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.

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.

DNA stability and lipid peroxidation in vitamin E–deficient rats in vivo and colon cells in vitro

2004 ◽  
Vol 44 (4) ◽  
pp. 195-203 ◽  
Author(s):  
S. J. Duthie ◽  
P. T. Gardner ◽  
P. C. Morrice ◽  
S. G. Wood ◽  
L. Pirie ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Dna Stability ◽  
Colon Cells

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.

Metallothionein response to stress in rats: role in free radical scavenging

1988 ◽  
Vol 255 (4) ◽  
pp. E518-E524 ◽  
Author(s):  
J. Hidalgo ◽  
L. Campmany ◽  
M. Borras ◽  
J. S. Garvey ◽  
A. Armario
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Liver Lipid ◽  
Radical Scavenging ◽  
Antioxidant Vitamin ◽  
Response To Stress ◽  
Liver Lipid Peroxidation

The possibility that liver metallothionein (MT) can function as an antioxidant in vivo has been studied in the rat. It was found that the stress of food and water deprivation with or without physical immobilization consistently increased liver lipid peroxidation (LLP), suggesting that liver MT induction by stress might be related to the stress-induced LLP. This was supported by results with the lipid peroxidation promoter dimethyl sulfoxide (DMSO) and the natural antioxidant vitamin E. Whereas DMSO administration increased LLP levels in basal and stress situations, vitamin E decreased them. Liver MT levels were increased by DMSO in basal and stress situations, whereas they were decreased by vitamin E during stress. These in vivo results are consistent with an antioxidant role of liver MT suggested by previous in vitro results. However, liver MT preinduction by Zn treatment did not result in a lower MT response to stress. Instead a positive synergistic effect between Zn and stress appeared to be present. This result indicates that the mechanism of action of MT as antioxidant remains unclear.

Improved cardiac performance after ischemia in aged rats supplemented with vitamin E and α-lipoic acid

2000 ◽  
Vol 279 (6) ◽  
pp. R2149-R2155 ◽  
Author(s):  
Jeff S. Coombes ◽  
Scott K. Powers ◽  
Karyn L. Hamilton ◽  
Haydar A. Demirel ◽  
R. Andrew Shanely ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Myocardial Ischemia ◽  
Lipoic Acid ◽  
Ischemia Reperfusion ◽  
Control Diet ◽  
Cardiac Performance ◽  
Aged Rats

The purpose of these experiments was to examine the effects of dietary antioxidant supplementation with vitamin E (VE) and α-lipoic acid (α-LA) on biochemical and physiological responses to in vivo myocardial ischemia-reperfusion (I-R) in aged rats. Male Fischer-334 rats (18 mo old) were assigned to either 1) a control diet (CON) or 2) a VE and α-LA supplemented diet (ANTIOX). After a 14-wk feeding period, animals in each group underwent an in vivo I-R protocol (25 min of myocardial ischemia and 15 min of reperfusion). During reperfusion, peak arterial pressure was significantly higher ( P < 0.05) in ANTIOX animals compared with CON diet animals. I-R resulted in a significant increase ( P < 0.05) in myocardial lipid peroxidation in CON diet animals but not in ANTIOX animals. Compared with ANTIOX animals, heart homogenates from CON animals experienced significantly less ( P < 0.05) oxidative damage when exposed to five different in vitro radical producing systems. These data indicate that dietary supplementation with VE and α-LA protects the aged rat heart from I-R-induced lipid peroxidation by scavenging numerous reactive oxygen species. Importantly, this protection is associated with improved cardiac performance during reperfusion.

Comparison of the effects of dietary vitamin E on in vivo and in vitro parameters of lipid peroxidation in the rabbit

1995 ◽  
Vol 19 (5) ◽  
pp. 617-626 ◽  
Author(s):  
Sheila A. Wiseman ◽  
Marline A.P. Van Den Boom ◽  
Nanneke J. De Fouw ◽  
Marjolein Groot Wassink ◽  
Jos A.F.Op Den Kamp ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Dietary Vitamin

scholarly journals Vitamin E and hepatotoxic agents

1969 ◽  
Vol 23 (2) ◽  
pp. 297-307 ◽  
Author(s):  
J. Green ◽  
J. Bunyan ◽  
M. A. Cawthorne ◽  
A. T. Diplock
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Rat Liver ◽  
Protective Action ◽  
Lipid Peroxides ◽  
Ultraviolet Region ◽  
Intraperitoneal Dose ◽  
And Control

1. It has been suggested that carbon tetrachloride damages rat liver by accelerating processes of lipid peroxidation at subcellular sites and that the protective action of vitamin E is due to its functioning as an antioxidant in vivo. Direct evidence for these mechanisms in vivo has been sought and is critically examined.2. The increased production of malondialdehyde by rat liver microsomal fractions during incubation with CCl4 was shown to be a function of the vitamin E status of the rat and of an in vitro reaction, which could not be correlated with the hepatotoxic action of CCI4.3. Evidence for the production of lipid peroxides by CCl4 in the livers of vitamin E-deficient and vitamin E-supplemented rats was sought (I) by measurement of ultraviolet spectral changes ('diene' formation) and (2) by direct micro-iodimetric determination of the peroxide. No differences in peroxide content were found between CC14-treated and control rats, nor were the spectrophotometric changes in the ultraviolet region related to the presence of vitamin E.4. The effect of CCI4 (2.0 ml/kg orally) on ATP levels in rat liver was studied at intervals from 3 to 68 h. The primary lesion leading to necrosis and fat accumulation after CCl4 treatment occurred many hours before the eventual slight decline in ATP. Although the levels of ATP were somewhat higher in vitamin E-deficient rats, vitamin E did not prevent the slight decline in ATP that took place. Since ATP is known to be highly sensitive to peroxidation, the results suggest that lipid peroxidation is not the primary event in CCl4 poisoning.5. The effect of CC14on the metabolism of [14C]D-α-tocopherol in the rat was studied. A single intraperitoneal dose of CCl4 (2.0 m/kg) did not increase the destruction of α-tocopherol in the liver or carcass after 24 h. Three smaller daily doses of CC14 (0.25 ml/kg) also did not increase α-tocopherol catabolism; on the contrary, significantly more α-tocopherol was found in the livers of rats treated with CCI4. These results suggest that CCl4 does not increase lipid peroxidation in vivo.

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