Contrasting effects of low or high copper intake on rat tissue lipid essential fatty acid composition

The effects of low copper intake or copper supplementation on the metabolism of stearic acid have been studied previously, but their effects on essential fatty acids have not been reported. Male Sprague-Dawley rats were fed for 12 weeks on pelleted semi-synthetic diets containing less than 1 mg/kg copper (low copper), 6 mg/kg (copper control), or 250 mg/kg copper (copper supplemented). The fatty acid composition of the total phopholipids and triglycerides of plasma, liver, heart and adipose tissue was analyzed by gas liquid chromatography. In low copper rats compared to controls, palmitic and oleic acids were decreased but stearic acid and docosahexaenoic acid were increased in plasma, liver and heart phopholipids. Arachidonic acid was also increased in plasma and liver phospholipids in low copper rats. In liver triglycerides, linoleic and arachidonic acids were increased but palmitic and oleic acid were decreased in low copper rats. Copper supplementation had the opposite effect; palmitic and oleic acids were increased in phospholipids and triglycerides whereas essential fatty acids were generally decreased. Hence, copper not only has a direct effect on the desaturation of stearic acid but also has significant effects on the tissue lipid composition of essential fatty acids.     

In vivo effect of pancreatic phospholipase A2 on the arachidonic acid cascade.

BACKGROUND: In acute pancreatitis, pancreatic phospholipase A2 increases in systemic circulation. Yet the pathophysiological significance is controversial, because previous in vitro studies have shown that the enzyme has little cytotoxicity or ability to activate the arachidonic acid cascade by itself in contrast to other isozymes. AIM OF THE STUDY: The aims of this study are to examine the effect of pancreatic phospholipase A2 on the arachidonic acid cascade in vivo; to explain the discrepancy, if present, between in vitro and in vivo findings; and to reassess the pathophysiological significance of circulating pancreatic phospholipase A2. METHODS: Pancreatic phospholipase A2 was infused intravenously in guinea pigs, and changes in the arachidonic acid cascade, plasma lipoprotein, and cardiopulmonary function were investigated. RESULTS: Plasma concentrations of 6-keto-prostaglandin F1alpha, prostaglandin E2, and thromboxane B2 increased after intravenous (iv) infusion of pancreatic phospholipase A2. Some of the plasma phospholipids such as phosphatidylcholine and phosphatidylethanolamine decreased, and free dihomo-gamma-linolenic acid, arachidonic acid, and eicosapentaenoic acid were detected in plasma. These changes were accompanied with decreases in blood pressure, heart rate, and base excess. CONCLUSION: Circulating pancreatic phospholipase A2 activates the arachidonic acid cascade, probably by supplying free eicosanoid precursors from plasma lipoprotein to eicosanoid-producing cells. It is supposed to be a cause of systemic complications in acute pancreatitis.     

Original Article: Albumin Prevents TxB, Formation from Thrombin-stimulated Human Platelets by Sequestering the Liberated Arachidonic Acid in the Extracellular Space

Albumin is the major protein in plasma and possesses high affinity binding sites for fatty acids. Previous studies have shown that albumin interferes at various levels with the metabolism of arachidonic acid by stimulated human platelets. The aim of our study was to further characterise the effect of serum albumin on the release of arachidonic acid from platelet phospholipids and on the formation of thromboxane B(2) In washed prelabeled human platelets, stimulated with thrombin (0.5 U/ml), the presence of albumin in the incubation medium leads to an accumulation of [(3)H]AA in the extracellular space and to a reduced formation of thromboxane B(2). In an albumin-free medium, the radioactivity of thromboxane B(2) is markedly greater, while that of arachidonate is much less. The effect of bovine serum albumin is dose-dependent (0.35%, 1.0% and 3.5%). These data suggest that arachidonic acid liberated by PLA(2)-activation is released to the extracellular space where it binds serum albumin and thus is no longer available for its metabolic conversion to thromboxane B(2).     

克山病病区粮饲养大鼠血栓素前列环素水平及其与硒维生素E的关系

研究了硒和维生素Ｅ（ＶＥ）对大鼠血浆和心肌血栓素（ＴＸＡ２）、前列环素（ＰＧＩ２）水平及ＴＸＡ２／ＰＧＩ２比值的影响。发现饲低硒、ＶＥ的克山病病区粮组动物在谷胱甘肽过氧化物酶降低和自由基净含量、脂质过氧化物（ＬＰＯ）浓度增高的同时，ＴＸＡ２水平增高、ＰＧＩ２水平降低、ＴＸＡ２／ＰＧＩ２比值增高；加硒或／和ＶＥ对纠正上述变化有相似而又不尽相用的效果，而以联合补充效果量佳。本研究结果提示硒和ＶＥ缺乏通过影响花生四烯酸代谢参与克山病缺血缺氧性心肌坏死的发生发展，其机制可能与二者缺乏，抗氧化能力降低，生成过量自由基和ＬＰＯ，抑制了ＰＧＩ２合成酶的作用并促进ＴＸＡ２形成有关。     

Effect of the streptozotocin diabetes upon the in vivo conversion of [I-14C] gamma-linolenic and dihomo-gamma-linolenic acids into arachidonic acid in rats (author's transl)]

Streptozotocin diabetic rats were administered the same tracer dose of either [1 14C] gamma-linolenic or [1 14C] dihomo-gamma-linolenic acid by stomach tube seven days after streptozotocin injection. They were killed 48 hours later and the radioactivity in individual fatty acids of the liver determined by radio-gas chromatography. Results were compared to those obtained in non diabetic rats similarly prepared. With either radioactive precursor, 14C radioactivity recovered in hepatic dihomo-gamma-linolenic acid was not significantly affected by the diabetic state. On the other hand, 14C radioactivity incorporated into arachidonic acid was considerably decreased in diabetic rats, compared with normal rats, when the weights of hepatic arachidonic acid were the same in the two groups of animals. These results suggest that streptozotocin diabetes causes a partial inhibition of the 5-desaturation of dihomo-gamma-linolenic acid in rat liver in vivo.     

Influence of vitamin E on the antiplatelet effect of acetylsalicylic acid in human blood

We analysed the in vitro interaction between acetylsalicylic acid and vitamin E on the principal antiplatelet sites of action of acetylsalicylic acid, i.e., platelet aggregation, prostanoid production in platelets and leukocytes, and nitric oxide synthesis. Aggregation was measured in whole blood and in platelet-rich plasma (PRP) with ADP, collagen or arachidonic acid as platelet inducers, and we measured the production of thromboxane B2, prostacyclin and nitric oxide. Vitamin E potentiated the antiplatelet effect of acetylsalicylic acid in both whole blood and PRP. In PRP induced with collagen the IC50 for acetylsalicylic acid alone was 339+/-11.26, and that of acetylsalicylic acid+vitamin E was 0.89+/-0.09 (P<0.05). Vitamin E did not enhance inhibition of platelet thromboxane production by acetylsalicylic acid. Vitamin E spared or even increased prostacyclin levels, and acetylsalicylic acid+vitamin E diminished the inhibition of prostacyclin synthesis by acetylsalicylic acid (IC50 acetylsalicylic acid alone=1.81+/-0.15 microM; IC50 acetylsalicylic acid+vitamin E= 12.92+/-1.10 microM, P<0.05). Vitamin E increased the effect of acetylsalicylic acid on neutrophil nitric oxide production 42-fold (P<0.05). We conclude that vitamin E potentiates the antiplatelet effect of acetylsalicylic acid in vitro, and thus merits further research in ex vivo studies.     

Significance of prostaglandin E2 in acute necrotising pancreatitis in rats.

Acute necrotising pancreatitis in rats was induced by injecting 5% sodium taurocholate into the pancreatic duct. Prostaglandin E2 (100 micrograms/kg subcutaneously twice) decreased the mortality rate from 100% to 60% (NS). When treatment with prostaglandin E2 was combined with simultaneous administration of either dazmegrel (UK 38,485, 50 mg/kg bodyweight) or Sibelium (Flunarizine R 14,950, 0.2 mg/kg body weight) a significant decrease in the mortality rate (p less than 0.05) was recorded. Dazmegrel is a selective thromboxane A2 synthetase inhibitor and prevents the formation of thromboxane A2. Flunarizine (a calcium entry blocker) decreases thromboxane A2 formation and also inhibits the effects of raised thromboxane A2 concentrations. As plasma thromboxane B2 (the stable metabolite of thromboxane A2) concentrations increase and the plasma prostaglandin E2 concentrations decrease in acute necrotising pancreatitis in rats, the results of the present study indicate that these prostaglandins play a role in the pathophysiology of the disease. It is suggested that restoration of the balance in prostanoid concentrations will have a beneficial effect on the course of acute necrotising pancreatitis.     

Plasma fatty acid composition and lipid peroxide levels in children with paucity of interlobular bile ducts

The total and free fatty acid composition of plasma and lipid peroxide concentrations was studied in 32 cholestatic children with syndromatic paucity of interlobular bile ducts (Alagille's syndrome). The mean lipid peroxide value in these patients was 8.80 +/- 3.70 nmol/ml, nearly 4 times higher than the mean control value. Compared to the control group, the patients exhibited significant variations in total fatty acids, and in particular a relative decrease in linoleic acid (from 29.5 +/- 6.1% in the controls to 19.1 +/- 8.03% in the patients) compensated by an increase in saturated and monounsaturated fatty acids. The plasma lipid peroxide levels were inversely correlated with the unsaturated/saturated fatty acids ratio in total fatty acids, and with the vitamin E status (vitamin E/total lipids). Most of the total and free fatty acid variations observed were largest in patients with severe jaundice. Dietary fat malabsorption and the increase in lipid peroxidation partly explain these results. Furthermore, in free fatty acids, we observed a marked increase in arachidonic acid (from 1.43 +/- 0.85% in the controls to 4.27 +/- 2.24% in the patients), suggesting abnormal eicosanoid synthesis.     

Platelet function, thromboxane formation and blood pressure control during supplementation of the Western diet with cod liver oil

Epidemiologic and experimental data suggest an antiatherothrombotic potential of omega-3 polyunsaturated fatty acids. Therefore, the Western diet, which supplies predominantly omega-6 polyunsaturated fatty acids, was supplemented with 40 ml/day of cod liver oil, which provides about 10 g of omega-3 polyunsaturated fatty acids daily, for 25 days in eight volunteers. The omega-3 polyunsaturated fatty acids were incorporated in platelet and erythrocyte membrane phospholipids at the expense of omega-6 polyunsaturated fatty acids. Bleeding time increased (p less than 0.01) and platelet count (p less than 0.05), platelet aggregation upon ADP and collagen (p less than 0.01-0.05), and associated thromboxane B2 formation (p less than 0.01) decreased. Blood pressure (p less than 0.05) and blood pressure response to norepinephrine (p less than 0.01) and angiotensin II (NS) fell, without major changes in plasma catecholamines, renin, urinary aldosterone, kallikrein, prostaglandins E2 and F2 alpha and red cell cation fluxes. Biochemical and functional changes were reversed 4 weeks after cod liver oil was discontinued. Formation of prostaglandins derived from eicosapentaenoic acid and interference of eicosapentaenoic acid with formation and action of prostaglandins derived from arachidonic acid were evident in vitro. Whatever the mechanism, this moderate supplement of omega-3 polyunsaturated fatty acids markedly changed membrane phospholipids, which was associated with a shift toward less reactive platelets and a blunted circulatory response to pressure hormones.     

Evening primrose oil in rheumatoid arthritis: changes in serum lipids and fatty acids.

The serum concentration of lipids and composition of fatty acids after overnight fasting were studied in 18 patients with rheumatoid arthritis treated for 12 weeks with either 20 ml of evening primrose oil containing 9% of gamma-linolenic acid or olive oil. The serum concentrations of oleic acid, eicosapentaenoic acid, and apolipoprotein B decreased and those of linoleic acid, gamma-linolenic acid, dihomo-gamma-linolenic acid, and arachidonic acid increased during treatment with evening primrose oil. During olive oil treatment the serum concentration of eicosapentaenoic acid decreased and those of high density lipoprotein-cholesterol and apolipoprotein A-I increased slightly. The decrease in serum eicosapentaenoic acid and the increase in arachidonic acid concentrations induced by evening primrose oil may not be favourable effects in patients with rheumatoid arthritis in the light of the roles of these fatty acids as precursors of eicosanoids.     

Effect of streptozotocin diabetes on the in vivo conversion of gamma-linolenic and dihomo-gamma-linolenic 14C acids to arachidonic acid in the rat kidney and in the rat body

Streptozotocin diabetic rats were administered the same tracer dose of either [1 14C] gamma-linolenic acid or [2 14C] dihomo-gamma-linolenic acid by stomach tube seven days after streptozotocin injection. They were killed 48 hours later and the radioactivity in individual fatty acids of the kidneys and the whole animal determined by radio-gas chromatography. Results were compared to those obtained in non diabetic rats similarly prepared. With either radioactive precursor, 14C radioactivity incorporated into arachidonic acid, only as specific radioactivity of this acid, were considerably decreased in diabetic rats compared with normal rats, while the weights of renal and whole rat arachidonic acid were the same in the two groups of animals. These results suggest that, in vivo, streptozotocin diabetes causes a partial inhibition of the delta 5-desaturation of dihomo-gamma-linolenic acid, considered as a secondary step in linoleic acid metabolism, both in the kidneys and the whole rat as in the liver.     

Plasma Lipoproteins and Fatty Acid Composition during a Moderate Eicosapentaenoic Acid Diet

ABSTRACT. The effect of a diet rich in marine fatty acids, especially eicosapentaenoic acid, on plasma lipids (total plasma cholesterol, HDL cholesterol, total triglycerides and apolipoproteins A and B) and fatty acid composition in plasma phosphatidylcholine (PC) was studied in 10 healthy men. They were maintained for 11 weeks on their normal diet which was partly replaced by 150–200 g of fatty fish per day. In the same individuals this diet had previously caused a delay in primary haemostasis and a decrease in platelet aggregability similar to that caused by acetylsalicylic acid, a known inhibitor of thromboxane A₂ formation. Apart from its effect on haemostasis, the fish diet substantially reduced serum triglycerides (by 43%, p < 0.01) but caused no changes in total plasma or HDL cholesterol or apolipoproteins A and B. After three weeks on the diet the proportion of plasma PC ω-3 polyunsaturated fatty acids increased (C20: 5 and C22: 6) and ω-6 fatty acids decreased (C18: 2 and C20:3). The relative plasma PC content of arachidonic acid was unaffected throughout. These alterations in plasma PC fatty acid composition were principally in accordance with those seen in platelet membrane PC. There was a linear correlation between the content of ω-3 and of ω-6 fatty acids in plasma PC with that of platelet PC as well as in predominate individual fatty acids of the two series. Six weeks after the volunteers had resumed their usual diet, total triglycerides and the fatty acid composition of plasma PC had returned to the original state.     

Diets rich in saturated n-9 and n-3 fatty acids differentially affect the fatty acid composition of phospholipids and function of rat platelets

The aim of the present study was to determine whether dietary intake of monounsaturated or long chain n-3 fatty acids could be effective in lowering platelet responsiveness through modulation of platelet phospholipid composition. Rats were fed diets containing 20% fat with equal cholesterol and 13a-tocopherol contents. These diets were supplemented with saturated, oleic or n-3 fatty acids, n-3 polyunsaturated fatty acids being added either pure, as eicosapentaenoic and docosahexaenoic ethyl esters, or as MaxEPA oil. Dietary n-3 fatty acids did not affect the oxidation status of plasma lipids. Oleic acid- and saturated fatty acid-rich diets led to similar enrichment of platelet phospholipids in arachidonic acid and to comparable thromboxane A(2) generation on stimulation with collagen or thrombin. Platelets of n-3-fed groups were differently enriched in eicosapentaenoic and docosahexaenoic acids at the expense of arachidonic acid. These groups displayed similar thromboxane A(2) production, although levels were lower than those for groups fed with oleic- or saturated fatty acid-rich diets. Only the MaxEPA diet led to a reduction in platelet reactivity, measurable as a small decrease in the aggregation induced by collagen. This diet was also responsible for a high cholesteroUphospholipid ratio and low a-tocopherol content in platelets. Overall results indicated that (i) only MaxEPA reduced platelet reactivity and (ii) this effect was moderate and apparently unrelated to platelet arachidonic acid content, membrane cholesterol to phospholipid ratio or thromboxane A(2) production.     

Effect of fatty acid administration on plasma thyroid hormones in the domestic fowl

In birds a severe stress is associated with a reduction in concentrations of plasma thyroxine. Studies in man and the rat have demonstrated that severe illness is associated with an increase in serum concentrations of free fatty acids, notably oleic acid, and that they are associated with a reduction in concentrations of serum thyroxine (T4) and/or triiodothyronine (T3). Since stress is associated with increased fatty acids in birds, we have, in the present study, examined the role of oleic acid and another polyunsaturated fatty acid, arachidonic acid, on thyroid function tests (plasma thyroxine, triiodothyronine, and T3 resin uptake (RT3U) index) and on the thyroidal response to exogenous thyroid-stimulating hormone (TSH) in the domestic fowl. In the first study we observed that the iv administration of arachidonic (10 mg/kg) or oleic acid (15 mg/kg) to groups of 10-week-old cockerels (six per group) was associated with a significant reduction in concentrations of plasma T4, whereas there was little change in saline-injected controls. However, administration of fatty acids to chickens was not associated with a significant change in RT3U index or in the levels of plasma T3. In the second study, groups of animals (n = 6) were injected with bovine TSH (0.5 IU/kg, im) or saline 2.5 hr after the fatty acid injection and blood samples were obtained at -2.5 to 24 hr after the TSH injection. A similar progressive increase in serum T4 was observed for the three groups studied whereas there was little change in the concentrations of plasma T3.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arachidonic acid deficiency in streptozotocin-induced diabetes.

Fatty acid compositions of phospholipids of heart, liver, kidney, aorta, and serum from rats having streptozotocin-induced diabetes were determined and compared with those of nondiabetic controls. Linoleic and dihomo-gamma-linolenic acids were increased whereas arachidonic acid was decreased in most tissues, suggesting an impairment of delta 5-desaturase activity. Acids derived from linolenic acid were increased in some diabetic tissues from diabetic animals although the linolenic content was normal, indicating less impairment in the desaturation of the omega 3 series of fatty acids. Diabetes suppressed all polyunsaturated acids in the whole animal, but the competition between omega 3 and omega 6 acids favored the excessive suppression of long-chain omega 6 acids and an increase in the proportion of omega 3 acids in lipids of vital tissues. These changes in fatty acid composition of the phospholipids may have significant effects on cellular functions and vasoregulatory control mechanisms in diabetes.     

Familial Bleeding Tendency with Partial Platelet Thromboxane Synthetase Deficiency: Reorientation of Cyclic Endoperoxide Metabolism

Three family members from three successive generations presented with a moderate bleeding tendency and a functional platelet defect. They had absent aggregation with arachidonic acid (0.6--3 microM), reversible aggregation with ADP (4 microgram) and cyclic endoperoxide analogues, single wave aggregation only with adrenaline (5.4 microgram) and a prolonged template bleeding time (> min). Malondialdehyde formation was reduced after N-ethylmaleimide stimulation (2--6 nmol/10(9) platelets; control values 8--12 nmol) and serum thromboxane B2 values were reduced (33--101 ng/ml; control values 200--700 ng/ml). When the platelets were incubated with [3H]arachidonic acid the final metabolite of the lipoxygenase pathway (HETE) was produced in normal amounts but the production of thromboxane B2 and HHT was decreased whereas prostaglandin F2a, and E2 and probably D2 were increased. Evidence for enhanced production of prostaglandin D2 was also provided by the rise in the patient's platelet cyclic AMP levels following stimulation with arachidonic acid. The patient's washed platelets stimulated the production of 6-keto PGF 1a by aspirin-pretreated cultured bovine endothelial cells. The plasma levels of 6-keto PGF1a (439--703 pg/ml; normal 181 +/- 46 pg/ml) were raised. The decreased production of thromboxane B2, HHT and malondialdehyde and increased formation of prostaglandin F2a, E2, D2 and of 6-keto PGF1a are compatible with a partial platelet thromboxane synthetase deficiency and reorientation of cyclic endoperoxide metabolism. The markedly prolonged bleeding time would result not only from reduced formation of thromboxane A2 but also from increased production of the aggregation inhibiting prostaglandins PGI2 and PGD2.     

Plasma eicosanoid levels in rats with nonketotic diabetes mellitus: effect of severity

Nonketotic diabetes mellitus (DM) is associated with increased platelet production of thromboxane (TX) A2 and decreased endothelial production of prostacyclin (prostaglandin [PG]I2), but measurements of stable derivatives of these substances in the circulation have yielded discordant results. We studied the relationship between the severity of nonketotic DM and the plasma levels of 13,14-dihydro-15-keto-PGE2, 6-keto-PGF1 alpha, and TXB2 (stable derivatives of PGE2, PGI2, and TXA2, respectively) in rats, using three commonly employed doses of streptozotocin (40, 50, and 60 mg/kg body weight) to induce nonketotic DM of varying severity. Small differences in the severity of DM were associated with considerable differences in the plasma levels of 13,14-dihydro-15-keto-PGE2 and 6-keto-PGF1 alpha but not TXB2. Each eicosanoid responded differently to variations in the severity of DM. The plasma 13,14-dihydro-15-keto-PGE2 level was significantly lower than normal in the rats given 40 mg/kg streptozotocin, was unchanged from normal in the rats given 50 mg/kg and was significantly higher than normal in the rats given 60 mg/kg. The plasma 6-keto-PGF1 alpha level was significantly increased in rats given 40 mg/kg and 60 mg/kg, but was unchanged in those given 50 mg/kg. The plasma TXB2 level was not significantly different from normal in any one of the three groups of rats with nonketotic DM. The effect of severity on the plasma levels of the PGE2 and PGI2 derivatives is unexplained, but may reflect the origin of these derivatives from diverse organs and tissues, and the differing effects of abnormal metabolic factors (eg, fatty acids, glucose, insulin, pH) on the synthesis of these derivatives.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hepatic Triacylglycerol Accumulation Induced by Ethanol and Carbon Tetrachloride: Interactions with Essential Fatty Acids and Prostaglandins

Triacylglycerol accumulation in the liver (fatty liver) caused by ethanol or carbon tetrachloride involves interactions with essential fatty acids and prostaglandins. The degree to which the fatty liver develops is dependent on total dietary fat intake. Both ethanol and carbon tetrachloride impair desaturation of linoleic acid and dihomo-gamma-linolenic acid and this appears to be relevant to the pathogenesis of fatty liver from two points of view. First, low arachidonic acid in liver phospholipids is associated with increased liver triacylglycerol content whether caused by ethanol, carbon tetrachloride, or essential fatty acid deficiency. Second, essential fatty acids including gamma-linolenic acid and arachidonic acid, as well as the prostaglandins, prevent ethanol- and carbon tetrachloride-induced fatty liver. Arachidonic acid and possibly the prostaglandins are therefore likely to be directly involved in lipoprotein and triacylglycerol secretion by the liver.     

Correlation between dietary polyunsaturated fatty acids and plasma homocysteine concentration in vitamin B6-deficient rats

BACKGROUND AND AIM: Vitamin B6 as cofactor of Delta6 desaturase is involved in polyunsaturated fatty acid metabolism; moreover, it is a cofactor of the trans-sulfuration pathway of homocysteine. Some studies report that low concentrations of pyridoxine, by increasing homocysteine levels, are associated with coronary artery disease, and carotid and arterial lesions. The aim of this study was to verify whether different dietary amounts of polyunsaturated fatty acids associated with low content of vitamin B6 could modulate homocysteinemia. METHODS AND RESULTS: Thirty-two rats were divided into two groups, one fed a diet with adequate vitamin B6 content the other a diet containing low amount of the same vitamin. Within each group, rats were divided into two subgroups differing in the polyunsaturated fatty acid content of the diet (63 and 33%, respectively). The vitamin B6-deficient diet induced an increase in homocysteine concentration compared to the vitamin B6-normal diet. This increase was tenfold in the subgroup fed high polyunsaturated fatty acid levels and twofold in the other subgroup. The fatty acid composition of liver phospholipids showed a lower arachidonic acid relative molar content and a lower 20:4/18:2 ratio in vitamin B6-deficient groups compared with B6-normal groups. CONCLUSIONS: On the basis of the different biological functions of pyridoxine and considering that some factors closely related to atherosclerosis are vitamin B(6) dependent, adequate pyridoxine availability could be necessary to assure a normal long chain fatty acid metabolism and to reduce the risk linked to hyperhomocysteinemia.     

Experimental diabetes treated with ficus carica extract: effect on oxidative stress parameters

Parameters related to oxidative stress were studied in rats divided into 4 groups: streptozotocin-induced diabetic rats (n=10), diabetic rats who received a single dose of a basic fraction of Ficus carica extract (n=14), diabetic rats who received a single dose of a chloroform fraction of the extract (n=10), and normal rats (n=10). Compared to normal animals, the diabetic animals presented significantly higher values for erythrocyte catalase normalized to haemoglobin levels (1.5±0.15 vs. 0.96±0.18 μg/mg) and for plasma vitamin E (73.4±43.9 vs. 12.0±1.6 mg/l), monounsaturated fatty acids (0.219±0.118 vs. 0.067±0.014 mg/ml), polyunsaturated fatty acids (PUFA, 0.567±0.293 vs. 0.175±0.040 mg/ml), saturated fatty acids (0.779±0.262 vs. 0.401±0.055 mg/ml), and linoleic acid (0.202±0.086 vs. 0.106 ±0.014 mg/ml). Both Ficus carica fractions tended to normalize the values of the diabetic animals' fatty acids and plasma vitamin E values. On studying the ratios of vitamins E and A to PUFA (129.4±77.5 diabetic and 68.8±9.1 μg/mg normal; 37.5±20.8 vs. 108.0±43.6 μg/mg) and to C18:2 (259.9±65.8 vs. 161.0±21.3 μg/mg; 68.3±37.9 vs. 252.7±102.1 μg/mg), we found statistically significant differences as a function of diabetes, with the vitamin E/C18:2 ratio being normalized by the administration of the chloroform fraction (to 152.1±80.3 μg/mg) and the vitamin A/C18:2 ratio being raised relative to the untreated diabetic rats by the administration of the basic fraction (91.9±14.5 μg/mg). Our work confirms that antioxidant status is affected in the diabetes syndrome, and that Ficus carica extracts tend to normalize it. Received: September 2000 / Accepted in revised form: September 2002 Correspondence to M.D. Torres