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1.
Methyl esters of dimeric fatty acids were prepared by fractionating a mixture of conjugated linoleic and oleic acids that
was heated for 24 hr at 300 C in the absence of air. Rats fed diets containing less than 1% dimers showed no significant difference
(P<0.05) in the growth rate, feed efficiency, liver: body weight ratio, and lipid: liver weight ratio from those fed normal
diets. A lymph cannulation study using14C labeled dimers showed that ca. 0.4% of the dimers fed were absorbed within 12 hr and were transported as free acids in the
lymph. Within a 28 hr period, 2% of the labeled dimers fed by gastric intubation were oxidized to14CO2, and 1% radioactivity was recovered from the urine. The metabolism of methyl oleate appeared normal for rats prefed diets
containing dimers. 相似文献
2.
Klaus Eder 《Lipids》1999,34(7):717-725
This study was carried out to investigate the effects of a dietary oxidized oil on lipid metabolism in rats, particularly
the desaturation of fatty acids. Two groups of rats were fed initially for a period of 35 d diets containing 10% of either
fresh oil or thermally treated oil (150°C, 6d). The dietary fats used were markedly different for lipid peroxidation products
(peroxide value: 94.5 vs. 3.1 meq O2/kg; thiobarbituric acid-reactive substances: 230 vs. 7 μmol/kg) but were equalized for their fatty acid composition by using
different mixtures of lard and safflower oil and for tocopherol concentrations by individual supplementation with dl-α-tocopherol acetate. In the second period which lasted 16 d, the same diets were supplemented with 10% linseed oil to study
the effect of the oxidized oil on the desaturation of α-linolenic acid. During the whole period, all the rats were fed identical
quantities of diet by a restrictive feeding system in order to avoid a reduced food intake in the rats fed the oxidized oil.
Body weight gains and food conversion rates were only slightly lower in the rats fed the oxidized oil compared to the rats
fed the fresh oil. Hence, the effects of lipid peroxidation products could be studied without a distortion by a marked reduced
food intake and growth. To assess the rate of fatty acid desaturation, the fatty acid composition of liver and heart total
lipids and phospholipids was determined and ratios between product and precursor of individual desaturation reactions were
calculated. Rats fed the oxidized oil had reduced ratios of 20∶4n−6/18∶2n−6, 20∶5n−3/18∶3n−3, 20∶4n−6/20∶3n−6, and 22∶6n−3/22∶5n−3
in liver phospholipids and reduced ratios of 20∶4n−6/18∶2n−6, 22∶5n−3/18∶3n−3, and 22∶6n−3/18∶3n−3 in heart phospholipids.
Those results suggest a reduced rate of desaturation of linoleic acid and α-linolenic acid by microsomal Δ4-, Δ5-, and Δ6-desaturases.
Furthermore, liver total lipids of rats fed the oxidized oil exhibited a reduced ratio between total monounsaturated fatty
acids and total saturated fatty acids, suggesting a reduced Δ9-desaturation. Besides those effects, the study observed a slightly
increased liver weight, markedly reduced tocopherol concentrations in liver and plasma, reduced lipid concentrations in plasma,
and an increased ratio between phospholipids and cholesterol in the liver. Thus, the study demonstrates that feeding an oxidized
oil causes several alterations of lipid and fatty acid metabolism which might be of great physiologic relevance. 相似文献
3.
Effect of an essential fatty acid (EFA) deficiency in the rat on the incorporation of leucine-14C and glucosamine-14C into serum and liver protein are reported. Weanling male rats of the Sprague-Dawley strain were raised on a fat-free diet
for 10–12 weeks and then switched to diets supplemented with 10% corn oil or 10% hydrogenated coconut oil. Leucine-14C or glucosamine-14C was injected into the tail veins of the animals of each group. At selected intervals up to 120 min after the injections,
the animals were sacrificed and the radioactivity of the liver and serum proteins was measured. The levels of triglyceride
(TG) in the serum and the liver were also determined. Less radio-activity was incorporated into the serum β-lipoprotein (β-LP)
fraction of the hydrogenated coconut oil than the corn oil fed animals injected with leucine-14C, but no differences were observed in the incorporation of radioactivity into the liver protein and both albumin and globulin
fractions of the serum of these groups of animals. In the similar experiments with glucosamine-14C less radioactivity was incorporated into the β-LP fraction of the serum and into the smooth endoplasmic reticulum of the
liver in the hydrogenated coconut oil (EFA deficient) than the corn oil fed animals. Time course studies also indicated that
less radioactivity was incorporated into the β-LP fraction than into the albumin and globulin fractions of the serum of the
hydrogenated coconut oil group. These findings suggest that an EFA deficiency results in an impairment of the synthesis or
release of lipoprotein. 相似文献
4.
Diets rich in polyunsaturated fatty acids (PUFA) are well known to suppress hepatic lipogenic enzymes compared to fat-free
diets or diets rich in saturated fatty acids. However, the mechanism underlying suppression of lipogenic enzymes is not quite
clear. The present study was undertaken to investigate whether lipid peroxidation products are involved in suppression of
lipogenic enzymes. Therefore, an experiment with growing male rats assigned to six groups over a period of 40 d was carried
out. Rats received semisynthetic diets containing 9.5% coconut oil and 0.5% fresh soybean oil (coconut oil diet, peroxide
value 5.1 meq O2/kg oil), 10% fresh soybean oil (fresh soybean oil diet, peroxide value 0.5 meq O2/kg oil), or 10% thermally treated soybean oil (oxidized soybean oil diet, peroxide value 74 meq O2/kg oil). To modify the antioxidant state of the rats, we varied the vitamin E supply (11 and 511 mg α-tocopherol equivalents
per kg of diet) according to a bi-factorial design. Food intake and body weight gain were not influenced by dietary fat and
vitamin E supply. Activities of hepatic lipogenic enzymes were markedly influenced by the dietary fat. Feeding either fresh
or oxidized soybean oil diets markedly reduced activities of fatty acid synthase, (FAS), acetyl CoA-carboxylase, (AcCX), glucose-6-phosphate
dehydrogenase, (G6PDH), 6-phosphogluconate dehydrogenase, and ATP citrate lyase (ACL) relative to feeding the coconut oil
diet. Moreover, feeding oxidized soybean oil slightly, but significantly, lowered activities of FAS, AcCX, and ACL compared
to feeding fresh soybean oil. Activities of hepatic lipogenic enzymes were reflected by concentrations of triglycerides in
liver and plasma. Rats fed the coconut oil diet had markedly higher triglyceride concentrations in liver and plasma than rats
consuming fresh or oxidized soybean oil diets, and rats fed oxidized soybean oil had lower concentrations than rats fed fresh
soybean oil. The vitamin E supply of the rats markedly influenced concentrations of thiobarbituric acid-reactive substances
in liver, but it did not influence activities of hepatic lipogenic enzymes. Because the vitamin E supply had no effect, and
ingestion of an oxidized oil had only a minor effect, on activities of hepatic lipogenic enzymes, it is strongly suggested
that neither exogenous nor endogenous lipid peroxidation products play a significant role in the suppression of hepatic lipogenic
enzymes by diets rich in PUFA. Therefore, we assumed that dietary PUFA themselves are involved in regulatio of hepatic lipogenic
enzymes. Nevertheless, the study shows that ingestion of oxidized oils, regardless of the vitamin E supply, also affects hepatic
lipogenesis, and hence influences triglyceride levels in liver and plasma. 相似文献
5.
The metabolism of malonaldehyde (MA) was investigated in vivo using male Wistar rats and in vitro using rat liver mitochondria.
Twelve hr after intubation with [1,3-14C] MA, 60–70%, 5–15% and 9–17% of administered radioactivity was recovered in expired CO2, feces and urine, respectively. In rats intubated with [1,2-14C] acetate, the corresponding values were 68–82%, 1–2% and 2–3%.14CO2 evolution was initially slower after14C-MA administration than after14C-acetate administration and more radioactivity was excreted in the feces and urine. In vitro experiments using [1,3-14C] MA showed that MA is metabolized primarily in the mitochondria via reactions involving O2 utilization and14CO2 production. The apparent Km and Vmax were 0.5 mM and 9.3 nmol/min/mg protein for O2 uptake, respectively, and 2.0 mM and 2.4 nmol/min/mg protein for14CO2 production. Addition of malonic acid to mitochondrial incubates at concentrations inhibitory to succinate dehydrogenase did
not affect MA-induced O2 uptake but enhanced14CO2 production from14C-MA.14C-Acetate appeared to be the major accumulating metabolite in rat liver mitochondrial preparations following a 120-min incubation
with14C-MA. A probable biochemical route for MA metabolism involves oxidation of MA by mitochondrial aldehyde dehydrogenase followed
by decarboxylation to produce CO2 and acetate. 相似文献
6.
Micheline Boquillon 《Lipids》1976,11(12):848-852
A test meal (300 mg casein, 600 mg sucrose, 100 mg corn oil, tracer dose of 9.103H oleic acid) was given to fasting adult rats with intestinal lymph fistulas. One group received an acute oral dose of ethanol
(3.2 g/kg body weight) simultaneously with the test meal. Controls received 2.5 ml of water instead of ethanol. Ingestion
of ethanol temporarily delayed the removal of lipid radioactivity from the stomachs. More than 25% of radioactivity fed remained
8 hr after feeding whereas with control rats less than 10% of lipid radioactivity fed remained 6 hr after feeding. In controls
and ethanoltreated rats, the amounts of exogenous lipids in the intestinal lumen and mucosa were low and similar enough. Quantities
of endogenous and exogenous lipids found in the lymph collected during 24 hr after feeding were similar in the two groups,
but the fat absorption peak was found after 6 hr in alcoholic rats and before 6 hr in controls. This delay was probably due
to the retention of lipids in the stomach. More of the exogenous lipid was always transported by small particles moving in
the region of α1 globulins in cellulose acetate electrophoresis than by larger particles remaining at the origin. This proportion was enhanced
in the ethanoltreated animals. The larger fat particles were richer in endogenous fatty acids in alcohol-treated rats than
in controls.
These experiments are a part of a thesis of “Doctorat d'Etat” (Speciality: Biology) no C.N.R.S. A0 11.965 presented in Dijon on February 6, 1976. 相似文献
7.
The metabolism of14C-sterculic acid, labeled in the methylene carbon of the cyclopropene ring, was investigated in Wistar rats. Comparison of
the distribution of radioactivity in tissue and excreta as a function of time showed that the free sterculic acid was metabolized
faster than the methyl ester and that the sterculic acid administered by intragastric intubation was absorbed and metabolized
at a faster rate than that administered by intraperitoneal injection. The concentration of label in blood serum reached a
maximum 2 hr after intubation and then rapidly declined. Incorporation of radioactivity into most organs peaked at 4 hr with
liver peaking at a maximum of 11% of the administered dose and other organs at less than 1%. Label in depot fat steadily increased
to 8% at 26 hr. Less than 1% of the administered dose was expired in CO2 in the same time period. Excretion of label reached a maximum of 48% in urine and 11% in feces by 16 hr. The majority of
the label in liver was in the fatty acid portion of the lipid fraction. The relative amount of label in microsomal and mitochondrial
subcellular fractions of liver changed with time suggesting that these organelles may be involved in the metabolism of sterculic
acid. Rats fed control diets appeared to metabolize sterculic acid in the same manner, but at a slower rate than rats acclimated
to dietary cyclopropene fatty acids. Low recovery of label in expired air showed that the methylene carbon of the cyclopropene
ring was not oxidized to CO2. These data suggest that rats readily absorb sterculic acid and excrete labeled compounds primarily in the urine.
Technical Paper No. 4409, Oregon Agricultural Experiment Station, Oregon State University, Corvallis, OR 97331. 相似文献
8.
Rats were fed for 5 weeks either 10% (w/w) menhaden oil (MO) or a 10% corn oil-lard (COL) mixture (1∶1) in diets with ≤5 IU
or ≤2 IU/kg vitamin E, respectively, or the same diets supplemented with d-α-tocopheryl succinate to a total of 35 and 180
IU vitamin E/kg, respectively. Slices of liver and heart from these rats were used to study lipid peroxidationin vitro. Thiobarbituric acid-reactive substances (TBARS) were measured in the medium after incubation of the slices at 37°C for 1
hr in the absence (uninduced) and presence of 0.5 mM tert-butyl hydroperoxide (induced). The release of TBARS from slices
of heart and liver from rats fed either lipid decreased with increasing levels of dietary vitamin E. At the same level of
dietary vitamin E, TBARS release was greater for slices of liver and heart from the MO-fed rats than from the COL-fed rats.
Application of the TBARS data to a model simulating the experimental conditions showed a good correlation (r=0.95, p<0.001)
between experimental and simulated values. Of the 16∶0–22∶6 fatty acids measured in liver from MO-fed rats, 15.4% was n−6
fatty acids and 29.9% was n−3 fatty acids; in liver from COL-fed rats, the respective values were 37.4% and 3.7%. Liver and
kidney vitamin E levels were unaffected by the dietary lipid. This study demonstrated that a dietary fish oil increased the
susceptibility of rat liver and heart toin vitro lipid peroxidation, and that vitamin E decreased TBARS in tissues from rats fed COL to lower levels than for tissues from
rats fed MO. The results suggest that there might also be an increased requirement for dietary antioxidants by humans using
fish oil supplements. 相似文献
9.
Eighteen-month-old Nebraska strain minipigs were fed diets containing 2% cholesterol and 20% corn oil, lard, or coconut oil
for 12 to 18 months. Concentrations of serum total lipid, total cholesterol, and total phospholipid increased 200 to 300%
with each diet. Changes in serum concentrations of Sf 20+ and Sf 0–20 lipoproteins varied with diets fed. Serum concentration of high density lipoprotein was increased in all cases. Intima
concentration of Sf 0–20 lipoprotein fraction was elevated by feeding the corn oil diet. There was no development of atherosclerosis as a result
of feeding the corn oil-cholesterol diet, but there was an increase in atherosclerosis as a result of feeding the lard or
coconut oil diet. There were no correlations between fatty acid patterns of several lipid fractions from serum and corresponding
lipid fractions from aortic intima of corn oil fed animals.
Deceased. 相似文献
10.
Incorporation of secondary autoxidation products (SP) of linoleic acid into the rat body was investigated. Radioactive SP
was administered orally to a group of 5 rats, and excretions of radioactive substances in feces, urine and respiration were
measured and compared with excretions from rats fed linoleic acid and its hydroperoxides. The SP-fed group excreted 45% and
the other groups about 10% of the administered radioactivity through feces. Urinary excretion accounted for 52% of activity
ingested in the SP group and less than 30% in the other groups. The14CO2 produced in each group was about 25% of the ingested activity. Incorporation of the radioactive substances of SP into tissues
and organs was measured periodically after administration of a single dose. The radioactive substances accumulated in the
liver between 12–24 hr after administration and accounted for 2.6% of the total amount given, the highest level of all tissues
and organs. This accumulation led to an elevation of serum transaminase activities, an increase in hepatic lipid peroxide,
as determined by thiobarbituric acid test, and a slight hypertrophy of liver (1.5-fold). Therefore, absorbed SP appeared to
contribute to the deleterious condition of the liver. 相似文献
11.
Lipogenesis, lipolysis, and stimulation of glucose conversion into lipid by insulin or prostaglandin E1 were studied in isolated fat cells of the epididymal fat pads of rats fed a fat-free diet or this diet supplemented with
10% hydrogenated coconut oil or 10% safflower seed oil. Changes in fatty acid composition, characteristic of an essential
fatty acid deficiency, were well advanced in the neutral lipid but had only started in the polar lipid of the fat cells of
the epididymal fat pads of animals 3 months after weaning. Cellularity of the epididymal fat pads, as indicated by protein
to lipid ratio of the fat cells, was influenced greatly by hydrogenated coconut oil in the diet irrespective of an essential
fatty acid deficiency. Lipogenesis was increased in the fat cells of the animals fed the hydrogenated coconut oil diet 5 weeks
after weaning but was not significantly different from that of the safflower fed animals 3 months after weaning. Incorporation
of glucose into lipid, oxidation to CO2, and basal lipolysis were not significantly different in the fat cells of the essential fatty acid deficient animals from
those fed safflower oil 3 months after weaning, except in animals of the fat-free group based upon cell lipid. However, conversion
of glucose to free fatty acid was significantly greater in the isolated fat cells of animals fed either the hydrogenated coconut
oil or the fat-free diet than in those of animals fed the safflower oil supplement. The incorporation of glucose into lipid
by isolated fat cells was stimulated significantly by insulin in young animals fed a fat-free diet, but the effect on lipogenesis
appeared to be reversed in the fat cells of animals receiving safflower seed oil 3 months after weaning. Prostaglandin E1 also appeared to stimulate the incorporation of glucose into lipid in the fat cells of the older animals receiving safflower
seed oil. Differences in osmolarity produced large differences in utilization of glucose and release of lipid from isolated
fat cells, but no significant differences were observed between the cells from animals fed the fat-free diet and those from
the controls fed safflower oil. The results demonstrated the effects of diets containing fat or no fat on enzyme activities
and membrane properties of fat cells of the epididymal fat pads of essential fatty acid deficient rats. 相似文献
12.
Male weanling rats were fed semi-synthetic diets high in saturated fat (beef tallow) vs high in linoleic acid (safflower oil)
with or without high levels of α-linolenic acid (linseed oil) for a period of 28 days. The effect of feeding these diets on
cholesterol content and fatty acid composition of serum and liver lipids was examined. Feeding linseed oil with beef tallow
or safflower oil had no significant effect on serum levels of cholesterol. Serum cholesterol concentration was higher in animals
fed the safflower oil diet than in animals fed the beef tallow diet without linseed oil. Feeding linseed oil lowered the cholesterol
content in liver tissue for all dietary treatments tested. Consumption of linseed oil reduced the arachidonic acid content
with concomitant increase in linoleic acid in serum and liver lipid fractions only when fed in combination with beef tallow,
but not when fed with safflower oil. Similarly, ω3 fatty acids (18∶3ω3, 20∶5ω3, 22∶5ω3, 22∶6ω3) replaced ω6 fatty acids (20∶4ω6,
22∶4ω6) in serum and liver lipid fractions to a greater extent when linseed oil was fed with beef tallow than with safflower
oil. The results suggest that the dietary ratio of linoleic acid to saturated fatty acids or of 18∶3ω3 to 18∶2ω6 may be important
to determine the cholesterol and arachidonic acid lowering effect of dietary α-linolenic acid. 相似文献
13.
G. Sarojini K. Chittema Rao P. Geervani 《Journal of the American Oil Chemists' Society》1985,62(6):993-996
Alkali refinedHibiscus sabdariffa seed oil (Mesta Oil) of the familyMalvales was heated and hydrogenated to eliminate the cyclopropene fatty acids (CPFA). Such processed oils were fed to weanling rats at 10% level of the diet for 4, 8 and 12 weeks. The food intake and gain in weight were found to be less in the refined oil group than in the peanut oil control group. The digestibility was found normal with all the processed oils. Serum and liver lipid composition with respect to total lipids, cholesterol and phospholipids were comparable to those fed with peanut oil. The liver architecture did not show any abnormalities withH. sabdariffa oil feeding. 相似文献
14.
Ana Maria P. Lottenberg Helena C. F. Oliveira Edna R. Nakandakare Eder C. R. Quintão 《Lipids》1992,27(5):326-330
The mechanism by which ω3 fatty acids lower plasma triacylglycerol levels was investigated. Rats were fed fish oil, olive
oil (10% fat by weight) or a nonpurified diet 4% fat by weight) for 15 days. Lipoprotein lipase was inhibited by intra-arterial
administration of Triton WR 1339 to estimate hepatic triacylglycerol output. Rats fed the olive oil diet showed a higher rate
of triacylglycerol formation than rats fed the ω3 fatty acid diet or the low-fat diet. All three groups showed identical rates
of removal from plasma of intraarterially administered artificial chylomicrons that had simultaneously been labeled with cholesteryl
[1-14C]oleate and [9,10(n)-3H]triolein. Liver radioactivity and total fat content were lowest in rats fed the fish oil diet, indicating that ω3 fatty
acids were preferentially metabolized in liver. Chylomicrons obtained from donor rats fed either fish oil containg [14C]cholesterol or olive oil containing [3H]cholesterol were removed at similar rates when infused together intraarterially into recipient animals. A slower formation
of plasma very low density lipoprotein triacylglycerols in rats fed fish oil is probably due to a faster rate of oxidation
of the fatty acid chains in the liver resulting in decreased plasma triacylglycerol concentrations. 相似文献
15.
B. Mandal S. Ghosh Majumdar C. R. Maity 《Journal of the American Oil Chemists' Society》1984,61(9):1447-1449
Karanja seed(Pongamia glabra) oil contains toxic flavonoids including 1.25% karanjin and 0.85% pongamol. After refining the oil resembles peanut oil in
composition and is free from toxic flavonoids, bitterness and unpleasant odors. Akashmoni seed(Acacia auriculaeformis) oil is rich in stearic acid (31%), and nearly two-thirds of its glyceride is GS2 U (disaturated monounsaturated), mostly SOS (saturated-stearic acid and unsaturated-oleic acid). Nutritional evaluations
of these two refined seed oils were carried out in rats by feeding the respective oils and peanut oil as control at 10% level
in a 20% protein diet for 12 weeks. The animals fed karanja oil showed poor growth performance, altered lipid metabolism and
fatty infiltration in liver. Akashmoni oil in the diet of rats did not reveal growth retardation or any abnormalities in evaluations
of lipid parameters of serum and liver or histopathological findings. The results of this study indicate that refined karanja
oil is toxic to rats and may not be desirable for edible purposes, while akashmoni oil may be desirable. 相似文献
16.
Jacqueline Dupont 《Lipids》1970,5(11):908-914
Female rats (200 g) were fed a nutritionally adequate diet containing 1% by weight of corn oil (low-fat, LF), 21% of corn
oil (CO) or 20% of beef tallow plus 1% of corn oil (BT) for two weeks. Food was removed for 8–12 hr, then each rat was refed
for 1 hr. Each rat was injected ip with Na-3H-acetate and U-14C-Na-palmitate, (P),-oleate (O) or-linoleate (L). Expired CO2 was collected for 2 hr. Liver, heart and serum were obtained for analysis of total lipid14C and3H and cholesterol14C and3H. Oxidation of L was twice as great as O or P when the LF diet was fed. CO and BT diets doubled oxidation of O to equal L,
and increased oxidation of P, 50%. In liver and serum P was retained to a greater extent than O or L on BT and CO diets. Incorporation
of acetate into total lipid was highest on LF diet and reduced by feeding either CO or BT. Incorporation of acetate into cholesterol
was greater when BT or CO was fed than for LF.14C was incorporated into cholesterol in such small amounts that it was barely detectable and could not be counted accurately.
Conclusions are that (a) dietary fat affects rate of oxidation of uniformly labeled palmitate and oleate, but not linoleate,
(b) acetate is a more ready precursor to cholesterol than is fatty acid carbon, and (c) the acetate incorporated into cholesterol
when polyunsaturated fat is fed is not derived directly from fatty acid carbon. The failure of incorporation of fatty acid
carbon into cholesterol within 2 hr of administration opens the question of compartmentation of acetate as to its metabolic
source.
Colorado Agricultural Experiment Station Scientific Series Paper No. 1510. 相似文献
17.
Fatty livers and the similarity between the skin lesions in kwashiorkor and those described in experimental essential fatty
acid (EFA) deficiency have led to the hypothesis that protein and EFA deficiencies may both occur in chronic malnutrition.
The relationship between serum very low density lipoprotein (VLDL) and hepatic lipid composition was studied after 28 d of
protein depletion to determine the interactions between dietary protein levels and EFA availability. Rats were fed purified
diets containing 20 or 2% casein and 5% fat as either soybean oil rich in EFA, or salmon oil rich in eicosapentaenoic (EPA)
and docosahexaenoic (DHA) acids, or hydrogenated coconut, oil poor in EFA. Animals were divided into six groups, SOC (20%
casein +5% soybean oil), SOd (2% casein +5% soybean oil), COC (20% casein +5% hydrogenated coconut oil), COd (2% casein +
5% hydrogenated coconut oil), SAC (20% casein +5% salmon oil) and SAd (2% casein +5% salmon oil). After 28 d, liver steatosis
and reduced VLDL-phospholipid contents (P<0.001) were observed in protein-deficient rats. In protein deficiency, triacylglycerol and phospholipid fatty acid compositions
in both liver and VLDL showed a decreased polyunsaturated-to-saturated fatty acid ratio. This ratio was higher with the salmon
oil diets and lower with the hydrogenated coconut oil diets. Furthermore, independent of the oil in the diet, protein deficiency
decreased linoleic and arachidonic acids in VLDL phospholipids. Conversely, despite decreased proportions of EPA at low protein
levels, DHA levels remained higher in rats fed salmon oil diets. While in rats fed the hydrogenated coconut oil-fed diets
the amount of 22∶5n−6 was lower in liver, it was higher in VLDL lipids at low protein levels. Both EPA and arachidonic acid
are precursors of eicosanoids and their diminution may be related to certain clinical symptoms seen in infants suffering from
kwashiorkor. 相似文献
18.
Interest in malondialdehyde (MDA) metabolism stems from its formation as a product of lipid peroxidation in the diet and in
the tissues; its reactivity with functional groups of nucleic acid bases, proteins and phospholipids; its mutagenicity in
bacteria, and its reported skin and liver carcinogenicity in animals. Administration of the Na enol salt of MDA in the drinking
water of mice over a range of 0.1–10.0 μg/g/day for 12 mo produced dose-dependent hyperplastic and neoplastic changes in liver
nuclei and increased mortality at the highest level but produced no gross hepatic tumors. Addition of MDA to the medium of
rat skin fibroblasts grown in culture caused nuclear abnormalities at concentrations as low as 10−6M despite an uptake of only 4%. [1,3-14C]MDA was rapidly oxidized to [14C]acetate in rat liver mitochondria and to14CO2 in vivo: however, ∼10% of the radioactivity was recovered in the urine. Chromatographic analysis of rat urine revealed the
presence of several compounds which yield MDA on acid hydrolysis. Total MDA excretion increased in response to conditions
which stimulate lipid peroxidation in vivo, including vitamin E deficiency, Fe or CCl4 administration, and enrichment of the tissues with PUFA. N-acetyl-e-(2-propenal)lysine was identified as a major urinary
metabolite of MDA in rat and human urine. This compound is derived primarily from N-α-(2-propenal)lysine released in digestion
as a product of reactions between MDA and the ε-amino groups of N-terminal lysine residues in food proteins. However, its
presence in the urine of animals fasted or fed MDA-free diets indicates that it is also formed in vivo. Identification of
the metabolites of MDA excreted in the urine may provide clues to the mechanisms of cellular damage caused by this compound
in the tissues. 相似文献
19.
Malondialdehyde (MDA) derivatives occur as normal constituents of rat and human urine. In a previous study, it was found that
MDA excretion in rats is responsive to MDA intake and to certain factors that increase lipid peroxidation in vivo: vitamin
E deficiency, iron administration and a high concentration of cod liver oil (CLO) fatty acids in the tissues. In the present
study, the effect on MDA excretion of several additional dietary and endogeneous factors was evaluated.
The composition of dietary fatty acids had a major influence on MDA excretion in fed animals, being highest for animals fed
n−3 fatty acids (20∶5 and 22∶6) from CLO, intermediate for those fed n−6 (18∶2) acids from corn oil (CO) and lowest for those
fed saturated acids from hydrogenated coconut oil (HCO). Diet was the main source of urinary MDA in all groups. Fasting produced
a marked increase in urinary MDA, which tended to be higher in rats previously fed CLO. Fasting MDA excretion was not affected
by the level of CO in the diet (5, 10 or 15%), indicating that feeding n−6 acids does not increase lipid peroxidation in vivo.
Adrenocorticotropic hormone and epinephrine administration increased urinary MDA, further indicating that lipolysis either
releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A
decrease in fasting MDA excretion was observed in rats previously fed a high level of antioxidants (vitamin E+BHT+vitamin
C) vs a normal level of vitamin E. MDA excretion increased following adriamycin and CCl4 administration. No increase was observed following short-term feeding of a choline-methionine-deficient diet, which has been
reported to increase peroxidation of rat liver nuclear lipids.
This study provides further evidience that urinary MDA can serve as a useful indicator of lipid peroxidation in vivo when
peroxidation of dietary lipids is precluded.
This research was performed in partial fulfillment of the requirements for the M.Sc. degree in Nutritional Sciences 相似文献
20.
The potential effects of oil specimens related to cases of toxic oil syndrome (TOS) on the liver microsomal lipid composition
from guinea pigs were investigated. For four weeks, animals were fed diets supplemented with either “case oil” (oil related
to cases of TOS) or “control oil” (oil unrelated to cases of TOS), either previously heated or not. Results were compared
with those from guinea pigs fed the same diet with no oil. The administration of case oil produced changes in liver microsomal
lipid composition. Statistically significant differences were also found between heated case and heated control oils. The
cholesterol/phospholipid molar ratios and the major phospholipid class distribution were unaffected under these diet conditions.
However, increases in the relative contents of linoleic and arachidonic acids and, simultaneously, a reduction in palmitic
and palmitoleic acid levels were observed by diet effects. Heated oil administration decreased the saturated/unsaturated ratios
in all cases. Our data suggest that changes observed in the fatty acid composition are attributable to the free fatty acid
contents of administered oils. The toxic constituents of case oil seem to be able to alter the liver microsomal lipid composition. 相似文献