Inhibitory effects of phenolic compounds on CCl4-induced microsomal lipid peroxidation

Summary The antiperoxidative effects of 35 phenolic compounds, most of them belonging to the flavonoid class, were investigated using CCl₄-induced peroxidation of rat liver microsomes. This system was rather insensitive to gallic acid, methyl gallate and ellagic acid. Nevertheless it was inhibited by flavonoids and structure/activity relationships were established. The most potent compounds were gardenin D, luteolin, apigenin (flavones), datiscetin, morin, galangin (flavonols), eriodictyol (flavanone), amentoflavone (biflavone) and the reference compound, (+)-catechin. The natural polymethoxyflavone gardenin D has shown a potency comparable to that of (+)-catechin and higher than that of silybin. Thus, it may be considered as a new type of natural antioxidant with potential therapeutical applications.     

Inhibitory effects of phenolic compounds on CCl4-induced microsomal lipid peroxidation

The antiperoxidative effects of 35 phenolic compounds, most of them belonging to the flavonoid class, were investigated using CCl4-induced peroxidation of rat liver microsomes. This system was rather insensitive to gallic acid, methyl gallate and ellagic acid. Nevertheless it was inhibited by flavonoids and structure/activity relationships were established. The most potent compounds were gardenin D, luteolin, apigenin (flavones), datiscetin, morin, galangin (flavonols), eriodictyol (flavanone), amentoflavone (biflavone) and the reference compound, (+)-catechin. The natural polymethoxyflavone gardenin D has shown a potency comparable to that of (+)-catechin and higher than that of silybin. Thus, it may be considered as a new type of natural antioxidant with potential therapeutical applications.     

Differential effect of silybin on the Fe2+-ADP and t-butyl hydroperoxide-induced microsomal lipid peroxidation

We have observed a differential effect of silybin dihemisuccinate on rat liver microsomal oxygen consumption and on lipid peroxidation induced by NADPH-Fe2+-ADP and t-butyl hydroperoxide. These results are ascribed to the antioxidant properties of the flavonoid. The differences observed in the effect of the catalysts may be a consequence of the different capacity of silybin to act as a scavenger of free radicals formed by NADPH-Fe2+-ADP or t-butyl hydroperoxide.     

Differential effect of silybin on the Fe2+-ADP and t-butyl hydroperoxide-induced microsomal lipid peroxidation

Summary We have observed a differential effect of silybin dihemisuccinate on rat liver microsonal oxygen consumption and on lipid peroxidation induced by NADPH-Fe²⁺-ADP and t-butyl hydroperoxide. These results are ascribed to the antioxidant properties of the flavonoid. The differences observed in the effect of the catalysts may be a consequence of the different capacity of silybin to act as a scavenger of free radicals formed by NADPH-Fe²⁺-ADP or t-butyl hydroperoxide.This research was supported in part by grant B-2019-8412 from Dirección de Investigación y Bibliotecas, Universidad de Chile.     

Acute60Co-gamma irradiation of rats decreases the inhibitory effect of succinate on the lipid peroxidation of liver mitochondria

Summary Succinate inhibits NADPH-dependent lipid peroxidation of liver mitochondria. This effect of succinate decreased 12 h after whole-body⁶⁰Co-gamma irradiation, depending on the dose of irradiation.     

Acute 60Co-gamma irradiation of rats decreases the inhibitory effect of succinate on the lipid peroxidation of liver mitochondria

Succinate inhibits NADPH-dependent lipid peroxidation of liver mitochondria. This effect of succinate decreased 12 h after whole-body 60Co-gamma irradiation, depending on the dose of irradiation.     

The effects of vitamin A nutritional status on microsomal lipid peroxidation and alpha-tocopherol level in rat liver

In vitamin A-deficient rats, liver glutathione peroxidase activity was decreased, alpha-tocopherol content was strongly enhanced, but microsomal liquid peroxidation remained unchanged.     

Effect of chronic ethanol treatment on peroxisomal acyl-CoA oxidase activity and lipid peroxidation in rat liver and heart

Summary Chronic ethanol administration was shown to increase catalase and acyl-CoA oxidase activities in rat myocardium but did not alter the activity of liver peroxisomal enzymes. As a result of alcohol consumption a 2–3-fold increase in the level of lipid peroxidation was observed in the heart tissue while in the liver the induction was much less pronounced.     

Effect of chronic ethanol treatment on peroxisomal acyl-CoA oxidase activity and lipid peroxidation in rat liver and heart

Chronic ethanol administration was shown to increase catalase and acyl-CoA oxidase activities in rat myocardium but did not alter the activity of liver peroxisomal enzymes. As a result of alcohol consumption a 2-3-fold increase in the level of lipid peroxidation was observed in the heart tissue while in the liver the induction was much less pronounced.     

Failure of carbon tetrachloride (CCl4) and trichlorobromo-methane (CCl3 Br) to alter polyribosomal profiles in the rat brain

Riassunto La disaggregazione dei polisomi di fegato di ratto trattato con CCl₄ o CCl₃Br non é riproducibile nei polisomi di cervello, neppure in animali pretrattati con fenobarbital.     

Products of the isoprostane pathway: unique bioactive compounds and markers of lipid peroxidation

We previously reported the discovery of prostaglandin F2-like compounds (F2-isoprostanes) formed by nonenzymatic free-radical-induced peroxidation of arachidonic acid. Quantification of F2-isoprostanes has proven to be a major advance in assessing oxidative stress status in vivo. Central in the pathway of formation of isoprostanes are prostaglandin H2-like endoperoxides, which also undergo rearrangement in vivo to form E-ring, D-ring, and thromboxane-ring compounds. E2- and D2-isoprostanes also undergo dehydration in vivo to form reactive cyclopentenone A2- and J2-isoprostanes, which are susceptible to Michael addition reactions with thiols. Recently, we described the formation of highly reactive gamma-ketoaldehydes (now termed isoketals) as products of isoprostane endoperoxide rearrangement which readily adduct to lysine residues on proteins and induce cross-links at rates that far exceed other aldehyde products of lipid peroxidation. Isoprostane-like compounds (neuroprostanes) and isoketal-like compounds (neuroketals) are formed from oxidation of docosahexaenoic acid, which is enriched in the brain, and measurement of neuroprostanes may provide a unique marker of oxidative neuronal injury.     

Uptake of alanine,phenylalanine and tyrosine by L1210 cells at 4°C: Possible effect of lipid solubility

Résumé L'introduction d'un groupe phényl facilite grandement le transfert del-alanine tandis que l'hydroxylation du groupe phényl diminue la facilité de transfert.

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Supported in part by a grant from Charles H. Hood Dairy Foundation. I thank Dr.John J. McCormack, and Dr.A. H. Schein, University of Vermont, for helpful discussions.     

Influence of hypophyseal intermediate lobe tissue and colloid on the reticuloendothelial cells of the liver

Zusammenfassung Gewebe des Hypophysenzwischenlappens und das Kolloid wirken auf Endothelzellen ein. Sie vermögen die retikuloendothelialen Zellen der Leber zur Mitose anzuregen. Diese Zellen scheinen eine wichtige Rolle bei der Übermittlung von endokrinen Stoffen und der Regulation des retikuloendothelialen Systems zu spielen.     

Influence of age on the total lipid,phospholipid and cholesterol contents of pancreas and liver of albino rats

Résumé Le cholestérol et les phospholipides du pancréas des rats diminuent à mesure que l'âge avance, tandisque le contenu total de lipides augmente sensiblement. Dans le foie, les phospholipides augmentent avec l'âge, mais le contenu total de lipide et de cholestérol n'augmentent pas dès que les souris atteignent l'âge de 5 à 6 mois.

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The author is grateful to the Indian Council fo Medical Research, New Delhi for a research grant to carry out this work.     

The effect of catecholamines and nicotine on the transmembranal potential of frog liver cells

Resumen La adrenalina (0.1 a 0.5 mg/rana) hiperpolarizó los hepatocitos deR. pipiens y depolarizó a dosis mas altas. El inhibidor de la monoamino oxidasa pargilina (100 mg/kg, 24–48 h antes) impidió este efecto.     

Mechanisms of NK cell activation: CD4+ T cells enter the scene

Natural killer (NK) cells are innate lymphocytes involved in immunosurveillance through their cytotoxic activity and their capacity to secrete inflammatory cytokines. NK cell activation is necessary to initiate effector functions and results from a complex series of molecular and cellular events. We review here the signals that trigger NK cells and discuss recent findings showing that, besides antigen-presenting cells, T cells can play a central role in the initiation of NK cell activation in lymph nodes.