scholarly journals Inhibition of the iron-catalysed formation of hydroxyl radicals from superoxide and of lipid peroxidation by desferrioxamine

1979 ◽  
Vol 184 (2) ◽  
pp. 469-472 ◽  
Author(s):  
J M C Gutteridge ◽  
R Richmond ◽  
B Halliwell
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Acetic Acid ◽  
Hydroxyl Radicals ◽  
Iron Chelator ◽  
Clinical Use ◽  
Membrane Phospholipids ◽  
Iron Salt ◽  
Iron Salts

The peroxidation of membrane phospholipids induced in vitro by ascorbic acid or by dialuric acid (hydroxybarbituric acid) does not occur in the absence of traces of metal ions. Peroxidation induced by adding iron salts to phospholipids can either be promoted or inhibited by the chelators EDTA, diethylenetriaminepenta-acetic acid and bathophenanthrolinesulphonate, depending on the ratio [chelator]/[iron salt]. The iron chelator desferrioxamine inhibits peroxidation at all concentrations tested, and it also inhibits the iron-catalysed formation of hydroxyl radicals (OH.) from superoxide (O2-.). Since desferrioxamine is approved for clinical use, it might prove a valuable tool in the treatment of inflammation, poisoning by autoxidizable molecules and radiation damage.

Phytochemical analysis and nephroprotective effect of cactus (Opuntia ficus-indica) cladodes on sodium dichromate-induced kidney injury in rats

2019 ◽  
Vol 44 (3) ◽  
pp. 239-247
Author(s):  
Mbarka Hfaiedh ◽  
Dalel Brahmi ◽  
Mohamed Nizar Zourgui ◽  
Lazhar Zourgui
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Wistar Rat ◽  
Phytochemical Analysis ◽  
Sodium Dichromate ◽  
Opuntia Ficus Indica

Environmental and occupational exposure to chromium compounds, especially hexavalent chromium, is widely recognized as potentially nephrotoxic in humans and animals. The present study aimed to assess the efficacy of cactus (Opuntia ficus-indica) against sodium dichromate-induced nephrotoxicity, oxidative stress, and genotoxicity. Cactus cladodes extract (CCE) was phytochemically studied and tested in vitro for its potential antioxidant activities. Additionally, the preventive effect of CCE against sodium dichromate-induced renal dysfunction in a Wistar rat model (24 rats) was evaluated. For this purpose, CCE at a dose of 100 mg/kg was orally administered, followed by 10 mg/kg sodium dichromate (intraperitoneal injection). After 40 days of treatment, the rats were sacrificed, and the kidneys were excised for histological, lipid peroxidation, and antioxidant enzyme analyses. The phenol, flavonoid, tannin, ascorbic acid, and carotenoid contents of CCE were considered to be important. Our analyses showed that 1 mL of CCE was equivalent to 982.5 ± 1.79 μg of gallic acid, 294.37 ± 0.84 μg of rutin, 234.78 ± 0.24 μg of catechin, 204.34 ± 1.53 μg of ascorbic acid, and 3.14 ± 0.51 μg of β-carotene. In vivo, pretreatment with CCE was found to provide significant protection against sodium dichromate-induced nephrotoxicity by inhibiting lipid peroxidation, preserving normal antioxidant activities, and protecting renal tissues from lesions and DNA damage. The nephroprotective potential of CCE against sodium dichromate toxicity might be due to its antioxidant properties.

Cardioselective Ammonium, Phosphonium, and Sulfonium Analogs of .alpha.-Tocopherol and Ascorbic Acid That Inhibit in Vitro and ex Vivo Lipid Peroxidation and Scavenge Superoxide Radicals

1995 ◽  
Vol 38 (15) ◽  
pp. 2880-2886 ◽  
Author(s):  
J. Martin Grisar ◽  
Gilbert Marciniak ◽  
Frank N. Bolkenius ◽  
Joelle Verne-Mismer ◽  
Eugene R. Wagner
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Ex Vivo ◽  
Superoxide Radicals ◽  
Alpha Tocopherol

scholarly journals In-vitro and In-vivo Antioxidant Activity of Ethanol Leaf Extract of Justicia carnea

2020 ◽  
pp. 48-60
Author(s):  
Udedi Stanley Chidi ◽  
Ani Onuabuchi Nnenna ◽  
Asogwa Kingsley Kelechi ◽  
Maduji Fitzcharles Chijindu ◽  
Okafor Clinton Nebolisa
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Activity ◽  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Leaf Extract ◽  
Dpph Radical ◽  
Β Carotene ◽  
In Vitro Antioxidant Activity

This study investigated the in-vitro antioxidant activity of ethanol leaf extract of Justicia carnea and its effect on antioxidant status of alloxan-induced diabetic albino rats. The in-vitro antioxidant activity was assayed by determining the total phenol, flavonoids, ascorbic acid, β-carotene and lycopene contents and by using 2,2 diphenyl-1-picrylhydrazyl (DPPH) radical, reducing antioxidant power and inhibition of lipid peroxidation antioxidant systems. Oxidative stress was produced in rats by single intraperitoneal injection of 150 mg/kg alloxan and serum concentration of malonaldehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were determined. Five experimental groups of rats (n=6) were used for the study. Two groups of diabetic rats received oral daily doses of 100 and 200 mg/kg Justicia carnea leaf extract respectively while gilbenclamide (5 mg/ml); a standard diabetic drug was also given to a specific group for 14 days. From the result, the leaf extract contained a higher concentration of flavonoids followed byphenols, ascorbic acid, lycopene and β-carotene. The extract displayed more potent reducing power ability with EC50 of 40 µg/ml compared to BHA (EC50 of 400µg/ml). The percentage DPPH radical scavenging activity of the extract was also higher with EC50 of 200µg/ml and increased with increase in concentration while BHA had EC50of 320µg/ml. The inhibition of lipid peroxidation also increased with increase in concentration with EC50 of 58µg/ml and comparable with BHA (EC50=60µg/ml). The effect of the plant extract on antioxidant enzyme activities was concentration-dependent. Administration of 100mg/kg of the plant extract resulted in a significant decrease (p<0.05) in serum MDA concentration, while 200 mg/kg of the extract caused a significant (p˂0.05) increase in superoxide dismutase (SOD) and catalase activities with a non-significant increase (p>0.05) in the serum level of MDA when compared with the diabetic untreated group. These findings suggest that ethanol leaf extract of Justicia carnea have antioxidant properties and could handle diabetes-induced oxidative stress.

scholarly journals L-Ascorbic Acid Inhibits UVA-Induced Lipid Peroxidation and Secretion of IL-1α and IL-6 in Cultured Human Keratinocytes In Vitro

1997 ◽  
Vol 108 (3) ◽  
pp. 302-306 ◽  
Author(s):  
Beate Tebbe ◽  
Shuling Wu ◽  
Christoph C. Geilen ◽  
Jürgen Eberle ◽  
Vitam Kodelja ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Human Keratinocytes

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (3) ◽  
pp. 671-679 ◽  
Author(s):  
M. A. Cawthorne ◽  
A. T. Diplock ◽  
I. R. Muthy ◽  
J. Bunyan ◽  
Elspeth A. Murrell ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Vitamin E ◽  
Lipid Peroxide ◽  
Toxic Effects ◽  
Peroxide Content ◽  
In Vitro Techniques ◽  
Sulphydryl Compounds

1. Vitamin E-deficient rats were found to be more susceptible than vitamin E-supplemented controls to the toxic effects of hyperbaric oxygen (60 lb/in.2 for 20 min). This agrees with the findings of other workers.2. Hyperbaric O2 treatment did not increase the metabolic destruction of a small amount (46.65 μg) of [14C-5-Me]D-α-tocopherol given to adult vitamin E-deficient rats 24 h previously. The O2 treatment also did not affect the soluble sulphydryl compounds and ascorbic acid of rat liver, nor the percentag haemolysis in vivo of rat blood.3. Hyperbaric O2 treatment did not increase the true lipid peroxide content of rat brain, compared to control rats treated with hyperbaric air, which has no toxic effects. Increases in ‘lipid peroxidation’ reported by previous workers are considered to have been due to the use of inadequate controls (untreated rats) and of in vitro techniques that are open to criticism.4. The toxic effects of hyperbaric O2 in the vitamin E-deficient rat cannot be attributed to peroxidation in vivo.5. Vitamin E was not found to protect rats against the effects of reduced O2 tension (anoxic anoxia). This finding contrasts with some reports by earlier workers. Reduced O2 tension had no effect on the metabolism of radioactive tocopherol, on blood haemolysis in vivo, or on the soluble sulphydryl compounds and ascorbic acid of liver.

scholarly journals Prophylactic neuroprotection against stroke: Low-dose, prolonged treatment with deferoxamine or deferasirox establishes prolonged neuroprotection independent of HIF-1 function

2011 ◽  
Vol 31 (6) ◽  
pp. 1412-1423 ◽  
Author(s):  
Yanxin Zhao ◽  
David A Rempe
Keyword(s):  
High Risk ◽  
Stroke Volume ◽  
Low Dose ◽  
Chronic Administration ◽  
Iron Chelator ◽  
Prolonged Treatment ◽  
Clinical Use ◽  
High Doses ◽  
Dependent Mechanism

Prophylactic neuroprotection against stroke could reduce stroke burden in thousands of patients at high risk of stroke, including those with recent transient ischemic attacks (TIAs). Prolyl hydroxylase inhibitors (PHIs), such as deferoxamine (DFO), reduce stroke volume when administered at high doses in the peristroke period, which is largely mediated by the hypoxia-inducible transcription factor (HIF-1). Yet, in vitro experiments suggest that PHIs may also induce neuroprotection independent of HIF-1. In this study, we examine chronic, prophylactic, low-dose treatment with DFO, or another iron chelator deferasirox (DFR), to determine whether they are neuroprotective with this paradigm and mediate their effects through a HIF-1-dependent mechanism. In fact, prophylactic administration of low-dose DFO or DFR significantly reduces stroke volume. Surprisingly, DFO remained neuroprotective in mice haploinsufficient for HIF-1 (HIF-1 +/ –) and transgenic mice with conditional loss of HIF-1 function in neurons and astrocytes. Similarly, DFR was neuroprotective in HIF-1 +/ mice. Neither DFO nor DFR induced expression of HIF-1 targets. Thus, low-dose chronic administration of DFO or DFR induced a prolonged neuroprotective state independent of HIF-1 function. As DFR is an orally administered and well-tolerated medication in clinical use, it has promise for prophylaxis against stroke in patients at high risk of stroke.

scholarly journals Sterodin®, a novel immunostimulating drug: Some toxicological and pharmacological evaluations in vivo, and drug-lipid interaction studies in vitro

2009 ◽  
Vol 59 (3) ◽  
pp. 325-334 ◽  
Author(s):  
Sarbani Ray ◽  
Partha Roy ◽  
Supratim Ray
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Blood Cells ◽  
White Blood Cells ◽  
Pharmacological Properties ◽  
Lipid Source ◽  
Interaction Studies ◽  
Lipid Interaction

Sterodin®, a novel immunostimulating drug: Some toxicological and pharmacological evaluations in vivo, and drug-lipid interaction studies in vitro Sterodin® is a novel non-specific immunostimulating drug produced by a combination of bile lipids and bacterial metabolites. In the present study, we investigated some of its (i) toxicological and (ii) pharmacological properties in vivo, and (iii) drug-lipid interaction (lipid peroxidation) in vitro. We also evaluated the possible (iv) Sterodin®-induced lipid peroxidation as well as the effect of ascorbic acid on this peroxidation. We found LD50 of Sterodin® to be 31.50 mL kg-1 body mass. In male albino mice, Sterodin® increased the total white blood cells and neutrophils count by 59 and 26%, respectively, on the 6th day, compared to day 0 after injection and stimulated phagocytic activity in vivo. We used goat liver as lipid source in drug-lipid interaction studies in vitro. Our experiments show that Sterodin® induces lipid peroxidation, which was prevented by ascorbic acid.

Lipid peroxidation of skeletal muscle: an in vitro study

1983 ◽  
Vol 3 (7) ◽  
pp. 609-619 ◽  
Author(s):  
M. J. Jackson ◽  
D. A. Jones ◽  
R. H. T. Edwards
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Free Radical ◽  
Vitamin E ◽  
Hydroxyl Radicals ◽  
Muscle Tissue ◽  
In Vitro Study ◽  
Muscle Tissues ◽  
In Vitro Technique

The process of lipid peroxidation of skeletal muscle has been examined in vitro by monitoring the autoxidation of skeletal-muscle homogenates. Skeletal-muscle tissue has been shown to have considerable capacity for autoxidation and the process has been found to be initiated by a free-radical-mediated mechanism, critically dependent on the presence of free iron in the homogenate. The initiating radicals have not been firmly identified, but the results suggest that neither superoxide or hydroxyl radicals are involved. An in vitro technique for assessment of the antioxidant capacity of muscle tissue has also been developed which is capable of demonstrating differences between muscle tissues with differing vitamin E contents.

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