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Biomedical subjects

B A Nassar

Publications and source records attributed to B A Nassar.

At least 19 recordsLinked to original sources
PubMed1992

The effect of chemical hepatocarcinogenesis on liver phospholipid composition in rats fed N-6 and N-3 fatty acid-supplemented diets.

The effect of dietary fats on essential fatty acid metabolism in rats subjected to chemically induced hepatocarcinogenesis was studied. Sixty male rats were fed a diet supplemented with one of the following three oil compositions: 10% hydrogenated coconut oil (HCO); 5% hydrogenated coconut oil and 5% gamma-linolenic acid (18:3n-6)-rich evening primrose oil (EPO); or 5% hydrogenated coconut oil and 5% marine oil (FO). Half of the animals in each dietary regimen were subjected to hepatocarcinogenesis induction using diethylnitrosamine and 2-acetylaminofluorene (2-AAF) followed by partial hepatectomy, whereas the other half underwent hepatectomy without receiving diethylnitrosamine and 2-acetylaminofluorene. Liver phospholipid composition was analyzed. In comparison to the HCO group, the EPO group showed raised levels of arachidonic acid (20:4n-6) and suppressed n-3 fatty acids. The FO group, on the other hand, showed suppressed levels of n-6 and increased n-3 fatty acids. Hepatocarcinogenesis suppressed the level of 20:4n-6 and this effect was greater in the FO rats. The levels of dihomo-gamma-linolenic acid (20:3n-6) were increased by the hepatocarcinogenic treatment, and this effect was further accentuated in the EPO rats. These results suggest that hepatocarcinogenesis may suppress the activity of delta-5-desaturase, which may be one of the reasons why tumor cell membranes have low levels of long chain fatty acids, especially 20:4n-6 cells, and have an impaired capacity to undergo lipid peroxidation.

Animals↗
PubMed1990

Release of essential fatty acids from the rat mesenteric vascular bed perfused in vitro: modulation by zinc.

The rat mesenteric vascular bed releases prostaglandins when perfused in vitro. The present study evaluated the effect of perfusion of the rat mesenteric vascular bed in vitro with a buffer containing 0, 3, 6, or 9 nM of added zinc on the release of essential fatty acids over a 150-min period. Long chain fatty acids in the mesenteric lipids and in total lipid of the perfusion effluent were assayed by gas liquid chromatography. The presence of 6 nM zinc in the perfusing buffer almost completely prevented the change in 16-22 carbon long chain fatty acids in the mesenteric phospholipids and decreased the release of free fatty acids in comparison to that occurring in the absence of additional zinc. The results suggest that physiological amounts of zinc in the perfusion medium reduce the release of essential fatty acid from rat mesenteric lipids.

Animals↗
PubMed1989

The prostaglandin outflow from perfused mesenteric vasculature of rats fed different fats.

The effects of dietary n-6 polyunsaturated fatty acids and replacement with saturated fat or fish oil on the prostaglandin outflow from perfused mesenteric vasculature in rats were studied. Seventy-two weanling male rats were fed ad libitum a semi-synthetic diet supplemented with 10% by weight of oil, composed wholly of n-6 fatty acid-rich evening primrose oil, or replaced partly or completely (25, 50, 75 or 100%) by n-6 fatty acid-deficient fish oil or hydrogenated coconut oil for 8 weeks. The outflows of 6-keto-PGF1 alpha, thromboxane B2, and prostaglandin E from the perfused mesenteric vasculature were measured at 60 min-time point after starting the perfusion. In general, the release of prostanoids from the mesenteric vasculature was significantly reduced in rats fed a diet in which evening primrose oil was partly or completely replaced by either hydrogenated coconut or fish oil. This was probably due to the insufficient conversion of linoleic acid to arachidonic acid. The extent of reduction was greater in fish oil-fed than in hydrogenated coconut oil-fed rats, while the levels of arachidonic acid in aortic phospholipids were similar between these two groups. This result implies that the greater reduction of prostaglandin synthesis in rats fed fish oil was due to the inhibitory effect of eicosapentaenoic and docosahexaenoic acids in fish oil on the conversion of arachidonate to eicosanoids.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

The influence of phenelzine and tranylcypromine on the release of prostaglandins from the rat mesenteric vascular bed.

We investigated the effects of phenelzine and tranylcypromine on the release of prostacyclin, thromboxane A2, prostaglandin E2, and prostaglandin E1 from the isolated perfused rat mesenteric vascular bed. Perfusion of the preparation with phenelzine in concentrations of 15, 45, and 135 microM for 150 min led to attenuated release of all four prostaglandins measured. Inhibition generally occurred with the lowest dose used and was most prominent with the highest concentration. Tranylcypromine also decreased prostaglandin formation. However, low doses were not effective in the suppression of prostacyclin release. Both drugs had an inhibitory effect on production of prostaglandin E1, which is a metabolite of dihomo-gamma-linolenic acid, the precursor of arachidonic acid, but this was only shown to be significant with phenelzine. In this work we demonstrate that phenelzine and tranylcypromine have an inhibitory effect on the production of 2-series prostaglandins derived from arachidonic acid, and possibly a similar effect on prostaglandins of the 1-series derived from dihomo-gamma-linolenic acid.

Alprostadil↗
PubMed1987

Effect of different ratios of dietary N-6 and N-3 fatty acids on fatty acid composition, prostaglandin formation and platelet aggregation in the rat.

Five groups of male Sprague-Dawley rats (150 g) were fed a fat-free diet supplemented with 10% by weight of evening primrose oil (Efamol, rich in linoleic acid and gamma-linolenic acid) and/or marine oil (Polepa, rich in eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3) combined in several ratios (Efamol/Polepa; 10.0%/0%; 7.5%/2.5%; 5.0%/5.0%; 2.5%/7.5%; 0%/10.0%). The n-6 fatty acid levels in aortic, platelet and plasma phospholipids decreased in proportion as Efamol was replaced with Polepa. The exception in phospholipids was dihomo-gamma-linolenic acid (20:3n-6), which increased when marine oil was provided in the diet with Efamol. The ratio of 20:3n-6 to arachidonic acid (20:4n-6) was positively correlated with 20:5n-3, docosapentaenoic acid (22:5n-3) or 22:6n-3 in aortic, platelet and plasma phospholipids under these dietary conditions. In contrast, 20:3n-6 in plasma cholesterol esters, triglycerides and free fatty acids did not show any increase in the presence of Polepa. Aortic prostaglandin (PG) production (6-keto-PGF1 alpha, PGE2 and PGE1) was reduced as Efamol was progressively replaced with Polepa. Aortic PG production was positively correlated with 20:4n-6 content in aortic phospholipids. Thrombin-induced thromboxane B2 production in whole blood was related to 20:4n-6 content in platelet phospholipids. However, ADP-induced platelet aggregation was significantly decreased only in the 7.5% Efamol/2.5% Polepa group as compared to the other 4 groups. These results suggest that combined treatment with Efamol and Polepa increases the ratio of 20:3n-6 to 20:4n-6 in tissue and plasma phospholipids. An appropriate ratio of these oils favorably affects aortic PG production and platelet ADP aggregation.

Adenosine Diphosphate↗
PubMed1987

The influence of dietary marine oil (Polepa) and evening primrose oil (Efamol) on prostaglandin production by the rat mesenteric vasculature.

The interactions of n-6 and n-3 fatty acids on prostaglandin metabolism in the isolated rat mesenteric vessels were studied. Sprague-Dawley rats (200-220 g) were fed for two weeks a fat-free semi-synthetic diet supplemented with 10% by weight of different combinations of Evening Primrose Oil (Efamol), a rich source of linoleic acid (LA) and gamma-linolenic acid (GLA), the immediate precursor of dihomo-gamma-linolenic acid (DGLA), and Polepa (POL), a marine oil rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. The combinations of supplement were as follows: 9% Efamol - 1% POL, 8% Efamol - 2% POL, 7% Efamol - 3% POL, 6% Efamol - 4% POL, 5% Efamol - 5% POL. The outflow of thromboxane (TxB2), prostacyclin (6-keto-PGF1 alpha), PGE2, and PGE1 was decreased in relation to the proportion of marine oil in the diet, except for the group which received 8% Efamol - 2% POL, and which showed an increase in 6-keto-PGF1 alpha, PGE2, and PGE1. The decrease in TxB2 was much greater than those of 6-keto-PGF1 alpha or PGE2, while PGE1 followed the same pattern as prostacyclin and PGE2. These results suggest that n-3 fatty acids, at high concentrations, inhibits conversion of both DGLA and AA to eicosanoids. Low concentrations of fish oil may, in contrast, increase formation of desirable 1 and 2 series eicosanoids.

Administration, Oral↗
PubMed1986

Changes of plasma lipids and long-chain n-3 and n-6 fatty acids in plasma, liver, heart and kidney phospholipids of rats fed variable levels of fish oil with or without cholesterol supplementation.

Diets supplemented with 10% by weight of oil, either wholly safflower oil or proportinally (25, 50, 75 or 100%) replaced by fish oil, were given to 60 rats which had previously been deprived of dietary fat for 6 weeks. Half the animals on each dietary regimen were also given 1% of cholesterol. After 4 weeks of feeding, the plasma lipid contents and the phospholipid fatty acid compositions of plasma, liver, heart and kidney were determined. In general, the concentrations of plasma lipids were significantly reduced in animals fed a diet containing 5% or more of fish oil in comparison with those fed only safflower oil. Cholesterol feeding increased the levels of plasma cholesterol, whereas it lowered those of plasma triacylglycerols and phospholipids. The levels of 20:4(n - 6) in all four tissues were sharply reduced, whereas those of 18:2(n - 6) increased when 25% of dietary safflower oil was replaced by fish oil. Both 18:2(n - 6) and 20:4(n - 6) were decreased as the contents of dietary fish oil were further increased. The levels of long-chain n-3 fatty acids, e.g., 20:5(n - 3), 22:5(n - 3) and 22:6(n - 3) were increased as the intake of fish oil increased. The incorporation of 22:6(n - 3) was greater in plasma, liver and heart phospholipids, whereas that of 20:5(n - 3) was greater in kidney phospholipids. Cholesterol feeding also increased the levels of 18:2(n - 6) and 20:5(n - 3), whereas it decreased the levels of 20:4(n - 6) and 22:6(n - 3) in plasma and liver. However, these changes were not observed in heart and kidney.

Animals↗
PubMed1986

The influence of dietary manipulation with n-3 and n-6 fatty acids on liver and plasma phospholipid fatty acids in rats.

The interrelations between linoleic acid (LA) metabolites and fish oil fatty acids were studied. Sprague-Dawley rats (200-220 g) were fed a fat-free semisynthetic diet supplemented with 10% (by weight) of different combinations of evening primrose oil (EPO), a rich source of LA and gamma-linolenic acid, and polepa (POL), a marine oil rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. The combinations of supplement were as follows: 9% EPO-1% POL, 8% EPO-2% POL, 7% EPO-3% POL, 6% EPO-4% POL and 5% EPO-5% POL. After two weeks on the respective diets, the animals were killed, and the fatty acid compositions of liver and plasma phospholipids were examined. The results showed that animals fed higher proportions of POL consistently contained higher levels of dihomo-gamma-linolenic acid (DGLA) (p less than 0.05), a metabolite of LA and GLA, and lower levels of arachidonic acid (AA) (p less than 0.01), a metabolite of DGLA through delta-5-desaturation. Thus, an inverse relationship between AA/DGLA ratio and EPA levels was found to exist (r = -0.765 in plasma and -0.792 in liver). However, there was no such relationship between AA/DGLA ratio and DHA levels. This result suggested that EPA but not DHA in fish oil exerts an inhibitory effect on the conversion of DGLA to AA.

Animals↗
PubMed1975

Seasonal and sexual variations in the responsiveness of rabbit hearts to prolactin.

Rabbit hearts perfused by the Langendorff technique were studied. The addition of ovine prolactin (NIH-P-S-10) to the perfusate in a concentration of 50 ng/ml produced rapid increases in both the amplitude and rate of contraction in 33 adult male hearts studied in winter. Prepubertal male animals showed no response, and only 1 out of 12 adult females responded. Pretreatment for 10 days with 2.5 mg/day testosterone propionate led to minimal inotropic but not chronotropic responses in 2 out of 4 prepubertal males and 2 out of 4 adult females to prolactin. Clear responses to prolactin were seen in 5 adult males pretreated with reserpine. Propanolol consistently reversed both the inotropic and chronotropic actions of prolactin. The original experiments were performed in January and February. When tested in May, adult males failed to respond to prolactin and this situation, persisted until October when responsiveness again appeared. The same prolactin preparation and procedures were used throughout indicating that the changes must have been due to seasonal variations in the cardiac responsiveness to the hormone.

Animals↗