A further study on memory and learning ability and lipid peroxide content in some brain regions of vitamin E deficient rats

1990 ◽  
Vol 183 (6) ◽  
pp. 2359 ◽  
Author(s):  
M. Moriyama ◽  
N. Oda ◽  
M. Nakagawa
1967 ◽  
Vol 21 (2) ◽  
pp. 475-495 ◽  
Author(s):  
J. Bunyan ◽  
Elspeth A. Murrell ◽  
J. Green ◽  
A. T. Diplock

1. A micro-adaptation of the iodimetric method has been used to determine lipid peroxides in the tissues of vitamin E-deficient rats and chicks.2. No increases in lipid peroxide were found in liver, kidney or adipose tissue of rats with nutritional liver necrosis due to deficiency of vitamin E and selenium. When liver necrosis was induced by giving rats a casein diet and silver acetate solution to drink, the peroxide value of the adipose tissue was not increased.3. Degeneration of the testes of vitamin E-deficient rats was not accompanied by a rise in the peroxide value of the tissue lipids.4. There was an increase in cathepsin activity of the kidneys of rats displaying the phenomenon of renal autolysis (post mortem), but there was no increase in lipid peroxide content.5. No rise in lipid peroxide was found in dystrophic chick breast muscle, in cerebellum, brain and adipose tissue of chicks with encephalomalacia nor in the liver of chicks with exudative diathesis.6. In rat liver, kidney, testis and leg muscle, peroxide values in the range 10–40 µ-equiv./g lipid were found, and these values were not altered either by a substantial change in the degree of unsaturation of the dietary lipid or by the addition of vitamin E to the diet. Dietary addition of N, N'-diphenyl-p-phenylenediamine (DPPD) or 6-ethoxy-1, 2-dihydro-2,2,4-trime-thylquinoline (ethoxyquin) also failed to affect the peroxide value of liver. The possibility that lipid peroxide is a normal metabolite of these tissues is discussed.7. Peroxide values of rat adipose tissue were never found to be greater than 40 µ-equiv./g lipid and were readily decreased by the addition of vitamin E to the diet or by a decrease in the unsaturation of the dietary lipid. The peroxide content of this tissue may depend upon the up-take of peroxidized dietary lipid.8. The conclusion from this study of true lipid peroxides in animal tissues is that the biological role of vitamin E is not connected with lipid peroxidation in vivo, in agreement with our previous studies on the metabolism of the fatty acid substrates of peroxidation and of α-tocopherol and other postulated biological antioxidants.


1967 ◽  
Vol 21 (3) ◽  
pp. 671-679 ◽  
Author(s):  
M. A. Cawthorne ◽  
A. T. Diplock ◽  
I. R. Muthy ◽  
J. Bunyan ◽  
Elspeth A. Murrell ◽  
...  

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.


2010 ◽  
Vol 112 (6) ◽  
pp. 1325-1334 ◽  
Author(s):  
Ge Liang ◽  
Christopher Ward ◽  
Jun Peng ◽  
Yifan Zhao ◽  
Baosheng Huang ◽  
...  

Background We hypothesized that isoflurane has a greater potency to induce neurodegeneration than sevoflurane in the developing brains of neonatal mice based on our previous studies in cell culture. Methods We treated 7-day-old mice with either 0.75% isoflurane or 1.1% sevoflurane ( approximately 0.5 minimum alveolar concentration) for 6 h and then obtained blood and brain samples at 2 h after the anesthesia treatment for determination of neuroapoptosis in different brain regions and the neurodegenerative biomarker S100beta in the blood. The mechanisms of neurodegeneration induced by isoflurane or sevoflurane were also compared by determining protein expressions of the cell cycle and apoptosis-related proteins. In separate groups, memory and learning ability were evaluated through the use of Morris Water Maze testing in mice at postnatal day 42 after anesthesia treatment at postnatal day 7. Results Isoflurane but not sevoflurane significantly increased the neurodegenerative biomarker S100beta in the blood. Isoflurane treatments significantly increased apoptosis indicated by the activation of caspase-3 and elevation of poly-(ADP-ribose) polymerase in different brain regions. An equipotent exposure of sevoflurane tended to increase apoptosis in hippocampal and cortex areas but was significantly less potent than isoflurane. Neither isoflurane nor sevoflurane significantly changed protein levels of glyceraldehyde-3-phosphate dehydrogenase, beta-site amyloid beta-precursor protein-cleaving enzyme, and cell cycle regulatory proteins (CDK4, cyclin D1). Isoflurane and sevoflurane at the selected exposures did not significantly alter memory and learning ability. Conclusion At equipotent exposures, isoflurane has a greater potency than sevoflurane to cause neurodegeneration in the developing brains of neonatal mice.


1991 ◽  
Vol 65 (04) ◽  
pp. 411-414 ◽  
Author(s):  
Keizo Umegaki ◽  
Hiromi Saegusa ◽  
Masato Kurokawa ◽  
Tomio Ichikawa

SummaryEffects of vitamin E on platelet function and serum lipid peroxide levels were investigated in DOCA-salt hypertensive rats. In the hypertensive rats, ADP- and collagen-induced platelet aggregation in whole blood were markedly attenuated and accompanied by a reduction of serotonin content as compared with the normotensive controls. These facts indicated the appearance of exhausted platelets, which have already been activated in vivo, due to the hypertension. Platelet vitamin E levels were decreased by 50%, while serum lipid peroxide levels were increased 3.6-fold in the hypertensive rats. Vitamin E administration (10 times the dietary intake) during the experimental periods did not influence either the aggregability or the serotonin content of platelets from the hypertensive rats. However, vitamin E administration significantly prevented the elevation of serum tipid peroxides due to the hypertension. These results suggest that vitamin E administration has little effect on platelet activation in vivo due to DOCA-salt hypertension.


2002 ◽  
Vol 8 (5) ◽  
pp. 253-256 ◽  
Author(s):  
Ling Li ◽  
Zhiqiang Shen ◽  
Weimin Yang ◽  
Wanling Wu ◽  
Weiping Liu ◽  
...  

The cerebroprotective effects of copper aspirinate [dimeric copper(II) bis(o-acetoxybenzoate)] were investigated in gerbils subjected to 10-min global cerebral ischemia followed b 60-min reperfusion. The results showed that intragastric copper aspirinate (7.5, 15.0 and 30.0 mg Kg−1 ) markedly promoted the recovery of the electroencephalogram amplitude, attenuated the increase of lipid peroxide content and the decrease of superoxide dismutase activity in the cortex during ischemia-reperfusion injury. It suggested that copper aspirinate possesses potential neuroprotective properties, the mechanism of which might be related to an increase of the activity of endogenous superoxide dismutase.


2021 ◽  
Vol 2 (2) ◽  
pp. 69-73
Author(s):  
Mohaya Farzin ◽  
Parastoo Jafarzade ◽  
Niloofar Faraji ◽  
Seyedeh Maral Mousavi ◽  
Mostafa Yousefi

1998 ◽  
Vol 178 (5) ◽  
pp. 1072-1076 ◽  
Author(s):  
Eduard Gratacós ◽  
Elena Casals ◽  
Ramón Deulofeu ◽  
Vicenç Cararach ◽  
Pedro L. Alonso ◽  
...  

1989 ◽  
Vol 67 (12) ◽  
pp. 1549-1559 ◽  
Author(s):  
Madhu Gupta ◽  
Pawan K. Singal

Effects of xanthine (2 mM) and xanthine oxidase (10 U/L) perfusion on myocardial function, lipid peroxide content, high-energy phosphates and their metabolites, and ultrastructure were examined in isolated perfused rat hearts to define the time course of myocardial injury due to exogenous supply of active oxygen species. Peak-developed force and dF/dt showed a decline within 5 min and complete contractile failure was seen at 20 min. Resting tension was higher at 10 min and reached a maximum value of 400% at 40 min. These changes in contractile parameters were reduced by superoxide dismutase (1.2 × 105 U/L), catalase (2 and 4 × 104 U/L), and mannitol (10 and 20 mM). Lipid peroxide content was significantly higher at 5 min and rose continuously with xanthine – xanthine oxidase (X–XO) perfusion. A close correlation was noted (r = 0.935) between increased lipid peroxide content and a decrease in peak-developed force. Creatine phosphate and adensoine triphosphate (ATP) showed a time-dependent decrease due to X–XO perfusion. Loss of ATP also correlated (r = 0.819) with the contractile failure. Adenosine diphosphate showed an increase at 5 min followed by a decrease at 20 and 40 min. Adenosine monophosphate, adenosine, and creatine content increased with X–XO perfusion. In a semiquantitative morphometric study, significant myocardial and vascular changes became apparent only after 10 min of X–XO perfusion. When a 5-min perfusion with X–XO was followed by a control perfusion, a recovery of developed force and normal structure was noted at 40 min. These data show that X–XO induced contractile failure involves partially reduced forms of oxygen such as superoxide, hydroxyl radicals, and hydrogen peroxide. The negative inotropic effect of a vascular supply of these active oxygen species may be related to increased lipid peroxidation as well as the loss of high-energy phosphates. Structural damage to myocytes and blood vessels and a rise in resting tension were delayed events requiring a continuous and longer exposure to radical species.Key words: myocardial failure, oxygen radicals, lipid peroxidation, myocardial high-energy phosphates, myocardial cell damage, antioxidant protection.


2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Makoto Suzuki ◽  
D. Craig Willcox ◽  
Matthew W. Rosenbaum ◽  
Bradley J. Willcox

Background. The Free Radical Theory of Aging mechanistically links oxidative stress to aging. Okinawa has among the world's longest-lived populations but oxidative stress in this population has not been well characterized.Methods. We compared plasma lipid peroxide (LPO) and vitamin E—plasma and intracellular tocopherol levels (total α, β, and γ), in centenarians with younger controls.Results. Both LPO and vitamin E tocopherols were lower in centenarians, with the exception of intracellular β-tocopherol, which was significantly higher in centenarians versus younger controls. There were no significant differences between age groups for tocopherol: cholesterol and tocopherol: LPO ratios. Correlations were found between α-Tocopherol and LPO in septuagenarians but not in centenarians.Conclusions. The low plasma level of LPO in Okinawan centenarians, compared to younger controls, argues for protection against oxidative stress in the centenarian population and is consistent with the predictions of the Free Radical Theory of Aging. However, the present work does not strongly support a role for vitamin E in this phenomenon. The role of intracellular β-tocopherol deserves additional study. More research is needed on the contribution of oxidative stress and antioxidants to human longevity.


Sign in / Sign up

Export Citation Format

Share Document