift of the prooxidant-antioxidant equilibrium towards the lipid peroxidation activation.

scholarly journals Antioxidant Action of Solid Preparation of Xingnaojing in SHRSP

2013 ◽  
Vol 8 (5) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Yang Liu ◽  
Naomi Yasui ◽  
Aya Kishimoto ◽  
Jian-ning Sun ◽  
Katsumi Ikeda
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Status ◽  
Total Antioxidant Status ◽  
Thiobarbituric Acid ◽  
Antioxidant Effect ◽  
Antioxidant Action ◽  
Thiobarbituric Acid Reactive Substances ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Total Antioxidant

We investigated the antioxidant action of a solid preparation of Xingnaojing (XNJ) and ascorbic acid (AA) in stroke-prone spontaneously hypertensive rats (SHRSP). The total antioxidant states in the plasma, systolic blood pressure, and heart rate were measured every 2 weeks, and lipid peroxidation, expressed as thiobarbituric acid-reactive substances in plasma, was measured in the 6th week. The results showed that AA and XNJ significantly increased the total antioxidant status in plasma and reduced malondialdehyde in the plasma. These data suggest that during 6-week administration, XNJ has antioxidant action on SHRSP, which may relate to its generalized inhibition of lipid peroxidation and promotion of the total antioxidant state. These results demonstrated that orally treated XNJ has an antioxidant effect on SHRSP plasma.

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