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

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.

Oxidation of alpha 1-protease inhibitor: role of lipid peroxidation products

1989 ◽  
Vol 66 (5) ◽  
pp. 2211-2215 ◽  
Author(s):  
V. Mohsenin ◽  
J. L. Gee
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Stearic Acid ◽  
Protease Inhibitor ◽  
Alpha Tocopherol ◽  
Inhibitory Capacity ◽  
Buffer Control

Previously we demonstrated that in vivo exposure of humans to NO2 resulted in significant inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the bronchoalveolar lavage fluid. However, alpha 1-PI retains its elastase inhibitory activity in vitro when exposed to 10 times the concentration of NO2 used in vivo. We suggested exogenous oxidants such as O2 and NO2 exert their effect in vivo in part through lipid peroxidation. We investigated the mechanism of inactivation of alpha 1-PI in the presence or absence of lipids under oxidant atmosphere. alpha 1-PI in solutions containing phosphate buffer (control), 0.1 mM stearic acid (saturated fatty acid, 18:0), or 0.1 mM linoleic acid (polyunsaturated fatty acid, 18:2) was exposed to either N2 or NO2 (50 ppm for 4 h). Elastase inhibitory capacity of alpha 1-PI was significantly diminished in the presence of 0.1 mM linoleic acid and under NO2 atmosphere (75 +/- 8% of control, P less than 0.01), whereas there was no change in elastase inhibitory capacity of alpha 1-PI in the presence or absence (buffer only) of 0.1 mM stearic acid under a similar condition (109 +/- 11 and 94 +/- 6%, respectively). The inactivated alpha 1-PI as the result of peroxidized lipid could be reactivated by dithiothreitol and methionine sulfoxide peptide reductase, suggesting oxidation of methionine residue at the elastase inhibitory site. Furthermore the inhibitory effect of peroxidized lipid on alpha 1-PI could be prevented by glutathione and glutathione peroxidase and to some extent by alpha-tocopherol.

Hypolipidemic drugs reduce lipoprotein susceptibility to undergo lipid peroxidation: in vitro and ex vivo studies

1992 ◽  
Vol 93 (1-2) ◽  
pp. 105-113 ◽  
Author(s):  
Ron Hoffman ◽  
Gerald J. Brook ◽  
Michael Aviram
Keyword(s):  
Lipid Peroxidation ◽  
Ex Vivo ◽  
Hypolipidemic Drugs

Mécanisme moléculaire de l'effet protecteur de la vitamine E dans l'athérosclérose

2002 ◽  
Vol 80 (7) ◽  
pp. 662-669 ◽  
Author(s):  
Abdelouahed Khalil
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Vascular Diseases ◽  
Epidemiologic Studies ◽  
Low Density Lipoproteins ◽  
Alpha Tocopherol ◽  
Low Density ◽  
Prooxidant Effect

Oxidation of low-density lipoproteins constitutes the first step of a very complex process leading to atherosclerosis. Vitamin E, and principally alpha-tocopherol, is considered as the principal inhibitor of lipid peroxidation. Some studies showed the beneficial role of vitamin E in the prevention and reduction of atherosclerosis and its associated pathologies. However, other in vitro studies advance a prooxidant role of vitamin E. The results of the epidemiologic studies are difficult to generalize without taking account of the clinical randomized tests. In this work, we reviewed the principal studies devoted to the role of vitamin E and discussed the assumption of a prooxidant effect of this molecule.Key words: vitamin E, low-density lipoproteins (LDL), lipid peroxidation, cardio-vascular diseases.

scholarly journals Suppression of lipid peroxidation in adrenal microsomes following ACTH administration to guinea pigs

2001 ◽  
Vol 168 (2) ◽  
pp. 333-338 ◽  
Author(s):  
JM Burczynski ◽  
JM Voigt ◽  
PA Longhurst ◽  
HD Colby ◽  
Keyword(s):  
Lipid Peroxidation ◽  
Guinea Pigs ◽  
Beta Carotene ◽  
Alpha Tocopherol ◽  
Inhibitory Effects ◽  
Hormone Production ◽  
Adrenal Hormone ◽  
Acth Treatment ◽  
Dose Dependent

Previous studies demonstrated high levels of lipid peroxidation (LP) in the guinea pig adrenal cortex. The present studies were done to determine if adrenal LP activity was influenced by ACTH, the major hormonal regulator of the gland. Guinea pigs were treated with ACTH for 1, 3 or 7 days. In addition, some guinea pigs received ACTH for 7 days and were killed 3 or 7 days later. After treatment, adrenal microsomal fractions were prepared and incubated in vitro with 1 mM ferrous sulfate to initiate LP. ACTH treatment caused a progressive decrease in adrenal LP; activity was almost totally inhibited within 3 days. The inhibitory effects of ACTH on LP were dose-dependent. Following cessation of ACTH treatment, adrenal LP gradually returned toward control levels. Microsomal concentrations of linoleic acid, a major substrate for adrenal LP, were increased by ACTH administration and then also returned to control levels after cessation of treatment. There were no significant changes in adrenal alpha-tocopherol or beta-carotene concentrations resulting from ACTH treatment. The results indicate that ACTH has a role in the regulation of adrenal LP. The actions of ACTH cannot be attributed to an increase in adrenal content of the antioxidants, alpha-tocopherol and beta-carotene, or to a decrease in LP substrate. The actions of ACTH to inhibit LP may contribute to an increase in adrenal hormone production by protecting steroidogenic enzymes from peroxidative degradation.

Estimate of antioxidant capacity and lipid peroxidation in plasma of healthy subjects

Open Medicine ◽  
2006 ◽  
Vol 1 (1) ◽  
pp. 23-34
Author(s):  
Anna Gorąca ◽  
Beata Skibska
Keyword(s):  
Ascorbic Acid ◽  
Uric Acid ◽  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Plasma Concentrations ◽  
Beta Carotene ◽  
Alpha Tocopherol ◽  
Elderly Subjects ◽  
Total Antioxidant

AbstractSerum contains various antioxidant molecules that may provide important protection against free radical attack. The aim of this work was to assess the total antioxidant capacity of plasma and a marker of lipid per oxidation [(thiobarbituric acid-reactive substances (TBARS)] in plasma of healthy smoking and non-smoking young and elderly subjects. In addition, we investigated plasma concentrations of α-tocopherol, β-carotene, and ascorbic acid. In in vitro experiments, the effects of exogenous compounds (ascorbic acid, uric acid, Trolox) on total ferric-reducing activity of plasma (FRAP) were also tested. We demonstrated that total antioxidant capacity of plasma obtained from healthy non-smoking young subjects was significantly higher than plasma antioxidant capacity of smoking elderly subjects. The concentration of TBARS in young non-smoking volunteers was lower than that in young smokers. The concentration of TBARS in elderly non-smoking volunteers was lower than in elderly smokers. Plasma concentrations of alpha-tocopherol, beta-carotene and ascorbic acid were significantly lower in elderly smoker than in elderly non-smokers of the same age. No difference in the plasma levels of alpha-tocopherol, beta-carotene and ascorbic acid were found in 22-year-old smoking and non-smoking subjects. In vitro addition of ascorbic acid, uric acid, or Trolox to plasma samples significantly increased their total antioxidant capacity. Decrease of FRAP values and increase of TBARS concentrations is a significant physiologic condition of the aging process. Supplementation of antioxidants could be useful for the enhancement of antioxidant screen in plasma.

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