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1.
Weanling rats were fed one of 3 diets containing 0, 11 or 200 international units (IU) dl-α-tocopherol acetate/kg diet for
4 weeks. Following this period, the drinking water was replaced with an 18% solution of ethanol (v/v). An isocaloric D-glucose
solution was substituted for the drinking water of a control group of rats fed the vitamin-E-deficient diet for 4 weeks. The
4 treatment groups were maintained on the diet and drinking regimen for 20 weeks. Basal levels of expired pentane were determined
at weeks 0, 1, 3, 5, 7 and 9. Chronic ethanol consumption did not influence basal pentane production during the 9-week treatment.
Basal levels of expired pentane were affected by dietary vitamin E. Rats supplemented with vitamin E had basal pentane levels
less than one-half of the level of rats fed a vitamin-E-deficient diet (p<0.001). After 14 weeks of treatment, the 2 groups of rats fed a vitamin-E-deficient diet were administered p.o. an acute
dose of 6 g of ethanol/kg body wt. Pentane expired above basal levels during the following 4-hr period correlated with the
amount of hepatic triglycerides determined at the conclusion of the experiment. The etiology of ethanol toxicity is a complex
and multifactorial system made up to many biological variables that influence lipid peroxidation. The appropriate choices
of experimental designs and methods are important in examining the role of lipid peroxidation. 相似文献
2.
The hypothesis that pentane is an in vivo product of lipid peroxidation was confirmed by a study of the effects of a nonbiological
antioxidant on pentane production in rats fed a diet deficient in vitamin E and supplemented with 0.01% N,N′-diphenyl-p-phenylenediamine
(DPPD). Seven rats were fed a vitamin E-deficient diet starting at 3 wk of age. After 5 wk, 0.01% DPPD was added to the diets
of three rats (group DPPD) while the diet of the other four rats remained unchanged (group OE). Within 2 wk of the diet change,
rats in group DPPD exhaled 65% less pentane than rats of the same age in group OE. After 5 wk of being fed the DPPD-supplemented
diet, rats in group DPPD were again fed the basal vitamin E-deficient diet; within 3 wk, these rats produced pentane levels
similar to those of rats in group OE. The effects of vitamin E depletion and repletion on in vivo lipid peroxidation in rats
were also studied. Three groups of three rats each were initially fed a vitamin E-deficient diet starting at 3 wk of age.
After 8, 8, and 5 wk of being fed this diet, the three groups were fed diets supplemented with 3.3 (group 0→3.3E), 11 (group
0→11 E), and 200 (group 200E) i.u. vitamin E acetate/kg diet, respectively. Another group of three rats (group 11 E) was fed
a diet supplemented with 11 i.u. vitamin E/kg starting at 3 wk of age for the duration of the study. There were significant
decreases in pentane production by rat groups 0→3.3E, 0→11E, and 200E within 2 wk of the change to the vitamin E-supplemented
diets. After about 5 wk of being fed their respective vitamin E-supplemented diets, pentane breath levels had stabilized.
Breath pentane levels were inversely proportional to the log of dietary vitamin E concentration. 相似文献
3.
The study investigated the relationship between lipid peroxidation and enzyme inactivation in rat hepatic microsomes and whether
prior inactivation of aldehyde dehydrogenase (ALDH) exacerbated inactivation of other enzymes. In microsomes incubated with
2.5 μM iron as ferric sulfate and 50 μM ascorbate, ALDH, glucose-6-phosphate (G6Pase) and cytochrome P450 (Cyt-P450) levels
decreased rapidly and concurrently with increased levels of thiobarbituric acid-reactive substances. Microsomal glutathioneS-transferase and nicotinamide adenine dinucleotide phosphate-cytochromec reductase were little affected during 1 hr of incubation. Addition of reduced glutathione partially protected, andN,N′-diphenyl-p-phenylenediamine and butylated hydroxytoluene completely protected microsomes against inactivation of ALDH, G6Pase and Cyt-P450,
as well as lipid peroxidation induced by iron and ascorbate. ALDH was more susceptible than G6Pase to inactivation by iron
and ascorbate, and was thus an excellent marker for oxidative stress. Inhibition of ALDH by cyanamide injection of rats exacerbated
the inactivation of G6Pase in microsomes incubated with 0.1 mM, but not 25 μM 4-hydroxynonenal (4-HN). 4-HN did not stimulate
lipid peroxidation. Thus, 4-HN may play a minor role in microsomal enzyme inactivation. In contrast, lipid, peroxyl radicals
play an important role in microsomal enzyme inactivation, as evidenced by the prevention of both lipid peroxidation and enzyme
inactivation by chain-breaking antioxidants. 相似文献
4.
One useful method to monitor in vivo lipid peroxidation is the measurement of volatile hydrocarbons, mainly pentane and ethane,
that derive from unsaturated fatty acid hydroperoxides. Vitamin E, the biological antioxidant, inhibits lipid peroxidation
and the production of pentane and ethane. The rates of pentane production by male Sprague-Dawley rats fed a diet that contained
10% vitamin E-stripped corn oil and 0, 1, 3, 5 or 10 IU dl-α-tocopherol acetate/kg were monitored over a 12-wk period. During
the eleventh and twelfth weeks, the rats were injected intraperitoneally with 3.3 and 13 mg of methyl ethyl ketone peroxide
(MEKP)/kg body wt, respectively. Pentane production was then measured at intervals over a 50-min period, and the total amount
of pentane produced over this time interval was estimated. An asymptotic function was found to describe the relationship between
exhaled pentane and the low levels of dietary vitamin E that were fed to the rats. As measured by pentane production, rats
had a higher minimal vitamin E requirement after they were treated with the potent peroxidation initiator MEKP than they did
prior to treatment. The level of pentane exhaled by rats injected with 13 mg MEKP/kg body wt was significantly correlated
with kidney and spleen tocopherol levels. 相似文献
5.
When highly unsaturated fatty acids are added to cell cultures, it can become important to include antioxidants in the culture
medium to prevent cytotoxic peroxidation. To find an optimal antioxidant for this purpose, the effect of 50 μM α-tocopherol,
γ-tocopherol, α-tocopheryl acetate, α-tocopheryl acid succinate, or α-tocopheryl phosphate, or of 1 μMN,N′-diphenyl-1,4-phenylenediamine, was investigated with respect to the agent's ability to prevent lactate dehydrogenase leakage
in long-term rat hepatocyte cultures supplemented with 0.5 mM highly unsaturated fatty acids. Formation of thiobarbituric
acid reactive substances in the cultures was also measured. α-Tocopheryl acid succinate was found to be the most effective
cytoprotective compound, followed byN,N′-diphenyl-1,4-phenylenediamine, α-tocopherol, γ-tocopherol and α-tocopheryl acetate, and α-tocopheryl phosphate was without
effect. 相似文献
6.
Factors involved in reduced glutathione (GSH) and vitamin E-mediated inhibition of NADPH-dependent rat liver microsomal lipid
peroxidation were examined. Lipid peroxidation was monitored over a time-course of 180 min by thiobarbituric acid reactive
product formation. The addition of 5 mM GSH to the reaction system containing microsomes from rats fed a diet supplemented
with 150 IU/kg of α-tocopherol acetate for eight weeks produced a lag in peroxidation of >30 min. This effect was not observed
for microsomes prepared from rats fed a diet deficient in vitamin E. Indeed, a prooxidant effect of 5 mM GSH was observed
in assays containing microsomes from rats fed a diet deficient in vitamin E. The inhibition by GSH of lipid peroxidation in
microsomes prepared from livers of vitamin E supplemented rats was not restricted by its availability, for it was found that
approximately 92% of the GSH remained in the reduced form after 60 min. Additional experiments revealed that the α-tocopherol
content of peroxidizing microsomes decreased rapidly in the absence of GSH. The addition of 5 mM GSH to the assay system markedly
depressed the loss of microsomal α-tocopherol. The results ofin vivo labeling of liver microsomes with [14C] α-tocopherol demonstrated that i) GSH addition to thein vitro peroxidizing medium reduced the disappearance of α-tocopherol, and ii) a compound that interfered with the determination
of α-tocopherol was separated by HPLC and was not an oxidation product of α-tocopherol. A portion of the microsomal14C-labeled α-tocopherol was converted to an unidentified product with HPLC retention characteristics that was similar, but
not identical, to α-tocopherol quinone. 相似文献
7.
The effect of a single dose of ethanol on lipid peroxidation in three groups of rats fed different amounts of vitamin E was
determined by the measurement of pentane in the breath. All rats had increased pentane production above basal levels by 15
min following oral administration of 6 g ethanol/kg body wt. The increase in total pentane production during a 13-hr test
period after intragastric administration of ethanol was greater in the rats fed the vitamin E-deficient diet than in the rats,
fed vitamin E-supplemented diets (α=2P=0.02). The results support the hypothesis that acute ethanol toxicity involves lipid
peroxidation and further demonstrate the usefulness in toxicological studies of monitoring pentane as an index of lipid peroxidation
in vivo. 相似文献
8.
Anu M. Turpeinen Georg Alfthan Liisa Valsta Eino Hietanen Jukka T. Salonen Hanna Schunk Kristiina Nyyssönen Marja Mutanen 《Lipids》1995,30(6):485-492
The effects of natural mixed diets on lipid peroxidation were investigated in humans. In the first study, 59 subjects were
fed a rapeseed oil-based diet rich in monounsaturated fatty acids (MUFA) and a sunflower oil-based diet rich in polyunsaturated
fatty acids (PUFA) in a cross-over manner for three and a half weeks. The lipid peroxidation products in plasma were determined
by measuring conjugated dienes and malondialdehyde (MDA). In a second study, plasma thiobarbituric acid reactive substances
(TBARS), lipid hydroperoxides, and the susceptibility of very low density lipoprotein + low-density lipoprotein (LDL) toin vitro oxidation were measured from subjects fed similar MUFA and PUFA diets for six week diets. No significant differences in plasma
MDA or conjugated diene concentrations were found after the rapeseed oil diet or the sunflower oil diet in Study 1. In the
second study, a small but significant decrease (P<0.05) in both lipid hydroperoxides and TBARS was observed in the LDL fraction after the sunflower oil diet. Thein vitro oxidation gave opposite results, showing increased oxidation after the sunflower oil diet. Despite a high intake of α-tocopherol
during the oil peroids, no increase in plasma α-tocopherol was noticed in either study. The results suggest that moderate
changes in the fatty acid composition in the Western-type diet may be adequate to affect lipoprotein susceptibility to oxidationin vitro, but there is considerable disparity with some indices ofin vivo lipid peroxidation. 相似文献
9.
The present study investigated the dietary effect of conjugated linolenic acid (CLnA) on lipid profiles and lipid peroxidations
in alloxan-induced diabetes mellitus in rats. Diabetic rats were fed with 20% sunflower oil (diabetic control), sunflower
oil supplemented with 0.5% CLnA, sunflower oil supplemented with 0.15% α-tocopherol, and sunflower oil containing 0.25% CLnA+0.15%
α-tocopherol. The results demonstrated that 0.5% CLnA, 0.15% α-tocopherol, and 0.25% CLnA+0.15% α-tocopherol each on supplementation
significantly lowered total cholesterol and non-HDL-cholesterol in comparison with the diabetic control group. The TAG level
was significantly lowered in both the 0.15% α-tocopherol and 0.25% CLnA+0.15% α-tocopherol groups. LDL lipid peroxidation
and erythrocyte membrane lipid peroxidation were reduced significantly in each of the experimental groups vs. the control
group. The CLnA+α-tocopherol diet induced a greater reduction in membrane lipid and liver lipid peroxidation than the α-tocopherol
diet alone. In conclusion, dietary CLnA exerts antioxidant activity as evidenced by reduced lipid peroxidation in chemically
induced diabetes mellitus. 相似文献
10.
Three series of experiments demonstrated that sesame seed and its lignans cause significant elevation of α-tocopherol content
in rats. In Experiment 1, 20% sesame seed (with a negligible amount of α-tocopherol) supplementing 10 (low), 50 (normal),
or 250 (high) mg/kg α-tocopherol diets (protein and fat concentrations in diets were adjusted to 200 and 110 g/kg, respectively)
all caused a significant increase of α-tocopherol in the blood and tissue of rats. In Experiment 2, groups of rats were fed
five different diets: a vitamin E-free control diet, a low α-tocopherol diet, and three low α-tocopherol diets supplemented
with 5, 10, and 15% sesame seed. Changes in lipid peroxides in liver, red blood cell hemolysis, and pyruvate kinase activity,
as indices of vitamin E deficiency, were examined. These indices were high in the low α-tocopherol diet, whereas supplementation
with even 5% sesame seed suppressed these indices completely and caused a significant increase of α-tocopherol content in
the plasma and liver. In Experiment 3 two diets containing sesame lignan (sesaminol or sesamin) and low α-tocopherol were
tested. Results in both of the sesame lignan-fed groups were comparable to those observed in the sesame seed-fed groups as
shown in Experiment 2. These experiments indicate that sesame seed lignans enhance vitamin E activity in rats fed a low α-tocopherol
diet and cause a marked increase in α-tocopherol concentration in the blood and tissue of rats fed an α-tocopherol-containing
diet with sesame seed or its lignans. 相似文献
11.
Measurements of pentane and ethane as indices of in vivo lipid peroxidation were made on samples of breath from vitamin C-sufficient
and vitamin C-deficient guinea pigs injected with 23 μl carbon tetrachloride (CCl4)/100 g body wt. Vitamin C-deficient animals produced significantly more pentane and ethane after CCl4 treatment than did vitamin C-sufficient guinea pigs. Pretreatment of vitamin C-deficient animals with 75 mg ascorbic acid/100
g body wt significantly lowered both pentane and ethane evolution. Protection against in vivo lipid peroxidation similar to
that provided by ascorbic acid was also found when vitamin C-deficient guinea pigs were pretreated with isoascorbic acid,
reduced glutathione, α-tocopherol or β-carotene. When animals were pretreated with the radical scavenger mannitol, a protective
effect was also observed as measured by pentane evolution. 相似文献
12.
Liver microsomes and mitochondria and heart sarcosomes from rats fed diets with varying α-tocopherol concentrations and lipid
contents were peroxidized over a 6 hr time period. Lipid peroxidation was measured by absorption of oxygen, production of
thiobarbituric acid (TBA) reactants and by development of fluorescence. The spectral characteristics of the fluorescent compounds
were the same for all peroxidizing systems; the excitation maximum was 360 nm and the emission maximum was 430 nm. As time
of peroxidation increased, uptake of oxygen and production of fluorescent compounds increased. These two parameters as well
as production of TBA reactants were dependent upon dietary antioxidant and all three had an inverse relationship with the
amount of dietary α-tocopherol. The relationship between absorption of oxygen and development of fluorescent compounds was
also dependent upon dietary polyunsaturated fats (PUFA). Subcellular particles from animals fed higher levels of PUFA produced
more fluorescent products per mole of oxygen absorbed than did those from animals on a diet with lower PUFA content. TBA reacting
products increased with time during the initial phase of peroxidation: in the microsomal systems their production stabilized
or decreased by 4–6 hr of peroxidation. Using the synthetic 1-amino-3-iminopropene derivative of glycine as standard for quantitation
of fluorescence, the molar ratios of oxygen absorbed per fluorescent compound produced were calculated. This ratio for subcellular
particles isolated from rats fed diets with PUFA ratios similar to those in the average American human diet was 393∶1. The
fluorescent compounds had the same spectral characteristics as the lipofuscin pigment that accumulates in animal tissues as
a function of age, oxidative stress or antioxidant deficiency. The fluorescent molecular damage represented by that accumulated
in human heart age pigment by 50 years of age was calculated to have been caused by approximately 0.6 μmole of free radicals
per gram of heart tissue. 相似文献
13.
Harold H. Draper Sanjiv Agarwal Dagmar E. Voparil Nelson Jae Joon Wee A. K. Ghoshal Emmanual Farber 《Lipids》1995,30(10):959-961
The effect of age and peroxidative stress on the concentration of a deoxyguanosine malondialdehyde adduct (dG-MDA) in rat
tissues was investigated. Vitamin E deficiency had not effect on the dG-MDA content of liver DNA in rats fed a diet containing
10% corn oil. When 2% cod liver oil was added to this diet, the dG-MDA content of liver DNA doubled in the positive controls
fed a high level of vitamin E (100 ppm dl-α-tocopherol), and there was a further increase when vitamin E was deleted. Neither
iron nitrilotriacetate administration nor choline deficiency had any effect on the dG-MDA content of liver DNA. Carbon tetrachloride
had a lowering effect. The failure of iron or carbon tetrachloride administration and of vitamin E deficiency to increase
liver dG-MDA is consistent with their failure in previous experiments to affect the urinary excretion of dG-MDA. In contrast,
these forms of peroxidative stress produce large increments in the urinary excretion of MDA adducts with lysine, reflecting
increased formation and degradation of MDA-modified proteins. DNA appears to be protected from modification by MDA produced
at extranuclear sites. The frequency of dG-MDA in different tissues of 4-month-old rats varied markedly: brain ≫ liver > kidneys
and testes. Higher concentrations of dG-MDA were found in the liver and kidneys, but not the testes, of 25-month-old rats.
The determinants of the concentration of dG-MDA in DNA merit further investigation. 相似文献
14.
Six groups of rats were fed diets low, but adequate, in α-tocopherol but high in γ-tocopherol. The six diets differed only
in their contents (0, 0.25, 0.5, 1.0, 2.0, and 4.0 g/kg, respectively) of sesamin, a lignan from sesame oil. After four weeks
ofad libitum feeding, the rats were sacrificed and the concentrations of α- and γ-tocopherols were measured in the plasma, livers, and
lungs. Sesamin-feeding increased γ-tocopherol and γ-/α-tocopherol ratios in the plasma (P<0.05), liver (P<0.001), and lungs (P<0.001). The increase was non-significant for α-tocopherol. Thus, sesamin appears to spare γ-tocopherol in rat plasma and
tissues, and this effect persists in the presence of α-tocopherol, a known competitor to γ-tocopherol. This suggests that
the bioavailability of γ-tocopherol is enhanced in phenol-containing diets as compared with purified diets. 相似文献
15.
Malondialdehyde (MDA) production and cytosolic aldehyde dehydrogenase (ALDH) response were examined in rat liver tissues after
feeding different levels of dietary vitamin E and/or selenium and polyunsaturated fat for 12–38 wk. MDA production was significantly
increased by vitamin E deficiency or by high levels of polyunsaturated fat intake, but not by selenium deficiency. The activity
of cytosolic ALDH increased upon increased production of MDA after 12–16 wk of feeding the lipid peroxidation-inducing diets.
However, ALDH activity was suppressed after 38 wk of feeding the vitamin E-deficient diet. The results indicate that the hepatic
cytosolic ALDH may be involved in the metabolism of MDA during a relatively short-term increase inin vivo lipid peroxidation, but that ALDH activity becomes suppressed after more severein vivo lipid peroxidation has been produced. Hepatic and plasma α-tocopherol levels and lipid peroxidation products were measured
for the various dietary groups. 相似文献
16.
A method is presented for the determination of 4-hydroxy-nonenal (HNE) in tissue homogenates followingin vitro lipid peroxidation induced by iron (Fe++). NHE is measured as the pentafluorobenzyl oxime derivative using liquid chromatography thermospray mass spectrometry.In vitro metabolism of HNEvia the glutathione/glutathione-S-transferase pathway was inhibited using iodoacetic and iodobenzoic acids. The assay has been used as an indicator of the
peroxidizability of tissue samples from animals both adequate in and depleted of α-tocopherol. The concentrations of HNE produced
in tissues taken from animals depleted of α-tocopherol were found to be up to 8 times higher than those taken from animals
supplemented with α-tocopherol. 相似文献
17.
Pascale Cogrel Isabelle Morel Gerard Lescoat Martine Chevanne Pierre Brissot Pierre Cillard Josiane Cillard 《Lipids》1993,28(2):115-119
The response of normal and transformed rat hepatocytes to oxidative stress was investigated. Isolated normal rat hepatocytes
and differentiated hepatoma cells (the Fao cell line was derived from the Reuber H 35 rat hepatoma) in suspension were incubated
with the ADP/Fe3+ chelate for 30 min at 37°C. Membrane lipid oxidation was assessed by measuring (i) free malondialdehyde (MDA) production
by a high-performance liquid chromatography (HPLC) procedure, (ii) membrane fatty acid disappearance as judged by capillary
gas chromatography, and (iii) α-tocopherol oxidation as determined by HPLC and electrochemical detection. The addition of
iron led to increased MDA production in normal as well as in transformed cells, and to simultaneous consumption of polyunsaturated
fatty acids (PUFA) and α-tocopherol. In addition, in Fao cells more α-tocopherol was consumed during lipid peroxidation while
less PUFA was oxidized. Lipid peroxidation was lower in tumoral hepatocytes than in normal cells. This could be due to a difference
in membrane lipid composition because of a lower PUFA content and a higher α-tocopherol level in Fao cells. During oxidation,
Fao cells produced 1.5 to 2 times less MDA than normal cells, while in the tumoral cells the amount of oxidized PUFA having
3 or more double bonds was 7 to 8 times lower. Therefore, measuring MDA alone as an index of lipid peroxidation did not allow
for proper comparison of the membrane lipid oxidizability of transformed cellsvs. the membrane lipid oxidizability of normal cells. 相似文献
18.
For four weeks, groups of eight male and eight female F344/N rats were fed diets containing 15.5, 20, 30 or 40% of energy
(en%) as fat. The fat was composed of corn oil and beef tallow with 9 en% from linoleate in all diets. Females had greater
mean hepatic α-tocopherol levels, whereas males had greater plasma α-tocopherol and cholesterol concentrations. In males,
the plasma ratio of α-tocopherol/cholesterol was significantly greater than in females (P<0.05). Plasma α-tocopherol increased with increasing en% fat (r=0.51,P<0.001) in both sexes, but dietary fat did not alter hepatic α-tocopherol levels. These results suggest that plasma α-tocopherol
may serve as a biomarker of total dietary fat intake and that in F344/N rats gender differences affect α-tocopherol and cholesterol
status. 相似文献
19.
Beneficial effects of dietary phytic acid (myo-inositol hexaphosphate; IP6) have often been explained by its strong iron ion-chelating ability, which possibly suppresses iron ion-induced oxidative
damage in the gastrointestinal tract. Because phytic acid is hydrolyzed during digestion, this work aimed to know whether
its hydrolysis products (IP2′ IP3′, IP4′ and IP5) could still prevent iron ion-induced lipid peroxidation. Studies using liposomal membranes demonstrated that hydrolysis
products containing three or more phosphate groups are able to inhibit iron ion-induced lipid peroxidation although their
effectiveness decreased with dephosphorylation. Similarly, they also prevented iron ion-induced decomposition of phosphatidylcholine
hydroperoxide. These results demonstrate that intermediate products of phytic acid hydrolysis still possess iron ion-chelating
ability, and thus they can probably prevent iron ion-induced lipid peroxidation in biological systems. 相似文献
20.
Weanling rats were fed diets containing 10% menhaden oil (MO) or 10% corn oil-lard (1∶1, COL) with low (≤5 IU/kg) or supplementary
(35 IU/kg) vitamin E for six weeks. The rats were killed 30 min after injection with 24 mg iron/kg as ferrous chloride because
thiobarbituric acid-reactive substances (TBARS) in liver homogenates were highest at 30 min after injection of iron into rats
fed a standard diet. Tissue homogenates were used either without incubation (zero-time) or after incubation at 37°C for 1
hr. In addition to TBARS and conjugated dienes, headspace hexanal and total volatiles (TOV) determined by capillary gas chromatography
were useful indices of lipid peroxidation since they were decreased by vitamin E supplementation and were increased with increasing
iron dose. Regardless of the dietary lipid used, vitamin E supplementation decreased headspace hexanal, TOV, TBARS and conjugated
dienes in both zero-time and incubated homogenates of liver and kidney. Dietary MO increased TBARS in both zero-time and incubated
homogenates of tissue from rats injected with iron. In contrast, dietary MO decreased hexanal and TOV in incubated tissue
homogenates. The study demonstrated the usefulness and limitations of using hexanal and TOV as indices of lipid peroxidation. 相似文献