scholarly journals The inhibitory effect of reduced glutathione on the lipid peroxidation of the microsomal fraction and mitochondria

1968 ◽  
Vol 106 (2) ◽  
pp. 515-522 ◽  
Author(s):  
B. O. Christophersen
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Protective Effect ◽  
Rat Liver ◽  
Microsomal Fraction ◽  
Unsaturated Fatty Acids ◽  
Reduced Glutathione ◽  
Inhibitory Effect ◽  
Inhibiting Effect ◽  
Heat Labile

1. GSH efficiently inhibited the ascorbate-stimulated lipid peroxidation of the unsaturated fatty acids in the fresh microsomal fraction and mitochondria of rat liver, whereas the peroxidation in heat-denatured particles was little inhibited. 2. Cysteamine and diethyldithiocarbamate inhibited the peroxidation in both fresh and boiled particles. Thioglycollate and 2-mercaptoethanol had no inhibiting effect. Cysteine and homocysteine both stimulated the lipid peroxidation even in the absence of ascorbate. 3. The added GSH disappeared at nearly the same rate in the presence of fresh and of boiled particles to which ascorbate had been added, although considerably more malonaldehyde was formed in the boiled particles. In the absence of ascorbate little GSH disappeared. 4. It is suggested that the protective effect of GSH against lipid peroxidation depends on the preservation of heat-labile structures in the microsomal fraction and mitochondria.

scholarly journals The Involvement of Energy Metabolism and Lipid Peroxidation in Lignin Accumulation of Postharvest Pumelos

Membranes ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 269
Author(s):  
Huiling Yan ◽  
Junjia Chen ◽  
Juan Liu
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Energy Metabolism ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Energy Charge ◽  
Succinic Dehydrogenase ◽  
Membrane Integrity ◽  
Lignin Accumulation ◽  
Juice Sacs

Lignification is especially prominent in postharvest pumelo fruit, which greatly impairs their attractiveness and commercial value. This study investigated the energy metabolism and lipid peroxidation and their relationship with accumulated lignin content in juice sacs of “Hongroumiyou” (HR) during 90 d of storage at 25 °C. The results indicated that, the alterations of energy metabolism in juice of sacs of postharvest pumelos was featured by a continuous decline in energy charge and ATP/ADP; an increase in succinic dehydrogenase (SDH) activity before 30 d and increases in activities of cytochrome c oxidase (CCO) and F0F1-ATPase before 60 d; but declines in activities of Ca2+-ATPase and H+-ATPase. Additionally, enhanced contents of H2O2, O2−, and –OH scavenging rate; increased malondialdehyde (MDA) content; and transformation of unsaturated fatty acids (USFA) to saturated fatty acids (USFA) and reduced USFA/SFA (U/S) could result in lipid peroxidation and membrane integrity loss. Moreover, correlation analysis showed that lignin accumulation was in close relation to energy metabolism and lipid peroxidation in juice sacs of postharvest pumelos. These results gave evident credence for the involvement of energy metabolism and lipid peroxidation in the lignin accumulation of HR pumelo fruit during postharvest storage.

Unsaturated fatty acids and cyclooxygenase inhibitors: effects on pial arterioles

1982 ◽  
Vol 242 (4) ◽  
pp. H629-H632
Author(s):  
W. I. Rosenblum
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Eicosatrienoic Acid ◽  
Inhibitory Effect ◽  
Cyclooxygenase Inhibitors ◽  
Dependent Manner ◽  
Double Bonds ◽  
Pial Arterioles ◽  
Dose Dependent

Cerebral surface arterioles of the mouse were constricted in a dose-dependent manner by three different unsaturated fatty acids each with one of its double bonds in the n-6 position: arachidonate, linoleic, and 11,14,17-eicosatrienoic acid (ETA) in doses of 10-200 micrograms/ml. The constriction was transient, and its magnitude was significantly reduced by pretreatment of the mice with intraperitoneal injections of indomethacin (5 mg/kg), aspirin (100 mg/kg), or sodium 2-amino-3-(4 chlorobenzyl)-phenylacetate (AHR-6293, 100 mg/kg). The inhibitory effect of these cyclooxygenase inhibitors suggests that this enzyme is involved in the response to these fatty acids and is in keeping with suggestions in the literature stating that such unsaturated fatty acids may interact with cyclooxygenase even when they cannot form prostaglandin (PG) endoperoxides, The PG endoperoxide formed by arachidonate or the analogous hydroperoxy compounds formed by linoleic or 11,14,17 ETA, may then alter cerebrovascular tone by production of reactive, O2-containing species. Alternate explanations for the data are also proposed.

scholarly journals Unsaturated Fatty Acids Associated with Glycogen May Inhibit Glucose-6 Phosphatase in Rat Liver

1997 ◽  
Vol 127 (12) ◽  
pp. 2289-2292 ◽  
Author(s):  
Nathalie Danièle ◽  
Jean-Claude Bordet ◽  
Gilles Mithieux
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Unsaturated Fatty Acids

scholarly journals Fatty acid metabolism in the perfused rat liver

1970 ◽  
Vol 119 (3) ◽  
pp. 525-533 ◽  
Author(s):  
H. A. Krebs ◽  
R. Hems
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Ketone Body ◽  
Unsaturated Fatty Acids ◽  
Ketone Bodies ◽  
Saturated Fatty Acids ◽  
Perfused Rat Liver ◽  
Body Formation ◽  
Body Production ◽  
Chain Fatty Acids

1. The formation of acetoacetate, β-hydroxybutyrate and glucose was measured in the isolated perfused rat liver after addition of fatty acids. 2. The rates of ketone-body formation from ten fatty acids were approximately equal and independent of chain length (90–132μmol/h per g), with the exception of pentanoate, which reacted at one-third of this rate. The [β-hydroxybutyrate]/[acetoacetate] ratio in the perfusion medium was increased by long-chain fatty acids. 3. Glucose was formed from all odd-numbered fatty acids tested. 4. The rate of ketone-body formation in the livers of rats kept on a high-fat diet was up to 50% higher than in the livers of rats starved for 48h. In the livers of fat-fed rats almost all the O2 consumed was accounted for by the formation of ketone bodies. 5. The ketone-body concentration in the blood of fat-fed rats rose to 4–5mm and the [β-hydroxybutyrate]/[acetoacetate] ratio rose to 11.5. 6. When the activity of the microsomal mixed-function oxidase system, which can bring about ω-oxidation of fatty acids, was induced by treatment of the rat with phenobarbitone, there was no change in the ketone-body production from fatty acids, nor was there a production of glucose from even-numbered fatty acids. The latter would be expected if ω-oxidation occurred. Thus ω-oxidation did not play a significant role in the metabolism of fatty acids. 7. Arachidonate was almost quantitatively converted into ketone bodies and yielded no glucose, demonstrating that gluconeogenesis from poly-unsaturated fatty acids with an even number of carbon atoms does not occur. 8. The rates of ketogenesis from unsaturated fatty acids (sorbate, undecylenate, crotonate, vinylacetate) were similar to those from the corresponding saturated fatty acids. 9. Addition of oleate together with shorter-chain fatty acids gave only a slightly higher rate of ketone-body formation than oleate alone. 10. Glucose, lactate, fructose, glycerol and other known antiketogenic substances strongly inhibited endogenous ketogenesis but had no effects on the rate of ketone-body formation in the presence of 2mm-oleate. Thus the concentrations of free fatty acids and of other oxidizable substances in the liver are key factors determining the rate of ketogenesis.

Lipid peroxidation as one mode of action in ochratoxin A toxicity in rats and chicks

1997 ◽  
Vol 77 (2) ◽  
pp. 287-292 ◽  
Author(s):  
Dirk Hoehler ◽  
Ronald R. Marquardt ◽  
Andrew A.F. Rohlich
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Ochratoxin A ◽  
Sunflower Oil ◽  
Mode Of Action ◽  
Unsaturated Fatty Acids ◽  
Corn Oil ◽  
Iron Catalyst ◽  
Different Tissues

The objective of this study was to determine whether lipid peroxidation is one mode of action in ochratoxin A (OA) toxicity in vivo. Lipid peroxidation was monitored by analyzing malondialdehyde (MDA) in different tissues by HPLC. A refinement study on the MDA assay was carried out, which showed the importance of the addition of an iron catalyst for the decomposition of hydroperoxides to yield a maximum amount of MDA from a given sample. The rat experiment was designed in a 2 × 2 factorial arrangement using 4 × 6 animals. The four different diets were fed for 21 d and contained either 1% corn oil and 9% tallow (Diets I and III) or 10% corn oil (Diets II and IV); in groups III and IV, 5 mg OA were added per kilogram of diet. For the chick experiment 4 × 8 Leghorn cockerels received diets for 14 d with no added sunflower oil (Diets I and III), whereas the diets of groups II and IV were supplemented with 2.5% sunflower oil. In groups III and IV, 2.5 mg OA were added per kilogram of diet. In both experiments OA decreased the performance of the animals significantly. In the rat experiment an increased lipid peroxidation due to a higher dietary level of unsaturated fatty acids could be obtained, when muscle samples were oxidatively stressed with Fe3+ and ascorbic acid. In the chick experiment there were very clear effects of the dietary treatment on the MDA concentrations of different tissues, as both a higher supply with unsaturated fatty acids and OA increased most of the MDA values significantly. These data suggest that lipid peroxides are formed in vivo by OA, but the effects may vary considerably from species to species, and may also be influenced by other factors. Key words: Ochratoxin A, lipid peroxidation, malondialdehyde, rat, chick

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