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Biomedical subjects

F Feo

Publications and source records attributed to F Feo.

At least 91 records · Page 5Linked to original sources
PubMed1978

The role of lipid-protein interactions in NADH-cytochrome c reductase (rotenone-insensitive) of rat liver mitochondria.

The phospholipid depletion of rat liver mitochondria, induced by acetoneextraction or by digestion with phospholipase A2 or phospholipase C, greatly inhibited the activity of NADH-cytochrome c reductase (rotenone-insensitive). A great decrease of the reductase activity also occurred in isolated outer mitochondrial membranes after incubation with phospholipase A2. The enzyme activity was almost completely restored by the addition of a mixture of mitochondrial phospholipids to either lipid-deficient mitochondria, or lipid-deficient outer membranes. The individual phospholipids present in the outer mitochondrial membrane induced little or no stimulation of the reductase activity. Egg phosphatidylcholine was the most active phospholipid, but dipalmitoyl phosphatidylcholine was almost ineffective. The lipid depletion of mitochondria resulted in the disappearance of the non-linear Arrhenius plot which characterized the native reductase activity. A non-linear plot almost identical to that of the native enzyme was shown by the enzyme reconstituted with mitochondrial phospholipids. Triton X-100, Tween 80 or sodium deoxycholate induced only a small activation of NADH-cytochrome c reductase (rotenone-insensitive) in lipid-deficient mitochondria. The addition of cholesterol to extracted mitochondrial phospholipids at a 1 : 1 molar ratio inhibited the reactivation of NADH-cytochrome c reductase (rotenone-insensitive) but not the binding of phospholipids to lipid-deficient mitochondria or lipid-deficient outer membranes. These results show that NADH-cytochrome c reductase (rotenone-insensitive) of the outer mitochondrial membrane requires phospholipids for its activity. A mixture of phospholipids accomplishes this requirement better than individual phospholipids or detergents. It also seems that the membrane fluidity may influence the reductase activity.

Animals↗
PubMed1978

Phenobarbital stimulation of cytochrome P-450 and aminopyrine N-demethylase in hyperplastic liver nodules during LD-ethionine carcinogenesis.

Microsomes isolated from hyperplastic liver nodules and hepatomas, induced by DL-ethionine, exhibited a reduced cytochrome P-450 content and aminopyrine N-demethylase activity when compared to the organelles of control and surrounding non-nodular liver. Phenobarbital administration to rats caused an increase of microsomal protein, cytochrome P-450 and aminopyrine N-demethylase in all tissue tested. In the hepatoma the rise of cytochrome P-450 and aminopyrine N-demethylase/g of tissue was very low and it is compensated by a slight increase of microsomal protein. In hyperplastic nodules as well as in control and surrounding livers, cytochrome P-450 and aminopyrine N-demethylase increased more than microsomal protein. However, the phenobarbital-induced stimulation was significantly lower in hyperplastic nodules than in control and surrounding livers.

Aminopyrine N-Demethylase↗
PubMed1977

[Complement].

Explore the source record for details and available documents.

Complement Activating Enzymes↗
PubMed1976

The influence of enrichment with cholesterol on the phagocytic activity of rat macrophages.

Prolonged treatment of rats with a cholesterol-rich diet induced hypercholesterolaemia and increased free cholesterol content of peritoneal macrophages. A 2-2 times increase in plasma membrane cholesterol was demonstrated in cholesterol-enriched macrophages. These cells showed a significant inhibition of phagocytosis. The inhibition was 37-0% and 81-7% for latex particles or lipid droplets, respectively.

Cell Membrane↗
PubMed1976

Effect of a cholesterol-rich diet on cholesterol content and phagocytic activity of rat macrophages.

Treatment for 11-13 weeks with a cholesterol-rich diet induced increases in free and esterified serum cholesterol. There was also an increase in free cholesterol of peritoneal macrophages. A 2.2 times rise in the cholesterol to phospholipid ratio of plasma membranes occurred in cholesterol-enriched macrophages. No changes were observed in phagolysosomes. Cholesterol-enriched macrophages showed a 35.8% inhibition of latex particles phagocytosis. When lipid droplets were substituted for latex the inhibition was 81.7%.

Animals↗
PubMed1975

Effect of cholesterol content on some physical and functional properties of mitochondria isolated from adult rat liver, fetal liver, cholesterol-enriched liver and hepatomas AH-130, 3924A and 5123.

The cholesterol to phospholipid ratio in mitochondria from hepatomas AH-130, 3924A and 5123 is higher than in the particles isolated from adult or fetal rat livers. Nearly all the cholesterol of hepatoma mitochondria is located in membranes. As in liver mitochondria, in the particles isolated from hepatoma AH-130 there is more cholesterol in the outer than in the inner membrane. In mitochondria from cholesterol-enriched liver and hepatomas, there occurs a decrease in extent of hypoosmotic and phosphate-induced swelling and a decrease of conformational changes linked to energy states. The phenomenon is more marked in particles which exhibit higher cholesterol to phospholipid ratios. A statistically significant negative correlation exists between the cholesterol to phospholipid ratio and extent of volume or conformational changes. No significant modifications of these parameters were found in fetal liver mitochondria. Cholesterol content does not influence K+ uptake by cholesterol-enriched or hepatoma mitochondria. Nor does cholesterol content affect the respiratory increment related to this uptake. As a consequence of K+ uptake, total mitochondrial water exchangeable with tritiated water rises 20% while sucrose-impermeable water rises 42-48% in both adult rat liver and hepatoma AH-130 mitochondria. Absorbance changes linked to ion uptake do not correspond merely to variations in mitochondrial water content. Water content is apparently not influenced by the cholesterol to phospholipid ratio. However, the ratio is significantly correlated to both extent and initial rate of absorbance decrease of mitochondrial suspensions during K+ uptake. The higher the ratio, the lower the extent and initial rate of absorbance decrease.

Animals↗
PubMed1975

Functional and structural alterations of liver ergastoplasmic membranes during DL-ethionine hepatocarcinogenesis.

Different functional and structural properties of rat liver microsomes were studied during hepatocarcinogenesis induced by 0.25% DL-ethionine. During the first to fourth months of ethionine feeding, great decreases of cytochrome P-450 content, reduced nicotinamide adenine dinucleotide phosphate-dependent lipid peroxidation, and animopyrine demethylase activity occurred. No changes in the reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase activity were observed. These functional alterations were paralleled by an increase in membrane-free ribosomes and by changes in the relative proportions of phospholipid fatty acids in microsomes. After the end of ethionine feeding, when hyperplastic nodules and/or hepatomas were present, the above functional and structural parameters were studied in the latter tissues, as well as in surrounding nonodular liver. Decreases in cytochrome P-450 content, lipid peroxidation, and animopyrine demethylase activity were documented in hyperplastic nodules and hepatomas. In hepatomas, the alterations were more marked and decrease of reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase activity was also found. All these functional parameters were quite normal in surrounding nonnodular liver. Similarly, alterations in phospholipid fatty acid composition disappeared in surrounding nonnodular liver, but they partially persisted in both hyperplastic nodules and hepatomas. In contrast, the increase in membrane-free ribosomes also occurred in surrounding nonnodular liver, although to a lower extent than in hyperplastic nodules and hepatomas. These data are discussed in relation to the problem of the cellular precursors of hepatomas.

Animals↗