Lipid Peroxides and Nutrition

Author(s):  
Takashi Kaneda ◽  
Teruo Miyazawa
Keyword(s):  
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.


1993 ◽  
Vol 70 (04) ◽  
pp. 707-711 ◽  
Author(s):  
Andrew D Blann ◽  
Charles N McCollum

SummaryThe effect of smoking on the blood vessel intima was examined by comparing indices of endothelial activity in serum from smokers with that from non-smokers. Serum from smokers contained higher levels of von Willebrand factor (p <0.01), the smoking markers cotinine (p <0.02) and thiocyanate (p <0.01), and was more cytotoxic to endothelial cells in vitro (p <0.02) than serum from non-smokers. The acute effects of smoking two unfiltered medium tar cigarettes was to briefly increase von Willebrand factor (p <0.001) and cytotoxicity of serum to endothelial cells in vitro (p <0.005), but lipid peroxides or thiocyanate were not increased by this short exposure to tobacco smoke. Although there were correlations between von Willebrand factor and smokers consumption of cigarettes (r = 0.28, p <0.02), number of years smoking (r = 0.41, p <0.001) and cotinine (r = 0.45, p <0.01), the tissue culture of endothelial cells with physiological levels of thiocyanate or nicotine suggested that these two smoking markers were not cytotoxic. They are therefore unlikely to be directly responsible for increased von Willebrand factor in the serum of smokers. We suggest that smoking exerts a deleterious influence on the endothelium and that the mechanism is complex.


1979 ◽  
Vol 88 (2) ◽  
pp. 856-858 ◽  
Author(s):  
V. E. Kagan ◽  
V. Z. Lankin ◽  
A. A. Shvedova ◽  
K. N. Novikov ◽  
S. K. Dobrina ◽  
...  

1995 ◽  
Vol 115 ◽  
pp. S76
Author(s):  
M. Zamaklar ◽  
N. Lalić ◽  
S. Kapor ◽  
V. Sajdl ◽  
P. Djodjević

1996 ◽  
Vol 39 (7) ◽  
pp. 588 ◽  
Author(s):  
D.R. Evans ◽  
P.Y. Puczkowski ◽  
M.J. Brandsma ◽  
J.S. Mahadik ◽  
S.P. Mahadik

2004 ◽  
Vol 19 (1) ◽  
pp. 79-82 ◽  
Author(s):  
D. Sreeramulu ◽  
B. A. Ramalakshmi ◽  
N. Balakrishna ◽  
N. Raghuramulu

Author(s):  
D Özmen ◽  
I Mutaf ◽  
B Özmen ◽  
J Mentes ◽  
O Bayindir

This study aims to explore the role of reactive oxygen radicals in the genesis of diabetic cataract. Lipid peroxide (LPO) concentrations in senile ( n = 30) and diabetic ( n = 14) cataractous lenses, were determined as thiobarbituric acid-reactive substances (TBARS) by a method modified from Satoh and Yagi, and reduced glutathione (GSH) concentrations were measured according to Beutler. Lens LPO levels (mean, SD; nmol TBARS/g protein) were significantly higher in diabetics (107·54, 18·12) than senile cataractous subjects (53·54, 15·48) ( P < 0·0001). Lens GSH levels (mean, SD; nmol/g protein) showed no significant difference between diabetics (4·29, 2·05) and senile cataractous subjects (4·68, 3·12). These results suggest that free radical damage is more effective in the genesis of diabetic cataract than in senile cataract.


2000 ◽  
Vol 352 (1) ◽  
pp. 27-36 ◽  
Author(s):  
Lixia TANG ◽  
Yong ZHANG ◽  
Zhongming QIAN ◽  
Xun SHEN

The mechanism of Fe2+-initiated lipid peroxidation in a liposomal system was studied. It was found that a second addition of ferrous ions within the latent period lengthened the time lag before lipid peroxidation started. The apparent time lag depended on the total dose of Fe2+ whenever the second dose of Fe2+ was added, which indicates that Fe2+ has a dual function: to initiate lipid peroxidation on one hand and suppress the species responsible for the initiation of the peroxidation on the other. When the pre-existing lipid peroxides (LOOH) were removed by incorporating triphenylphosphine into liposomes, Fe2+ could no longer initiate lipid peroxidation and the acceleration of Fe2+ oxidation by the liposomes disappeared. However, when extra LOOH were introduced into liposomes, both enhancement of the lipid peroxidation and shortening of the latent period were observed. When the scavenger of lipid peroxyl radicals (LOOP), N,N´-diphenyl-p-phenylene-diamine, was incorporated into liposomes, neither initiation of the lipid peroxidation nor acceleration of the Fe2+ oxidation could be detected. The results may suggest that both the pre-existing LOOH and LOOP are necessary for the initiation of lipid peroxidation. The latter comes initially from the decomposition of the pre-existing LOOH by Fe2+ and can be scavenged by its reaction with Fe2+. Only when Fe2+ is oxidized to such a degree that LOOP is no longer effectively suppressed does lipid peroxidation start. It seems that by taking the reactions of Fe2+ with LOOH and LOOP into account, the basic chemistry in lipid peroxidation can explain fairly well the controversial phenomena observed in Fe2+-initiated lipid peroxidation, such as the existence of a latent period, the critical ratio of Fe2+ to lipid and the required oxidation of Fe2+.


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