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1.
Effect of sesamin on mitochondrial and peroxisomal β-oxidation of arachidonic and eicosapentaenoic acids in rat liver 总被引:1,自引:0,他引:1
The effects of dietary sesamin on the hepatic metabolism of arachidonic (AA) and eicosapentaenoic (EPA) acids, were investigated
with respect to their β-oxidation and secretion as triacylglycerol (TG). For 2 wk, rats were fed three types of dietary oils:
(i) corn oil (control) group; (ii) FPA group: FPA ethyl esters/rapeseed oil=2∶3; (iii) AA group: AA ethyl esters/palm oil/perilla
oil=2∶2∶1, with or without 0.5% (w/w) of sesamin. Dietary sesamin significantly increased the activities of hepatic mitochondrial
and peroxisomal fatty acid oxidation enzymes (mitochondrial carnitine acyltransferase I, acyl-CoA dehydrogenase, and peroxisomal
acyl-CoA oxidase). Dietary FPA increased mitochondrial carnitine acyltransferase I and peroxisomal acyl-CoA oxidase. Dietary
AA, however, had an effect on peroxisomal acyl-CoA oxidase only. In whole liver and the TG fraction, EPA and AA concentrations
were significantly increased by dietary EPA and AA, respectively, and were decreased by dietary sesamin. In hepatic mitochondria
and peroxisomes, EPA concentration was increased by dietary EPA, but AA was not changed by dietary AA. The addition of dietary
sesamin to the EPA-supplemented diet significantly decreased the EPA concentration compared to concentrations found with consumption
of dietary EPA alone. These results suggest that sesamin increased β-oxidation enzyme activities and reduced hepatic EPA and
AA concentrations by degradation. The stimulating effect of sesamin on β-oxidation, however, was more significant in the EPA
group than in the AA group. Hepatic AA concentration was altered by the joint effect of sesamin through esterification into
TG and the stimulation of β-oxidation. 相似文献
2.
NMRI mice were fed diets supplemented with 0.05, 0.2, or 2% (w/w) docosahexaenoic acid (DHA), a polyunsaturated fatty acid
present in fish oil, for 3 d, 3 wk, or 3 mon. The doses of DHA were chosen to supply the mice with concentrations of DHA which
approximate those that have been reported to be beneficial to patients with peroxisomal disease. Diets containing 0.05 or
0.2% DHA did not change hepatic, myocardial, and renal catalase (EC 1.11.1.6) activity except for a slight but significant
increase (to 120%) in myocardial catalase activity in mice treated with the 0.05% DHA diet for 3 mon. A diet with 2% DHA induced
myocardial catalase activity to 150% after both 3 d and 3 wk of administration. In the liver of mice fed this diet for 3 wk,
hepatic catalase activity was increased to 140% while no induction of palmitoyl-CoA oxidase (EC 1.3.99.3), urate oxidase (EC
1.7.3.3), andl-α-hydroxyisovalerate oxidase (EC 1.1.3.a) was observed. With the light microscope, no changes in peroxisomal morphology were
visually evaluated in catalase stained sections of liver, myocardium, and kidney of mice fed either diet. Our results show
that in healthy mice a low dietary DHA dose (<0.2%; this corresponds to a dose prescribed to peroxisomal patients) has no
effect on several hepatic peroxisomal H2O2-producing enzymes, including the rate-limiting enzyme of the peroxisomal fatty acid β-oxidation. This may indicate that such
a DHA dose will not add a strong load on the often disturbed fatty acid metabolism in the liver of patients with peroxisomal
disorders. 相似文献
3.
Repeated administration of highly purified eicosapentaenoic acid (as ethyl ester) resulted in a decrease in plasma triglycerides
and high density lipoprotein (HDL) cholesterol. This was accompanied by a stimulation in the activities of carnitine palmitoyltransferase,
fatty acyl-CoA oxidase and peroxisomal β-oxidation in the liver. The results suggest that the triglyceride-lowering effect
observed with eicosapentaenoic acid may be due to a reduced supply of fatty acids for hepatic triglyceride synthesis because
of increased fatty acid oxidation. Eicosapentaenoic acid feeding marginally affected the triglyceride content of heart and
mitochondrial and peroxisomal enzyme activities. 相似文献
4.
The aim of the present study was to investigate whether eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) was responsible
for the triglyceride-lowering effect of fish oil. In rats fed a single dose of EPA as ethyl ester (EPA-EE), the plasma concentration
of triglycerides was decreased at 8 h after acute administration. This was accompanied by an increased hepatic fatty acid
oxidation and mitochondrial 2,4-dienoyl-CoA reductase activity. The steady-state level of 2,4-dienoyl-CoA reductase mRNA increased
in parallel with the enzyme activity. An increased hepatic long-chain acyl-CoA content, but a reduced amount of hepatic malonyl-CoA,
was obtained at 8 h after acute EPA-EE treatment. On EPA-EE supplementation, both EPA (20:5n-3) and docosapentaenoic acid
(DPA, 22:5n-3) increased in the liver, whereas the hepatic DHA (22:6n-3) concentration was unchanged. On DHA-EE supplementation
retroconversion to EPA occurred. No statistically significant differences were found, however, for mitochondrial enzyme activities,
malonyl-CoA, long-chain acyl-CoA, plasma lipid levels, and the amount of cellular fatty acids between DHA-EE treated rats
and their controls at any time point studied. In cultured rat hepatocytes, the oxidation of [1-14C]palmitic acid was reduced by DHA, whereas it was stimulated by EPA. In thein vivo studies, the activities of phosphatidate phosphohydrolase and acetyl-CoA carboxylase were unaffected after acute EPA-EE and
DHA-EE administration, but the fatty acyl-CoA oxidase, the rate-limiting enzyme in peroxisomal fatty acid oxidation, was increased
after feeding these n-3 fatty acids. The hypocholesterolemic properties of EPA-EE may be due to decreased 3-hydroxy-3-methylglutaryl-CoA
reductase activity. Furthermore, replacement of the ordinary fatty acids, i.e., the monoenes (16:1n-7, 18:1n-7, and 18:1n-9)
with EPA and some conversion to DPA concomitant with increased fatty acid oxidation is probably the mechanism leading to changed
fatty acid composition. In contrast, DHA does not stimulate fatty acid oxidation and, consequently, no such displacement mechanism
operates. In conclusion, we have obtained evidence that EPA, and not DHA, is the fatty acid primarily responsible for the
triglyceride-lowering effect of fish oil in rats. 相似文献
5.
The effect of eicosapentaenoic acid (EPA) on fatty acid oxidation and on key enzymes of triglyceride metabolism and lipogenesis
was investigated in the liver of rats. Repeated administration of EPA to normolipidemic rats resulted in a time-dependent
decrease in plasma triglycerides, phospholipids and cholesterol. The triglyceride-lowering effect was observed after one day
of feeding whereas lowering of plasma cholesterol and phospholipids was observed after five days of treatment. The triglyceride
content of liver was reduced after two-day treatment. At that time, increased mitochondrial fatty acid oxidation occurred
whereas mitochondrial and microsomal glycerophosphate acyltransferase was inhibited. The phosphatidate phosphohydrolase activity
was unchanged. Adenosine triphosphate:citrate lyase, acetyl-CoA carboxylase, fatty acid synthetase and glucose-6-phosphate
dehydrogenase were inhibited during the 15 d of EPA treatment whereas peroxisomal β-oxidation was increased. At one day of
feeding, however, when the hypotriglyceridemic effect was established, the lipogenic enzyme activities were reduced to the
same extent in palmitic acid-treated animals as in EPA-treated rats. In cultured rat hepatocytes, the oxidation of [14C]palmitic acid to carbon dioxide and acid-soluble products was stimulated in the presence of EPA. These results suggest that
the instant hypolipidemia in rats given EPA could be explained at least in part by a sudden increase in mitochondrial fatty
acid oxidation, thereby reducing the availability of fatty acids for lipid synthesis in the liver for export,e.g., in the form of very low density lipoproteins, even before EPA induced peroxisomal fatty acid oxidation, reduced triglyceride
biosynthesis and diminished lipogenesis. 相似文献
6.
Differential utilization of eicosapentaenoic acid and docosahexaenoic acid in human plasma 总被引:1,自引:0,他引:1
It has recently been shown that the ω3 fatty acid status in humans can be predicted by the concentration of eicosapentaenoic
(EPA) and docosahexaenoic (DHA) acids in plasma phospholipids [Bjerve, K.S., Brubakk, A.M., Fougner, K.J., Johnsen, H., Midjthell,
K., and Vik, T. (1993)Am. J. Clin. Nutr., in press]. In countries with low intake of ω3 fatty acids, the level of EPA in plasma phospholipids is often only about
one-fifth the concentration of DHA. The purpose of this study was to investigate whether this difference in the concentration
of these two fatty acids was due to a selective loss of EPA relative to DHA or to a lower dietary intake of EPA. Seven female
volunteers ingested four grams of MaxEPA daily for 2 wk and in the following 4 wk they ate a diet almost completely devoid
of the long-chain ω3 fatty acids. The concentrations of the ω3 fatty acids in the plasma cholesteryl esters, triglycerides
and phospholipids and the high density lipoprotein phospholipids were examined at weekly intervals throughout the study. There
was a more rapid rise in the concentration of EPA than in DHA levels in the supplementation period in all lipid fractions,
but there was a disproportionate rise in DHA relative to EPA in the plasma lipids compared with the ratio in the supplement.
In the depletion phase there was a rapid disappearance of EPA from all fractions, such that pre-trial levels were reached
by one week post-supplementation. The disappearance of DHA was slower, particularly for the plasma phospholipids: at 4 wk
post-supplementation, the DHA concentration in this fraction was still 40% above the pre-trial value. It is suggested that
the low plasma EPA values relative to DHA are the result of increased β-oxidation of EPA and/or low dietary intake, rather
than a rapid conversion of EPA to DHA. One practical result of this experiment is that, compared with DHA, the maintenance
of increased EPA levels in plasma (and therefore tissues) would require constant inputs of EPA due to its more rapid loss
from the plasma. 相似文献
7.
Earl H. Harrison J. Scott Lane Scott Luking Marc J. Van Rafelghem Melvin E. Andersen 《Lipids》1988,23(2):115-119
Perfluoro-n-decanoic acid (PFDA) produces toxic effects in rodents similar to those caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin.
A single, intraperitoneal dose (50 mg/kg) of PFDA to Sprague-Dawley rats caused disruption of the endoplasmic reticulum, mitochondrial
swelling and increases in intracellular lipid droplets in hepatocytes similar to effects reported previously in dioxin toxicity.
PFDA treatment led to large decreases in the activity of plasma membrane alkaline phosphodiesterase and mitochondrial cytochrome
c oxidase without affecting lysosomal N-acetyl-β-glucoaminidase, endoplasmic reticulum NADPH-cytochrome c reductase or peroxisomal
catalase activities. PFDA treatment led to moderate peroxisome proliferation and to very large (20–40-fold) increases in the
activity of fatty acyl-CoA oxidase, the rate-limiting enzyme in the peroxisomal system of fatty acid β-oxidation. 相似文献
8.
Maud Sabine Cansell Aurélie Battin Pascal Degrace Joseph Gresti Pierre Clouet Nicole Combe 《Lipids》2009,44(3):237-247
The study was undertaken to determine whether eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3),
esterified in phospholipids (PL) as liposomes or in triglycerides (TG) as oil, exhibited comparable fates in liver lipids
and whether these fates were associated with gene expressions related to fatty acid (FA) metabolism. PL and TG mixtures with
close contents in EPA and DHA were administered to rats over 2 weeks. Most relevant events occurred after 3 days for both
treatments. At that time, liposomes, compared with oil, increased the liver content in PL with a FA composition enriched in
n-6 FA, comparable in DHA and much lower in EPA. Moreover, liposomes increased the activity and mRNA levels of carnitine palmitoyltransferase
(CPT) I. In contrast, fish oil exerted opposite effects on CPT I and increased the genic expression of lipogenic enzymes.
Liposomes, unlike fish oil, apparently increased the mRNA levels of acyl-CoA oxidase and the activity of the peroxisomal FA-oxidising
system. Concomitantly, mRNA levels of hepatic lipoprotein receptors were increased with both diets, but intracellular proteins
involved in free FA uptake and lipid synthesis were up-regulated only with liposome-treated rats. The quasi absence of EPA
in hepatic PL of liposome-treated rats on the short term could result from increased β-oxidation activities through metabolic
regulations induced by more available free EPA and other PUFA. 相似文献
9.
Changes of the transcriptional and fatty acid profiles in response to n−3 fatty acids in SH-SY5Y neuroblastoma cells 总被引:2,自引:2,他引:0
Synthesis of docosahexaenoic acid (DHA) from its metabolic precursors contributes to membrane incorporation of this FA within the central nervous system. Although cultured neural cells are able to produce DHA, the membrane DHA contents resulting from metabolic conversion do not match the high values of those resulting from supplementation with preformed DHA. We have examined whether the DHA precursors down-regulate the incorporation of newly formed DHA within human neuroblastoma cells. SH-SY5Y cells were incubated with gradual doses of alpha-linolenic acid (alpha-LNA), EPA, or docosapentaenoic acid (DPA), and the incorporation of DHA into ethanolamine glycerophospholipids was analyzed as a reflection of synthesizing activity. The incorporation of EPA, DPA, and preformed DHA followed a dose-response saturating curve, whereas that of DHA synthesized either from alpha-LNA, EPA, or DPA peaked at concentrations of precursors below 15-30 microM and sharply decreased with higher doses. The mRNA encoding for six FA metabolism genes were quantified using real-time PCR. Two enzymes of the peroxisomal beta-oxidation, L-bifunctional protein and peroxisomal acyl-CoA oxidase, were expressed at lower levels than fatty acyl-CoA ligase 3 (FACL3) and delta6-desaturase (delta6-D). The delta6-D mRNA slightly increased between 16 and 48 h of culture, and this effect was abolished in the presence of 70 microM EPA. In contrast, the EPA treatment resulted in a time-dependent increase of FACL3 mRNA. The terminal step of DHA synthesis seems to form a "metabolic bottleneck," resulting in accretion of EPA and DPA when the precursor concentration exceeds a specific threshold value. We conclude that the critical precursor- concentration window of responsiveness may originate from the low basal expression level of peroxisomal enzymes. 相似文献
10.
The purpose of this study was to investigate in healthy humans the effect of eicosapentaenoic acid (EPA) and docosahexaenoic
acid (DHA) intake, alone or in combination with dL-α-tocopherol acetate (vitamin E) supplements on lipid peroxidation. Eightly
men were randomly assigned in a double-blind fashion to take daily for 6 wk either menhaden oil (6.26 g, n−3 fatty acids)
or olive oil supplements with either vitamin E (900 IU) or its placebo. Antioxidant vitamins, phospholipid composition, malondialdehyde
(MDA), and lipid peroxides were measured in the plasma at baseline and week 6. At the same time, breath alkane output was
measured. Plasma α-tocopherol concentration increased in those receiving vitamin E (P<0.0001). In those supplemented with n−3 fatty acids, EPA and DHA increased in plasma phospholipids (P<0.0001) and plasma MDA and lipid peroxides increased (P<0.001 and P<0.05, respectively). Breath alkane output did not change significantly and vitamin E intake did not prevent the increase
in lipid peroxidation during menhaden oil supplementation. The results demonstrate that supplementing the diet with n−3 fatty
acids resulted in an increase in lipid peroxidation, as measured by plasma MDA release and lipid peroxide products, which
was not suppressed by vitamin E supplementation. 相似文献
11.
Fourteen healthy male volunteers were given two separate high-saturated-fat meals with and without the addition of 4 g highly
purified ethyl esters of either eicosapentaenoic acid (EPA) (95% pure, n=7) or docosahexaenoic acid (DHA) (90% pure, n=7) supplied as 1-g capsules each containing 3.4 mg vitamin F. The chylomicrons were isolated 6 h after the meals, at peak concentrations
of n−3 fatty acids (FA). Addition of n−3 FA with the meal caused a 10.4-fold increase in the concentration of n−3 FA in chylomicrons
compared to the saturated fat meal without addition of n−3 FA. After the saturated-fat meal, the concentration of thiobarbituric
acid-reactive substances (TBARS) was 327.6±34.6 nmol/mmol triacylglycerol (TAG), which increased to 1015.8±212.0 nmol/mmol
TAG (P<0.0001, n=14) after EPA and DHA were added to the meal. There was no significant correlation between the concentrations of TBARS and
vitamin E in the chylomicrons collected 6 h after the test meal. The present findings demonstrate an immediate increase in
chylomicron peroxidation ex vivo provided by intake of highly purified n−3 FA. The capsular content of vitamin E was absorbed into chylomicrons, but the amount
of vitamin E was apparently not sufficient to protect chylomicrons against lipid peroxidation ex vivo. Daily intake of 4 g n−3 FA either as EPA or DHA for 5 wk did not change the plasma concentration of TBARS. Although not
significantly different between groups, DHA supplementation decreased total glutathione in plasma (P<0.05) and EPA supplementation increased plasma concentration of vitamin E (P<0.05). The other lipid-soluble and polar antioxidants in plasma remained unchanged during 5 wk of intervention with highly
purified n−3 FA. 相似文献
12.
Weanling rats were fed a riboflavin-deficient diet. The mitochondrial fatty acid oxidation in liver was depressed in riboflavin
deficiency but restored after supplementation of riboflavin. Among the enzymes involved in this system, only the acyl-CoA
dehydrogenase (EC 1.3.99.2 and 1.3.99.3) activities varied with the change in fatty acid oxidation. An accumulation of the
apoforms of acyl-CoA dehydrogenases was found in riboflavin deficiency. The levels of electron transfer flavoprotein and other
enzymes involved in the β-oxidation system remained unchanged. The peroxisomal fatty acid oxidation and levels of individual
enzymes of this system remained constant. No accumulation of the apoform of acyl-CoA oxidase was observed under simple, riboflavin-deficient
conditions. However, accumulation of a large amount of apo-acyl-CoA oxidase was observed when the peroxisomal system was induced
by administration of a peroxisome proliferator, di(2-ethylhexyl)phthalate, under riboflavin-deficient conditions. 相似文献
13.
Gabriella Calviello Paola Palozza Piergiorgio Franceschelli Gianna Maria Bartoli 《Lipids》1997,32(10):1075-1083
In view of the promising future for use of n-3 polyunsaturated fatty acids (PUFA) in the prevention of cancer and cardiovascular
diseases, it is necessary to ensure that their consumption does not result in detrimental oxidative effects. The aim of the
present work was to test a hypothesis that low doses of eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) do not induce
harmful modifications of oxidative cell metabolism, as modifications of membrane fatty acid composition occur. Wistar rats
received by gavage oleic acid, EPA, or DHA (360 mg/kg body weight/day) for a period of 1 or 4 wk. Fatty acid composition and
α-tocopherol content were determined for plasma, red blood cell (RBC) membranes, and liver, kidney, lung, and heart microsomal
membranes. Susceptibility to oxidative stress induced by tert-butylhydroperoxide was measured in RBC. EPA treatment increased EPA and docosapentaenoic acid (DPA) content in plasma and
in all the membranes studied. DHA treatment mainly increased DHA content. Both treatments decreased arachidonic acid content
and n-6/n-3 PUFA ratio in the membranes, without modifying the Unsaturation Index. No changes in tissue α-tocopherol content
and in RBC susceptibility to oxidative stress were induced by either EPA or DHA treatment. The data suggest that EPA and DHA
treatments can substantially modify membrane fatty acids, with-out increasing susceptibility to oxidative stress, when administered
at low doses. This opens the possibility for use of low doses of n-3 PUFA for chemoprevention without risk of detrimental
secondary effects. 相似文献
14.
The aim of the present study was to investigate the hepatic regulation and β-oxidation of long-chain fatty acids in peroxisomes
and mitochondria, after 3-thia- tetradecylthioacetic acid (C14-S-acetic acid) treatment. When palmitoyl-CoA and palmitoyl-l-carnitine were used as substrates, hepatic formation of acid-soluble products was significantly increased in C14-S-acetic acid treated rats. Administration of C14-S-acetic acid resulted in increased enzyme activity and mRNA levels of hepatic mitochondrial carnitine palmitoyltransferase
(CPT)-II. CPT-II activity correlated with both palmitoyl-CoA and palmitoyl-l-carnitine oxidation in rats treated with different chain-length 3-thia fatty acids. CPT-I activity and mRNA levels were,
however, marginally affected. The hepatic CPT-II activity was mainly localized in the mitochondrial fraction, whereas the
CPT-I activity was enriched in the mitochondrial, peroxisomal, and microsomal fractions. In C14-S-acetic acid-treated rats, the specific activity of peroxisomal and microsomal CPT-I increased, whereas the mitochondrial
activity tended to decrease. C14-S-Acetyl-CoA inhibited CPT-I activity in vitro. The sensitivity of CPT-I to malonyl-CoA was unchanged, and the hepatic malonyl-CoA concentration increased after C14-S-acetic acid treatment. The mRNA levels of acetyl-CoA carboxylase increased. In hepatocytes cultured from palmitic acid-
and C14-S-acetic acid-treated rats, the CPT-I inhibitor etomoxir inhibited the formation of acid-soluble products 91 and 21%, respectively.
In contrast to 3-thia fatty acid treatment, eicosapentaenoic acid treatment and starvation increased the mitochondrial CPT-I
activity and reduced its malonyl-CoA sensitivity. Palmitoyl-l-carnitine oxidation and CPT-II activity were, however, unchanged after either EPA treatment or starvation. The results from
this study open the possibility that the rate control of mitochondrial β-oxidation under mitochondrion and peroxisome proliferation
is distributed between an enzyme or enzymes of the pathway beyond the CPT-I site after 3-thia fatty acid treatment. It is
suggested that fatty acids are partly oxidized in the peroxisomes before entering the mitochondria as acylcarnitines for further
oxidation. 相似文献
15.
Eicosapentaenoic and docosahexaenoic acid affect mitochondrial and peroxisomal fatty acid oxidation in relation to substrate preference 总被引:1,自引:0,他引:1
Decreased triacylglycerol synthesis within hepatocytes due to decreased diacylglycerol acyltransferase (DGAT) activity has
been suggested to be an important mechanism by which diets rich in fish oil lower plasma triacylglycerol levels. New findings
suggest that eicosapentaenoic acid (EPA), and not docosahexaenoic acid (DHA), lowers plasma triacylglycerol by increased mitochondrial
fatty acid oxidation and decreased availability of fatty acids for triacylglycerol synthesis. To contribute to the understanding
of the triacylglycerol-lowering mechanism of fish oil, the different metabolic properties of EPA and DHA were studied in rat
liver parenchymal cells and isolated rat liver organelles. EPA-CoA was a poorer substrate than DHA-CoA for DGAT in isolated
rat liver microsomes, and in the presence of EPA, a markedly lower value for the triacyl[3H]glycerol/diacyl[3H]glycerol ratio was observed. The distribution of [1-14C]palmitic acid was shifted from incorporation into secreted glycerolipids toward oxidation in the presence of EPA (but not
DHA) in rat liver parenchymal cells. [1-14C]EPA was oxidized to a much greater extent than [1-14C]DHA in rat liver parenchymal cells, isolated peroxisomes, and especially in purified mitochondria. As the oxidation of EPA
was more effective and sensitive to the CPT-I inhibitor, etomoxir, when measured in a combination of both mitochondria and
peroxisomes, we hypothesized that both are involved in EPA oxidation, whereas DHA mainly is oxidized in peroxisomes. In rats,
EPA treatment lowered plasma triacylglycerol and increased hepatic mitochondrial fatty acid oxidation and carnitine palmitoyltransferase
(CPT)-I activity in both the presence and absence of malonyl-CoA. Whereas only EPA treatment increased the mRNA levels of
CPT-I, DHA treatment increased the mRNA levels of peroxisomal fatty acyl-CoA oxidase and fatty acid binding protein more effectively
than EPA treatment. In conclusion, EPA and DHA affect cellular organelles in relation to their substrate preference. The present
study strongly supports the hypothesis that EPA, and not DHA, lowers plasma triacylglycerol by increased mitochondrial fatty
acid oxidation. 相似文献
16.
Specific susceptibility of docosahexaenoic acid and eicosapentaenoic acid to peroxidation in aqueous solution 总被引:3,自引:0,他引:3
The peroxidation of different polyunsaturated fatty acids (PUFA) after photoirradiation in aqueous solution was evaluated
by measuring fatty acid loss and malonaldehyde production in medium. The oxidation rates of eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA), two highly unsaturated fatty acids of the n−3 series, were surprisingly lower (14 and 22%, respectively)
than the oxidation rates of linoleic, α-linolenic, γ-linolenic, dihomo γ-linolenic, and arachidonic acids (62–90%). The quantities
of malonaldehyde (MA) produced were assayed simultaneously by gas chromatography (GC) and high performance liquid chromatography
(HPLC). MA production was found to be related to both the degree of unsaturation and the metabolic series of the fatty acid.
The maximum value was observed with arachidonic acid (MA production from 2 mM arachidonic acid in aqueous solution was estimated
at 44.9±6.0 μM by GC and 46.8 ±4.0 μM by HPLC). Eicosapentaenoic acid and docosahexaenoic acid produced lower MA quantities
compared to arachidonic acid (MA production from 2 mM EPA and 2 mM DHA was estimated at 17.9±1.5 μM and 37.9±0.7 μM, respectively,
by GC, and 26.3±4.9 μM and 37.3±4.2 μM, respectively, by HPLC). The MA yield, defined as the amount of MA (nmols) produced
per 100 nanomoles of oxidized fatty acid, was used to express the susceptibility of individual PUFA to peroxidation. The MA
yield correlated well with the degree of unsaturation, but was independent of carbon chain length and metabolic series. The
study suggests that adequate assessment of lipid peroxidation cannot be achieved by measuring MA formation alone, but it also
requires knowledge of the fatty acid composition of the system studied. 相似文献
17.
Helvi M. Vidgren Jyrki J. Ågren Ursula Schwab Tiina Rissanen Osmo Hänninen Matti I. J. Uusitupa 《Lipids》1997,32(7):697-705
The effects of n-3 fatty acid supplementation in the form of fresh fish, fish oil, and docosahexaenoic acid (DHA) oil on the
fatty acid composition of plasma lipid fractions, and platelets and erythrocyte membranes of young healthy male students were
examined. Altogether 59 subjects (aged 19–32 yr, body mass index 16.8–31.3 kg/m2) were randomized into the following diet groups: (i) control group; (ii) fish diet group eating fish meals five times per
week [0.38±0.04 g eicosapentaenoic acid (EPA) and 0.67±0.09 g DHA per day]; (iii) DHA oil group taking algae-derived DHA oil
capsules (1.68 g/d DHA oil group taking algae-derived DHA oil capsules (1.68 g/d DHA in triglyceride form); and (iv) fish
oil group (1.33 g EPA and 0.95 g DHA/d as free fatty acids) for 14 wk. The fatty acid composition of plasma lipids, platelets,
and erythrocyte membranes was analyzed by gas chromatography. The subjects kept 4-d food records four times during the study
to estimate the intake of nutrients. In the fish diet, in DHA oil, and in fish oil groups, the amounts of n-3 fatty acids
increased and those of n-6 fatty acids decreased significantly in plasma lipid fractions and in platelets and erythrocyte
membranes. A positive relationship was shown between the total n-3 polyunsaturated fatty acids (PUFA) and EPA and DHA intake
and the increase in total n-3 PUFA and EPA and DHA in all lipid fractions analyzed. DHA was preferentially incorporated into
phospholipid (PL) and triglyceride (TG) and there was very little uptake in cholesterol ester (CE), while EPA was preferentially
incorporated into PL and CE. The proportion of EPA in plasma lipids and platelets and erythrocyte membranes increased also
by DHA supplementation, and the proportion of linoleic acid increased in platelets and erythrocyte membranes in the DHA oil
group as well. These results suggest retroconversion of DHA to EPA and that DHA also interferes with linoleic acid metabolism. 相似文献
18.
The effect of oral administration of purified (95%) eicosapentaenoic acid on serum lipids, hepatic peroxisomal enzymes, antioxidant
enzymes and lipid peroxidation was compared with that of palmitic acid fed mice and corresponding controls. After 10 d, a
dose of 1000 mg eicosapentaenoic acid per day/kg body weight lowered serum triglycerides by 45%, while no significant change
in serum cholesterol level was noted in comparison to palmitic acid fed mice and controls. Hepatic acyl-CoA oxidase and catalase
activities increased by 50% and 30%, respectively, in the eicosapentaenoic acid fed group. In addition, the hepatic reduced
glutathione content and the activities of glutathione transferase, glutathione peroxidase and glutathione reductase, increased
significantly during eicosapentaenoic acid treatment. The levels of hepatic lipid peroxides were lower after eicosapentaenoic
acid feeding, while no significant change was noted in the palmitic acid fed mice when compared to the controls. Taken together,
the present data demonstrate for the first time that at hypolipidemic doses eicosapentaenoic acid feeding i) enhances the
hepatic antioxidant defense, and ii) does not cause a significant differential induction of the two peroxisomal enzymes, acyl-CoA
oxidase and catalase, as was noted after administration of hypolipidemic peroxisome proliferating compounds, such as clofibrate
in rodents. 相似文献
19.
Atlantic salmon (Salmo salar) (90 g) were fed four different diets for 21 weeks (final weight 344 g). The levels of n-3 highly unsaturated fatty acids
(HUFA) ranged from 11% of the total fatty acids (FA) in the low n-3 diet to 21% in the intermediate n-3 diet, to 55 and 58%
in the high n-3 diets. The high n-3 diets were enriched with either docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA).
Increasing dietary levels of n-3 HUFA led to increasing percentages (from 31 to 52%) of these FA in liver lipids. The group
fed the highest level of DHA had higher expressions of peroxisome proliferator-activated receptor (PPAR) β and the FA β-oxidation
genes acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase (CPT)-II, compared to the low n-3 groups. The high n-3 groups
had reduced activity of mitochondrial cytochrome c oxidase and β-oxidation capacity, together with increased activities of
superoxide dismutase (SOD) and caspase-3 activities. In the group fed the highest level of n-3 HUFA, decreased percentages
of major phospholipids (PL) in the mitochondrial and microsomal membranes of the liver were also apparent. The percentage
of mitochondrial cardiolipin (Ptd2Gro) was 3.1 in the highest n-3 group compared to 6.6 in the intermediate group. These data clearly show an increased incidence
of oxidative stress in the liver of fish fed the high n-3 diets. 相似文献
20.
Gudmundur G. Haraldsson Björn Kristinsson Ragnheidur Sigurdardottir Gudmundur G. Gudmundsson Harald Breivik 《Journal of the American Oil Chemists' Society》1997,74(11):1419-1424
The objective of this study was to investigate the use of lipases as catalysts for producing concentrates of eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA) from fish oil as an alternative to conventional chemical procedures. Transesterification
of fish oil with ethanol was conducted under anhydrous solvent-free conditions with a stoichiometric amount of ethanol. Among
the 17 lipases tested, the results showed that Pseudomonas lipases had the highest activity toward the saturated and monounsaturated fatty acids in the fish oil, much lower activity
toward EPA and DHA and, at the same time, good tolerance toward the anhydrous alcoholic conditions. With 10 wt% of lipase,
based on weight of the fish oil triacylglycerol substrate (15% EPA and 9% DHA initial content), a 50% conversion into ethyl
esters was obtained in 24 h at 20°C, in which time the bulk of the saturated and monounsaturated fatty acids reacted, leaving
the long-chain n-3 polyunsaturated fatty acids unreacted in the residual mixture as mono-, di-, and triacylglycerols. This
mixture comprised approximately 50% EPA+DHA. Total recovery of DHA and EPA was high, over 80% for DHA and more than 90% for
EPA. The observed fatty acid selectivity, favoring DHA as a substrate, was most unusual because most lipases favor EPA. 相似文献