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Biomedical subjects

C A Drevon

Publications and source records attributed to C A Drevon.

At least 91 records · Page 5Linked to original sources
PubMed1992

Effect of dietary supplementation with n-3 polyunsaturated fatty acids on physical properties and metabolism of low density lipoprotein in humans.

The effects of marine n-3 polyunsaturated fatty acids were investigated in relation to the chemical and physical properties of low density lipoprotein (LDL) and how these changes affected LDL metabolism in humans. The subjects received supplements of six capsules daily, each capsule containing 1 g of either highly concentrated ethyl esters of n-3 fatty acids (85% eicosapentaenoic acid and docosahexaenoic acid) (n = 12) or corn oil (56% linoleic and 26% oleic acid) (n = 11). After 4 months of oil supplementation, the following changes were observed in the lipid moiety of the n-3-enriched LDL particles compared with LDL from the corn oil group: LDL cholesteryl ester, as well as the amount of total lipids of LDL, was significantly lower (0.97 +/- 0.12 versus 1.19 +/- 0.23 mg/mg protein and 1.88 +/- 0.40 versus 2.45 +/- 0.31 mg/mg, respectively; mean +/- SD, n = 6, p less than 0.05); the amount of eicosapentaenoic and docosahexaenoic acids and the unsaturation index increased (104.0 versus 29.4 micrograms/mg protein and 6.64 versus 5.49, respectively); and differential scanning calorimetry showed that LDL cholesteryl ester melting temperature was lowered by 2 degrees C (27.6 +/- 0.8 degrees versus 29.5 +/- 0.2 degrees C). The only effect observed on the protein moiety was an increase in the ratio of apolipoprotein (apo) B to cholesterol (0.66 +/- 0.17 versus 0.82 +/- 0.14 mg/mg cholesterol; p less than 0.05). Circular dichroism spectra of LDL indicated an alpha-helix content of 46 +/- 5% in apo B from both groups. No difference was observed by 13C nuclear magnetic resonance spectroscopy in the ratio of "active" to "normal" lysine residues of apo B. No detectable differences in the size of n-3 fatty acid-enriched LDL particles versus control LDL could be measured by either electron microscopy of negatively stained LDL (24.5 +/- 2.0 versus 25.0 +/- 1.5 nm) or dynamic light scattering (24.9 +/- 0.9 versus 24.9 +/- 0.4 nm). LDL from the fish oil and corn oil groups showed similar susceptibility to Cu(2+)-catalyzed lipid peroxidation, as indicated by the amount of lipid peroxides formed during the oxidation time, and degradation of oxidatively modified LDL in J774 macrophages as a function of Cu2+ oxidation time. No effect of n-3 fatty acids was observed on LDL metabolism. Specific uptake and degradation of n-3 fatty acid-enriched LDL were similar to those for control LDL in HepG2 cells as well as in human skin fibroblasts, and they showed the same ability to stimulate cholesteryl ester synthesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Role of liver endothelial and Kupffer cells in clearing low density lipoprotein from blood in hypercholesterolemic rabbits.

The role of liver endothelial and Kupffer cells in the hepatic uptake of cholesterol-rich low density lipoprotein (LDL) was studied in rabbits fed a diet containing 2% (w/w) cholesterol for 3 weeks. 125I-labeled tyramine cellobiose-labeled cholesterol-rich LDL was injected intravenously into rabbits, and parenchymal and nonparenchymal liver cells were isolated 24 h after injection. The hepatic uptake was 9 +/- 3% of injected dose in cholesterol-fed rabbits 24 h after injection, as compared to 36 +/- 9% in control-fed rabbits (n = 6 in each group; significant difference, P less than 0.005). Endothelial and Kupffer cells took up 2.7 +/- 0.5% and 1.2 +/- 0.8% of injected dose in the hypercholesterolemic rabbits, as compared to 1.9 +/- 0.8% and 0.8 +/- 0.3% in control animals. The amount accounted for by the parenchymal cells was markedly reduced in the cholesterol-fed rabbits to 7.3 +/- 2.7% of injected dose, as compared to 32.8 +/- 7.6% in controls (P less than 0.02). On a per cell basis, the nonparenchymal cells of cholesterol-fed rabbits took up as much LDL as the parenchymal cells (0.6 +/- 0.2, 0.7 +/- 0.1, and 0.6 +/- 0.4% of injected dose per 10(9) parenchymal, endothelial, and Kupffer cells, respectively). This is in marked contrast to the control animals, in which parenchymal cells took up about 6 times more LDL per cell than endothelial and Kupffer cells (3.2 +/- 0.9, 0.7 +/- 0.3, and 0.5 +/- 0.1% of injected dose per 10(9) cells). Thus, 30% of the hepatic uptake of LDL in the cholesterol-fed rabbits took place in nonparenchymal cells, as compared to 6% in controls. Consistent with these data, the concentrations of cholesteryl ester in endothelial and Kupffer cells in rabbits fed the high cholesterol diet were about twofold higher than in parenchymal cells (428 +/- 74 and 508 +/- 125 micrograms/mg protein, respectively, vs. 221 +/- 24 micrograms/mg protein in parenchymal cells). In contrast to cells from normal rabbits, Kupffer and endothelial cells from cholesterol-fed rabbits accumulated significant amounts of Oil Red O-positive material (neutral lipids). Electron microscopic examination of these cells in situ as well as in culture revealed numerous intracellular lipid droplets. Slot blot hybridization of RNA from liver parenchymal, endothelial, and Kupffer cells showed that cholesterol feeding reduced the level of mRNA specific for the apoB,E receptor to a small and insignificant extent in all three cell types (to 70-80% of that observed in control animals).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Influence of eicosapentaenoic acid (20:5, n-3) on secretion of lipoproteins in CaCo-2 cells.

CaCo-2 cells, grown on filter membranes, were used to study the effects of fatty acids on cellular metabolism of triacylglycerol and phospholipids. The rate of triacylglycerol secretion was enhanced more than 2-fold, from 1 to 2 weeks after reaching confluency, in the presence of 0.6 mM fatty acids. Triacylglycerol secretion and oxidation of oleic acid increased 2- and 9-fold, respectively, with this culture system, as compared to cells grown on conventional plastic dishes. Eicosapentaenoic acid (20:5 n-3), when compared to oleic acid, did not reduce formation of triacylglycerol or enhance phospholipid synthesis in CaCo-2 cells during short term (less than 24 h) experiments, when the cells resided on membranes, regardless of what type of radioisotopes were used as precursors in the incubation media. However, the n-3 fatty acid was preferentially incorporated into phosphatidylinositol, lysophosphatidylcholine, and sphingomyelin, as compared to oleic acid. The disappearance from the apical medium and cellular uptake of labeled eicosapentaenoic and oleic acid were similar during incubations up to 24 h, and the metabolism of these fatty acids to acid-soluble materials and CO2 was equal. Light scattering analysis indicated that secreted lipoproteins of density less than 1.006 g/ml were in the same size-range as chylomicrons derived from human plasma. Assessment of secreted apolipoprotein B showed that by incubating CaCo-2 cells with oleic acid, apolipoprotein B levels increased approximately 1.4-fold when compared to cells incubated with eicosapentaenoic acid, whereas the amount of triacylglycerol and size-range of particles were similar for the two fatty acids. Our data indicate that CaCo-2 cells grown on filter membranes exhibit enterocyte-like characteristics with the ability to synthesize and secrete chylomicrons. Eicosapentaenoic acid and oleic acid are absorbed, metabolized, and influence secretion of lipoprotein particles in a similar way, except for some differences in incorporation of the fatty acids into certain phospholipid classes and a reduced secretion of apolipoprotein B. The culture conditions, including time after confluency and cellular support, are critical for the rate of secretion in the presence of eicosapentaenoic acid and oleic acid.

Apolipoproteins B↗
PubMed1992

Accuracy of a quantitative food frequency questionnaire applied in elderly Norwegian women.

The accuracy (reproducibility and relative validity) of a self-administered quantitative food frequency questionnaire including 180 food items was evaluated. A total of 38 elderly women kept multiple weighed diet records for a total of 14 days over a 6-week period and filled in the questionnaire both before and after this period. Spearman rank correlations between the nutrient intakes from the two questionnaires varied from 0.43 for carbohydrate to 0.88 for energy percentage from alcohol. The median correlation was 0.70. Seven women whose recorded average energy intake was less than 1.17 times their measured basal metabolic rate were excluded from the analysis comparing the questionnaire and the diet records. The first questionnaire gave on the average 10% higher nutrient median values than the records, while the second questionnaire did not in general produce higher values. Unadjusted correlation coefficients comparing intakes measured by the two methods ranged from 0.31 for vitamin C to 0.79 for energy percentage from carbohydrate, the median coefficient being 0.61. On the average 77% of the subjects were classified in the same (+/- 1) quintile in the first food frequency questionnaire and the diet records. The present study indicates that the self-administered quantitative food frequency questionnaire is useful for measuring individual or group intakes for a variety of nutrients.

Aged↗
PubMed1992

Reduced concentration of hepatic alpha-tocopherol in patients with alcoholic liver cirrhosis.

The concentration of alpha-tocopherol was measured in liver biopsy specimens obtained from 83 patients with alcoholic and non-alcoholic liver diseases. The mean hepatic vitamin E content (as alpha-tocopherol) was significantly lower in 23 patients with alcoholic cirrhosis (17.6 +/- 12.1 nmol/mg wet weight liver), compared with 12 patients with normal liver histology (39.2 +/- 29.7 nmol/mg, P less than 0.01). The mean serum concentration of alpha-tocopherol was lower in patients with alcoholic cirrhosis (13.9 +/- 7.0 mumol/l) than in individuals with alcoholic fatty liver (21.3 +/- 9.3 mumol/l, P less than 0.01) and patients with normal liver histology (23.4 +/- 11.6 mumol/l, P less than 0.01). A decreased ratio of serum alpha-tocopherol/total serum lipids was also observed in patients with alcoholic cirrhosis, compared with patients with normal liver histology (P less than 0.05). There was a significant correlation between concentrations of alpha-tocopherol in liver and serum (r = 0.43, P less than 0.001). Furthermore, serum alpha-tocopherol correlated with retinol (r = 0.53, P less than 0.001), selenium (r = 0.45, P less than 0.001), and albumin (r = 0.37, P less than 0.001) in serum. We suggest that the reduced content of hepatic alpha-tocopherol observed in some patients may play a role in ethanol-induced lipid peroxidation.

Adolescent↗
PubMed1991

Uptake and degradation of filamentous actin and vitamin D-binding protein in the rat.

Tissue uptake and degradation of 125I-tyramine-cellobiose-labelled filamentous actin, vitamin D-binding protein (DBP) and actin-DBP complex were studied in the rat. Actin and actin-DBP complex were cleared from plasma at a faster rate than was DBP. About 40% of injected actin was recovered in the liver between 10 and 30 min after administration. Of the total radioactivity recovered in the liver, about 35% and 40% was detected in parenchymal and endothelial cells respectively when labelled actin or DBP-actin complex was injected intravenously. When labelled DBP alone was injected, approx. 55% of the radioactivity recovered in liver was in the Kupffer cells. These results suggest that actin is targeting the DBP-actin complex to the endothelial and parenchymal liver cells. Filamentous actin was also taken up in large amounts and at a rapid rate in parenchymal as well as non-parenchymal liver cells in vitro. Our data indicate that the rat has a mechanism to clear actin and the DBP-actin complex from plasma and that both parenchymal and non-parenchymal liver cells are involved in this process.

Actins↗
PubMed1991

Effect of dietary deficiency and supplementation with all-rac-alpha-tocopherol on hepatic content in rats.

We studied the effect of dietary deficiency and supplementation with vitamin E in the form of all-rac-alpha-tocopherol in relation to the content of alpha-tocopherol in parenchymal and nonparenchymal liver cells. The cells were isolated by centrifugal elutriation from rats fed diets containing normal, low or high amounts of vitamin E. The parenchymal cells contained about 90% of total hepatic alpha-tocopherol content in rats fed a nonpurified diet (reference group). However, the Kupffer and the endothelial/stellate cells contained four and two times more alpha-tocopherol, respectively, than the parenchymal cells per milligram of cell protein. When the rats were deprived of vitamin E for 8 wk, the content of alpha-tocopherol in parenchymal cells was reduced to 30% of values obtained from rats fed the nonpurified diet, and nonparenchymal cells contained very low levels of alpha-tocopherol (less than 5% of reference values). A diet enriched in vitamin E resulted in a sixfold increase in the content of alpha-tocopherol in parenchymal cells but in small changes in nonparenchymal cells compared to the reference diet. Accordingly, the parenchymal cells may have storage capacity for alpha-tocopherol. The light mitochondrial and microsomal fractions contained high amounts of alpha-tocopherol. These fractions were subdivided by density gradient centrifugation to examine the alpha-tocopherol content in different cell organelles. The lysosomes and the Golgi apparatus were found to contain high levels of alpha-tocopherol, whereas peroxisomes contained small amounts.

Animals↗
PubMed1991

Absorption, transport and metabolism of vitamin E.

Vitamin E includes eight naturally occurring fat-soluble nutrients called tocopherols and dietary intake of vitamin E activity is essential in many species. alpha-Tocopherol has the highest biological activity and the highest molar concentration of lipid soluble antioxidant in man. Deficiency of vitamin E may cause neurological dysfunction, myopathies and diminished erythrocyte life span. alpha-Tocopherol is absorbed via the lymphatic pathway and transported in association with chylomicrons. In plasma alpha-tocopherol is found in all lipoprotein fractions, but mostly associated with apo B-containing lipoproteins in man. In rats approximately 50% of alpha-tocopherol is bound to high density lipoproteins (HDL). After intestinal absorption and transport with chylomicrons alpha-tocopherol is mostly transferred to parenchymal cells of the liver were most of the fat-soluble vitamin is stored. Little vitamin E is stored in the non-parenchymal cells (endothelial, stellate and Kupffer cells). alpha-Tocopherol is secreted in association with very low density lipoprotein (VLDL) from the liver. In the rat about 90% of total body mass of alpha-tocopherol is recovered in the liver, skeletal muscle and adipose tissue. Most alpha-tocopherol is located in the mitochondrial fractions and in the endoplasmic reticulum, whereas little is found in cytosol and peroxisomes. Clinical evidence from heavy drinkers and from experimental work in rats suggests that alcohol may increase oxidation of alpha-tocopherol, causing reduced tissue concentrations of alpha-tocopherol. Increased demand for vitamin E has also been observed in premature babies and patients with malabsorption, but there is little evidence that the well balanced diet of the healthy population would be improved by supplementation with vitamin E.

Absorption↗
PubMed1990

Effect of 3- and 4-thia-substituted fatty acids on glycerolipid metabolism and mitochondrial beta-oxidation in rat liver.

Treatment of normolipidemic rats by alkylthiopropionic acid (CETTD), resulted in a dose- and time-dependent increase in total dihydroxyacetone phosphate acyltransferase (DHAPAT) activity, in extent comparable to that of 3-thiadicarboxylic acid (BCMTD) and alkylthioacetic acid (CMTTD). Thus, in CETTD- and CMTTD-treated rats, the specific DHAPAT activity increased in the microsomal, peroxisomal and mitochondrial fractions. In contrast, repeated administration of the peroxisome proliferator, BCMTD, decreased the specific DHAPAT activity both in the peroxisomal fraction and in purified peroxisomes. A three-fold increase in specific activity was, however, revealed in the mitochondrial fraction. Whether the variation of the DHAPAT activity in the mitochondrial and microsomal fractions among the feeding groups can be explained by increased number of enlarged and small peroxisomes sedimenting in the fractions, are to be considered. Subcellular fractionation studies confirmed previous findings that rat liver glycerophosphate acyltransferase (GPAT) was located both in mitochondria and the microsomal fraction. BCMTD was considerably more potent than CMTTD in stimulating the microsomal and mitochondrial GPAT activities. Administration of CETTD marginally affected the isoenzymes of GPAT. Diacylglycerol acyltransferase (DGAT) activity was increased by 35% in BCMTD and CMTTD treated rats, but by administration of CETTD the enzyme activity was decreased by more than 80%. The acyl-CoA cholesterol acyltransferase (ACAT) activity was marginally affected in animals treated with BCMTD, CMTTD and CETTD. Thus, the results indicate that the initial steps in the synthesis of triacylglycerols and ether glycerolipids as well as the last step in triacylglycerol synthesis could not be identified as mediating the fat accumulation or the lowering of triacylglycerol content in liver of CETTD, or BCMTD and CMTTD treated rats. On the other hand, CMTTD increased the palmitoyl-CoA oxidation in mitochondria, and CETTD considerably inhibited the activity. Therefore, it is conceivable that the development of fatty liver with CETTD is mostly due to inhibition of mitochondrial beta-oxidation.

Acyltransferases↗
PubMed1990

Absorption, transport and distribution of vitamin E.

Vitamin E is the term used for eight naturally occurring fat-soluble nutrients called tocopherols. alpha-Tocopherol is essential, has the highest biological activity and predominates in many species. In humans vitamin E is the most important lipid soluble antioxidant and deficiency may cause neurological dysfunction, myopathies and diminished erythrocyte life span. alpha-Tocopherol is absorbed via the lymphatic pathway and transported in association with chylomicrons. In plasma, alpha-tocopherol is found in all lipoprotein fractions but mostly is associated with apo B-containing lipoproteins. alpha-Tocopherol is associated with very-low-density lipoprotein when it is secreted from the liver. In the rat, about 90% of total body mass of alpha-tocopherol is recovered in the liver, skeletal muscle and adipose tissue. Most alpha-tocopherol is located in the mitochondrial fractions and in the endoplasmic reticulum, whereas little is found in cytosol and peroxisomes. New clinical evidence from heavy drinkers and from experimental work in rats suggests that alcohol may increase oxidation of alpha-tocopherol. Increased demand for vitamin E has also been observed in premature infants and patients with malabsorption, but there is little evidence that the healthy population requires supplementation of vitamin E to a well-balanced diet.

Absorption↗
PubMed1990

Regulation of fatty acid oxidation and triglyceride and phospholipid metabolism by hypolipidemic sulfur-substituted fatty acid analogues.

The mechanisms behind the hypotriglyceridemic effect of 1,10-bis(carboxymethylthio)decane (3-thiadicarboxylic acid) and tetradecylthioacetic acid and the development of fatty liver caused by 3-tetradecylthiopropionic acid (Aarsland et al. 1989. J. Lipid Res. 30: 1711-1718.) were studied in the rat. Repeated administration of S-substituted non-beta-oxidizable fatty acid analogues to normolipidemic rats resulted in a time-dependent decrease in plasma triglycerides, phospholipids, and free fatty acids. This was accompanied by an acute reduction in the liver content of triglycerides and an increase in the hepatic concentration of phospholipids. Mitochondrial fatty acid oxidation was stimulated, whereas lipogenesis was inhibited. The activity of phosphatidate phosphohydrolase decreased while the activity of CTP:phosphocholine cytidylyltransferase increased. These results suggest that the observed triglyceride-lowering effect was due to increased mitochondrial fatty acid oxidation accompanied by a reduction in the availability of the substrate i.e., free fatty acid, along with an enzymatic inhibition (phosphatidate phosphohydrolase). Administration of 3-tetradecylthiopropionic acid led to a drastic increase in the hepatic triglyceride content. Levels of plasma triglyceride phospholipid and free fatty acid also increased. Phosphatidate phosphohydrolase activity was stimulated whereas CTP:phosphocholine cytidylyltransferase was inhibited. Mitochondrial fatty acid oxidation was decreased. These data indicate that the development of fatty liver as an effect of 3-tetradecylpropionic acid is probably due to accelerated triglyceride biosynthesis, which is mediated by an increase in the availability of fatty acid along with stimulation of phosphatidate phosphohydrolase. The results of the present study speak strongly in favor of the hypothesis that phosphatidate phosphohydrolase is a major rate-limiting enzyme in triglyceride biosynthesis. Furthermore, they point out that the biosynthesis of triglycerides and phospholipids might be coordinately regulated. Such regulation is possibly mediated via phosphatidate phosphohydrolase and CTP:phosphocholine cytidylyltransferase. Whether the increase in hepatic phospholipids via increased CDP-pathway accounts for an increase of lipid components for proliferation of peroxisomes (3-thiadicarboxylic acid and tetradecylacetic acid) should be considered.

Animals↗
PubMed1989

Low-density-lipoprotein receptors in different rabbit liver cells.

Receptor-dependent uptake mechanisms for low-density lipoprotein (LDL) were studied in rabbit liver parenchymal and non-parenchymal cells. Hybridization studies with a cDNA probe revealed that mRNA for the apo (apolipoprotein) B,E receptor was present in endothelial and Kupffer cells as well as in parenchymal cells. By ligand-blotting experiments we showed that apo B,E-receptor protein was present in both parenchymal and non-parenchymal cells. Studies of binding of homologous LDL in cultured rabbit parenchymal cells suggested that about 63% of the specific LDL binding was mediated via the apo B,E receptor. Approx. 47% of the specific LDL binding was dependent on Ca2+, suggesting that specific Ca2+-dependent as well as Ca2+-independent LDL-binding sites exist in liver parenchymal cells. Methylated LDL bound to the parenchymal cells in a saturable manner. Taken together, our results showed that apo B,E receptors are present in rabbit liver endothelial and Kupffer cells as well as in the parenchymal cells, and that an additional saturable binding activity for LDL may exist on rabbit liver parenchymal cells. This binding activity was not inhibited by EGTA or reductive methylation of lysine residues in apo B. LDL degradation in parenchymal cells was mainly mediated via the apo B,E receptor.

Animals↗
PubMed1989

[Dietary advice in hyperlipidemia. A challenge for the health care service].

We propose practical dietary advice for patients with hyperlipidemias, based on data obtained from new results in epidemiology, clinical trials and laboratory experiments. We suggest a schedule for obtaining reliable data on dietary habits, to be used as a basis for advice to the individual patient. If the dietary fat intake can be reduced from about 40% to 25% of the total energy it is possible to achieve an average reduction in serum cholesterol of 10-20%. It is very important that doctors and other health personnel become involved in providing dietary advice in connection with treatment and prevention of coronary heart disease.

Coronary Disease↗
PubMed1989

Eicosapentaenoic acid inhibits hepatic production of very low density lipoprotein.

Synthesis and secretion of triacylglycerol and cholesterol ester by cultured hepatocytes were highest in the presence of oleic, palmitic, stearic and linoleic acid, and lowest with eicosapentaenoic (EPA) and docosahexaenoic acid. Cellular formation and secretion of triacylglycerol and cholesterol ester were reduced by 50-80% in the presence of EPA in comparison with oleic acid. Reduced formation of triacylglycerol and cholesterol ester was also observed when EPA was given together with oleic acid. EPA caused higher incorporation of (3H)water into phospholipid and lower incorporation into triacylglycerol and cholesterol ester as compared with oleic acid. Rat liver microsomes incorporated EPA-CoA into triacylglycerol and cholesterol ester to a lesser extent than oleoyl-CoA. Decreased formation of triacylglycerol and cholesterol ester was also observed when EPA-CoA was given together with oleoyl-CoA, whereas palmitoyl-CoA, stearoyl-CoA, linolenoyl-CoA and arachidonoyl-CoA had no inhibitory effects. In conclusion, inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase and acyl-CoA:cholesterol acyltransferase by EPA may be important for decreased hepatic synthesis and secretion of triacylglycerol and cholesterol ester.

Acyl Coenzyme A↗
PubMed1989

Effect of n-3 fatty acid supplement to patients with atopic dermatitis.

The effects of dietary supplement with n-3 fatty acids to patients with atopic dermatitis were investigated in a 12-week, prospective, double-blind study. The experimental group received daily 10 g of fish oil, containing 3 g n-3 fatty acids, of which eicosapentaenoic acid represented about 1.8 g. The controls received an isoenergetic placebo supplement containing olive oil. Compliance was monitored by gas chromatographic analysis of fatty acid pattern in serum phospholipids. Results favoured the experimental group with regard to scale (P less than 0.05), itch (P less than 0.05) and overall subjective severity (P less than 0.02) as compared to the controls.

Adolescent↗
PubMed1989

Effect of chronic ethanol consumption on the content of alpha-tocopherol in subcellular fractions of rat liver.

The effects of long-term administration of ethanol (35% of total energy for 6-8 weeks) on the distribution and concentration of alpha-tocopherol in subcellular fractions of rat liver have been studied. Marker enzymes were measured in all fractions. The highest concentration of alpha-tocopherol was found in the light mitochondrial fraction both in ethanol-fed and control rats, 754 +/- 104 and 1127 +/- 126 pmol/mg protein, respectively. The microsomal, heavy mitochondrial, and nuclear fractions also had high concentrations of alpha-tocopherol, whereas the cytosolic fraction contained minor amounts. In the light mitochondrial fraction we found the highest concentration of alpha-tocopherol in lysosomes, whereas small amounts were detected in peroxisomes. In the microsomal fraction the highest concentration was found in the Golgi apparatus. The content of alpha-tocopherol in the light mitochondrial fraction was reduced by 33% (p less than 0.02) in the ethanol-fed group as compared to the controls. In the other fractions no significant differences between the two groups were observed. Long term administration of ethanol promoted, however, a further enrichment of alpha-tocopherol (178% higher than controls) in the Golgi apparatus, possibly due to reduced secretion of very low density lipoprotein-associated alpha-tocopherol.

Animals↗