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The effect of flavone treatment on human otosclerotic ossicle organ cultures.

We studied the effect of 7-isopropoxy-isoflavone (Ipriflavone) on the collagen synthesizing activity in human otosclerotic auditory ossicle samples from whole organ cultures during incubation for 96 h, and compared this effect with that found in normal meatal cortical bone. Ipriflavone led to a dose-dependent increase in the collagen synthesizing activity in both the healthy and the otosclerotic bone samples. At the highest Ipriflavone concentration used (50 microM), collagen synthesis increased 6-fold in the cortical bone and 9-fold in the otosclerotic bone, as compared with untreated controls. These findings indicate that the otosclerotic bone cavities are filled in vitro with organic matrix.

Adult↗

Carbohydrate binding activities of Bradyrhizobium japonicum: IV. Effect of lactose and flavones on the expression of the lectin, BJ38.

BJ38 is a galactose/lactose-specific lectin (M(r) approximately 38,000) found at one pole of Bradyrhizobium japonicum. It has been implicated in mediating the adhesion of the bacteria to soybean roots, leading to the establishment of a nitrogen-fixing symbiosis. When the ligand lactose is added to cultures of the bacteria for at least 1 h prior to harvesting the cells for BJ38 isolation, the yield of the protein was found to be elevated in a dose-dependent fashion. Half maximal stimulation was observed at approximately 50 microM; the effect was saturated at approximately 1 mM, where a 10-fold higher yield of BJ38 was obtained. Saccharides with a lower affinity for BJ38 than lactose yielded a correspondingly smaller induction effect when compared at a concentration of 1 mM. The higher level of BJ38 induced by lactose is also manifested by an elevated amount of BJ38 detectable at the cell surface and by a higher number of B. japonicum cells adsorbed onto soybean cells. Surprisingly, the induction of BJ38 expression seen with lactose was also observed with certain, but not all, flavonoids that induce the nod genes of the bacteria; genistein mimicked the induction observed with lactose, whereas luteolin failed to stimulate BJ38 production.

Carbohydrate Metabolism↗

[Flavonols and flavones of vegetables. VI. On the changes of the flavonols of onions (authors transl)].

The epidermis of onion scales exclusively contains glucosides of quercetin as flavonols, while the dry outer skins contain quercetin in the free state mainly. First spiraeoside (quercetin-4'-glucoside) is built; the formation of diglucosides follows during storage and increases continously. The mesophyll appears to be free of flavonols. The flavonol concentration decreases from the outer to the inner scales, with higher levels in the outer than in the inner epidermis. In the green leaves the flavonol synthesis is light-dependent and also kaempferol glucosides are formed beside quercetin glucosides, but not spiraeoside and the known diglucosides of the scales. During drying on the field an accumulation of flavonols takes place in the drying leaves. This production is associated with the formation of free quercetin and spiraeoside, but not of free kaempferol.

Flavonoids↗

[Flavonols and flavones of vegetables. VII. Flavonols of leek, chive and garlic (author's transl)].

Green leaves of leek and chive mainly contain kaempferol glycosides, with mono- and di-glycosides dominating in leek and di- and tri-glycosides in chive. In leek glucose is dominant as sugar component compared to xylose; in chive we found glucose and galactose. Kaempferol-3-beta-D-glucoside and kaempferol-3-xylosyl-beta-D-glucoside were isolated from leek and the 3-beta-D-glucosides of kaempferol, quercetin and isorhamnetin as by-glycosides from chive. In leek traces of quercetin-3-glucoside were identified by tlc, but no spiraeoside (quercetin-4'-glucoside) could be detected in the two species. The bulbs of garlic and leek contain only few milligram of glycosides of kaempferol and quercetin per kg fresh weight.

Flavonoids↗

Flavones and flavonol glycosides from Eupatorium cannabinum L.

The 6-methoxyflavones hispidulin and eupafolin have been identified for the first time from the aerial parts of Eupatorium cannabinum L. The presence of the previously known flavonol glycosides astragalin, kaempferol-3-rutinoside, hyperoside, isoquercitrin and rutin could be confirmed. Hispidulin, eupafolin and rutin were screened for cytotoxicity in vitro.

Animals↗

Dissociation of cell death from covalent binding of paracetamol by flavones in a hepatocyte system.

Paracetamol metabolism and toxicity were studied in isolated rat hepatocytes. Cell damage, due to paracetamol, was shown to be dose dependent and was worse in cells from animals pre-treated with phenobarbitone. Exposure to 10 mM paracetamol for 1 hr caused a loss of intracellular reduced glutathione (GSH) and a later progressive leakage of isocitrate dehydrogenase (ICD). Treatment with (+)catechin, 3-O-methyl(+)catechin and promethazine reduced or prevented the paracetamol-induced ICD leakage. Similarly, studies on covalent binding of paracetamol showed that 3-O-methyl(+)catechin, which "protected" the cells, did so without affecting the amount of material bound covalently to cellular protein. Incubation in tissue culture for 24 hr, after prior treatment with paracetamol +/- the protective agent, showed that the protected cells remained viable and attached to tissue culture plates much better than did the "unprotected" cells. These results suggest that the protective effect is much more than just a temporarily delayed cell death. GSH loss and covalent binding of paracetamol metabolites to cell protein are not sufficient causes of cell death, although they may act as starting points in the chain of events leading to cell death.

Acetaminophen↗

The effect of some flavone drugs on the conversion of prostacyclin to 6-oxoprostaglandin E1.

Flavonoid drugs (rutin, naringenin and quercetin) were compared with indomethacin and sulphasalazine as inhibitors of rat and rabbit renal 9-hydroxyprostaglandin dehydrogenase, prostaglandin synthesis (bovine seminal vesicle microsomes) and inactivation (rabbit colon 100,000 g supernatant), vascular PGI2 formation (rat aortic rings) and for effects on platelet aggregation and on the isolated rat stomach strip. Rutin and naringenin potently inhibited rabbit renal conversion of PGI2 and PGF2 alpha to 6-oxoPGE1 and PGE2, respectively, but had no effect on rat renal 9-hydroxyprostaglandin dehydrogenase activity, prostaglandin breakdown, vascular PGI2 synthesis, platelet aggregation or the anti-aggregatory effect of PGI2 and 6-oxoPGE1. High concentrations (100 microM) of both drugs inhibited the spasmogenic effect of PGI2 on the rat stomach strip. Naringenin and quercetin (1 mM) inhibited whilst rutin (1 mM) stimulated microsomal prostaglandin synthesis. These results suggest that rutin and naringenin may be useful experimental tools to study the biological roles of 6-oxoPGE1.

Alprostadil↗