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Biomedical subjects

A B Awad

Publications and source records attributed to A B Awad.

49 records · Page 3Linked to original sources
PubMed1982

Age-dependent alterations in lipids and function of rat heart sarcolemma.

The objective of the present study was to examine the effect of age on heart sarcolemma structure and function. Sarcolemmal fractions were prepared from hearts of young (1-1.5 months) and adult (10-12 months) rats and assayed for marker enzyme activities. The membrane fractions were found to be devoid of other cellular organelles upon examination by electron microscopy. They were enriched with 5'-nucleotidase and devoid of succinate dehydrogenase activity. The only age-related lipid compositional changes noted in these membranes were changes in the fatty acid composition of membrane phospholipids with increasing age. Most changes were detected in phosphatidylcholine and phosphatidylethanolamine with very little alteration of sphingomyelin and phosphatidylserine plus phosphatidylinositol fatty acids. Polyunsaturated fatty acids, especially 18:2 and 20:4, were decreased with saturated fatty acids increased in membrane phosphatidylcholine and phosphatidylethanolamine fractions as the animal develops. There was a decrease in the specific activities of (Na+ + K+)-ATPase and 5'-nucleotidase of these membranes with age. On the other hand, membrane (K+)-rho-nitrophenylphosphatase was not affected by age.

5'-Nucleotidase↗
PubMed1981

Effect of dietary lipids on composition and glucose utilization by rat adipose tissue.

Feeding rats diets rich in either safflower oil or coconut oil resulted in a significant change in the lipid composition of epididymal fat pads as compared with those obtained from rats fed a commercial stock diet. A safflower oil diet resulted in an increase in tissue cholesterol and a decrease in phospholipid concentration as compared with the stock diet. A coconut oil diet resulted in a decrease in both tissue cholesterol and phospholipid concentrations as compared with the stock diet. Adipose tissue fatty acid composition was also altered due to these dietary manipulations. Glucose utilization by adipose tissue from animals fed the safflower oil diet was 2 and 10 times greater than glucose utilization by adipose tissue from animals fed the stock and coconut oil diets, respectively. The coconut oil diet resulted in an increase in the percentage of glucose incorporated into adipose tissue diglycerides, free fatty acids and cholesterol esters and a decrease in the percentage of glucose incorporated into triglycerides as compared with animals fed the stock or safflower oil diet. The incorporation of glucose into adipose tissue fatty acids was depressed by a saturated fatty acid diet as compared with either a polyunsaturated fatty acid diet or the stock diet.

Adipose Tissue↗
PubMed1981

Trans fatty acids in tumor development and the host survival.

Because trans fatty acids exist in the American diet and their relationship to cancer incidence has been proposed, studies were designed to investigate their possible role in the development of Ehrlich tumor cells in inbred CBA mice. Feeding elaidic acid (18:1 delta 9, trans) to Ehrlich ascites tumor-bearing animals resulted in tumors that incorporated more thymidine into their cells and into their acid-insoluble fraction as compared with those grown in animals fed the natural oleic acid (18:1 delta 3, cis)-rich diet. Elaidic acid diet feeding at 5% in the diet also resulted in a reduction in the host survival rate. This reduction ranged from 23 to 45%.

Animals↗
PubMed1981

Uptake and oxidation of elaidic acid by Ehrlich ascites tumor cells.

The present studies were designed to investigate some aspects of trans fatty acid metabolism by Ehrlich ascites tumor cells, i.e., uptake, oxidation and incorporation into cellular lipids. Elaidic acid (18:1delta9, trans) was compared with its cis counterpart (oleic acid) and with stearic acid (18:0) in its metabolism. These studies indicate that tumor cells take up elaidic acid at the same rate as stearic acids. Stearic acid is taken up at a higher rate than oleic acid. The oxidation of these fatty acids to CO2 by tumor cells followed the same pattern of uptake, i.e., elaidic acid was oxidized at the same rate as stearic acid but at a higher rate than oleic acid. In that tumor cells are different from the normal cells that are known to oxidize trans fatty acids at a slower rate as compared with their cis counterparts. The incorporation of these fatty acids into tumor cell lipids was found to be different. These data indicate that tumor cells handle elaidic acid differently than normal cells in some aspects of its metabolism.

Animals↗
PubMed1978

The effect of elaidic acid incorporation upon the lipid composition of Ehrlich Ascites tumor cells and of the host's liver.

The incorporation of elaidic acid into Ehrlich ascites tumor cells (EATC) upon feeding the host an elaidic acid-rich diet has been investigated in the present study. The EATC lipids contained only one-half the concentration of elaidic acid found in the lipids of either the host livers or of livers from normal mice. On the other hand, elaidic acid incorporation into tumor cells was close to that of ascites fluid. This incorporation was mainly into phospholipids; the highest into choline phospholipids and ethanolamine phospholipids. Some changes in the EATC fatty acid composition were noted due to this incorporation. EATC phospholipids had reduced polyunsaturated fatty acids as compared with oleic acid-grown cells. The same was true with respect to ascites fluid phospholipids, but neutral lipids were not altered. Tumor development was accompanied by an increase in elaidic acid of the host's liver. Elaidic acid incorporation into tumor cells resulted in a reduction in the amount of all major lipids in the tumor. In contrast, elaidic acid had no effect on lipid composition of livers from normal mice and and-tumor bearing mice, and also had no effect upon the lipids of the ascites fluid that bathes the tumor cells. The incorporation of elaidic acid into the lipids of EATC, normal liver and host liver did not affect the relative composition of phospholipids in these tissues. The development of the tumor did result in decreases in triacylglycerols and esterified cholesterol, and increases in phospholipids and free cholesterol in the livers of host animals.

Animals↗
PubMed1976

Modification of the Ehrlich ascites tumor cell nuclear lipids.

The fatty acid composition of Ehrilich ascites tumor cell nuclei was differend when the tumor-bearing mice were fed diets rich in either coconut or sunflower oil. When coconut oil was fed, the monoenoic fatty acid content of many of the nuclear lipids was increased and their polyenoic fatty acid content was reduced as compared with the sunflower oil diet. By contrast, only small changes were produced in the saturated fatty acid contents of the nuclear lipids. The nuclear membrane choline phospholipid, ethanolamine phospholipid and combined serine phospholipid plus inositol phospholipid fractions exhibited statistically significant changes in fatty acid composition, but the sphingomyelins were not altered appreciably by dietary lipid modification. The fatty acid composition of the small quantity of phospholipids associated with the chromatin was much more resistant to diet-induced mosification. Except for sphingomyelin, the fatty acid composition of the chromatin phospholipids was different from that of the corresponding nuclear membrane phospholipids, containing much larger amounts of fatty acids having less than 16 carbon atoms. The fatty acid compositons of the nuclear triaclglycerols and cholesterol esters, which were associated almost entirely with the chromatin, were modified by the dietary lipid modifications. There were no changes in the DNA, RNA or lipid content of these nuclei. Therefore, this experimental system can be used to prepare mamalian nuclei that differ appreciably only in their fatty acyl composition.

Animals↗
PubMed1976

Modification of the fatty acid composition of Ehrlich ascites tumor cell plasma membranes.

The fatty acyl group composition of Ehrlich ascites tumor cell plasma membranes was modified by feeding the tumor-bearing mice diets rich in either coconut or sunflower oil. When coconut oil was fed, the oleate content of the membrane phospholipids was elevated and the linoleate content reduced. The opposite occurred when sunflower oil was fed. Qualitatively similar changes were observed in the plasma membrane phosphatidylethanolamine, phosphatidylcholine and mixed phosphatidylserine plus phosphatidylinositol fractions. These diets also produced differences in the sphingomyelin fraction, particularly in the palmitic and nervonic acid contents. Unexpectedly, the saturated fatty acid content of the plasma membrane phospholipids was somewhat greater when the highly polyunsaturated sunflower oil was fed. The small quantities of neutral lipids contained in the plasma membrane exhibited changes in acyl group composition similar to those observed in the phospholipids. These fatty acyl group changes were not accompanied by any alteration in the cholesterol or phospholipid contents of the plasma membranes. Therefore, the lipid alterations produced in this experimental model system are confined to the membrane acyl groups.

Animals↗
PubMedDate not supplied

Dietary phytosterol inhibits the growth and metastasis of MDA-MB-231 human breast cancer cells grown in SCID mice.

The objective of the present study was to investigate the effect of dietary phytosterols on the growth and metastasis of the human breast cancer MDA-MB-231 cell line xenografted in SCID mice. Two groups of animals were fed AIN-93G diet supplemented with 0.2% cholic acid and 2% sterol (cholesterol or phytosterol mixture) for 15 days before inoculation of the tumor into the right inguinal mammary fat pad. Tumor growth and food consumption were recorded weekly throughout the 8 weeks of the experiment. At the end of the experiment, the animals fed phytosterol had a 40% lower serum cholesterol and 20 and 30 fold higher serum beta-sitosterol and campesterol, respectively as compared to those fed cholesterol. There was no difference between the two groups in body weight and food consumption. However, the tumor size in animals fed phytosterols was 33% smaller (P < 0.03) and had 20% fewer metastases to lymph nodes and lungs than the cholesterol group. At termination, the tumor weight of the animals fed the phytosterol diet was also less (P < 0.07) than that of the cholesterol group. It is concluded that dietary phytosterols retard the growth and spread of breast cancer cells.

Animals↗
PubMedDate not supplied

beta-Sitosterol inhibits HT-29 human colon cancer cell growth and alters membrane lipids.

The purpose of the present study was to examine the effect of beta-sitosterol, the main dietary phytosterol on the growth of HT-29 cells, a human colon cancer cell line. In addition, the incorporation of this phytosterol into cellular membranes and how this might influence the lipid composition of the membranes were investigated. Tumor cells were grown in DMEM containing 10% FBS and supplemented with sterols (cholesterol or beta-sitosterol) at final concentrations up to 16 microM. The sterols were supplied to the media in the form of sterol cyclodextrin complexes. The cyclodextrin used was 2-hydroxypropyl-beta-cyclodextrin. The sterol to cyclodextrin molar ratio was maintained at 1:300. The study indicated that 8 and 16 microM beta-sitosterol were effective at cel growth inhibition as compared to cholesterol or to the control (no sterol supplementation). After supplementation with 16 microM beta-sitosterol for 9 days, cell growth was only one-third that of cells supplemented with equimolar concentration of cholesterol. No effect was observed on total membrane phospholipid concentration. At 16 microM beta-sitosterol supplementation, membrane cholesterol was reduced by 26%. Cholesterol supplementation resulted in a significant increase in the cholesterol/phospholipid ratio compared to either beta-sitosterol supplemented cells or controls. There was a 50% reduction in membrane sphingomyelin (SM) of cells grown in 16 microM beta-sitosterol. Additional changes were observed in the fatty acid composition of minor phospholipids of beta-sitosterol supplemented cells, such as SM, phosphatidylserine (PS), and phosphatidylinositol (PI). Only in the case of PI, was there an effect of these fatty acid changes on the unsaturation index, beta-sitosterol incorporation resulted in an increase in the U.I. It is possible that the observed growth inhibition by beta-sitosterol may be mediated through the influence of signal transduction pathways that involve membrane phospholipids.

Cell Division↗
PubMedDate not supplied

beta-Sitosterol inhibits growth of HT-29 human colon cancer cells by activating the sphingomyelin cycle.

The present study examined the SM cycle as a mechanism to explain the inhibitory effect of SIT on HT-29 cell growth. SIT was the main phytosterol in the diet. Supplementation of SIT at 16 microM for 5 days in the media inhibited growth by 55% as compared to cholesterol. SIT supplementation had no effect on sphingosine production. Ceramide production increased 45% with SIT supplementation as compared to cholesterol. Sterol supplementation had no effect on phospholipase C, a key enzyme in the PKC pathway. We concluded that the activation of the SM cycle may play a role in growth inhibition of HT-29 cells by SIT.

Colonic Neoplasms↗