RESUMEN
Iron toxicity is a major challenge faced by plants in hypoxic soils; however, the consequences of such combined stress for soybean (Glycine max) remain to be determined. Here we assessed the physiological responses of soybean plants exposed to hypoxia and a high concentration of iron. Soil-grown plants cultivated in a greenhouse until the vegetative stage were transferred to a hydroponic system containing nutrient solution and subjected to two oxygen conditions (normoxia (6.2 mg L-1) and hypoxia (0.33 mg L-1)) and two iron concentrations (Fe-EDTA) (0.09 and 1.8 mM) for 72 h. During hypoxia, high concentrations of iron in the nutrient solution resulted in increased iron accumulation in roots and leaves. Under this condition, the concentrations of zinc, nitrogen, potassium, and calcium decreased in the roots, while the concentration of nitrogen and magnesium decreased in the leaves. Additionally, during hypoxia, the higher concentration of iron led to an increase in the activity of the antioxidant enzymes in roots and leaves, while decreased the levels of the photosynthetic pigments, leaf gas exchange, and plant growth. In conclusion, high iron concentration in the root medium results in a considerably more severe damage condition to soybean plants under hypoxia compared to plants grown under low iron availability.
Asunto(s)
Glycine max , Raíces de Plantas , Hipoxia , Hierro , Minerales , Estrés Oxidativo , Fotosíntesis , Hojas de la PlantaRESUMEN
Inhibitory effects on glycogenolysis have been reported for glibenclamide in the presence of insulin after stimulation of glycogenolysis by glucagon. Inhibition of oxidative phosphorylation, which has been equally reported for this drug, however, should stimulate glycogenolysis. The present work aimed to find an answer to the question of how glibenclamide affects glycogen catabolism in the liver of fed rats undergoing substrate- and hormone-free perfusion. The experimental system was the isolated perfused liver of ad libitum fed rats. Metabolites in the outflowing perfusate were assayed enzymatically. Oxygen uptake was measured polarographically. Glibenclamide (25-500 microM) stimulated glucose production and lactate release, with a clear correlation between concentrations and effects. Maximal stimulations were 132 and 127% for lactate production and glucose release, respectively. At low glibenclamide concentrations (up to 100 microM) both oxygen uptake and pyruvate production were stimulated, but at higher concentrations inhibition took place. Uric acid production was stimulated by glibenclamide. All effects of glibenclamide are probably due to decreases in oxidative phosphorylation. Stimulation of glucose release is the opposite of what should be expected for a hypoglycemic drug and it also contrasts with some reports of diminishing effects in the presence of glucagon plus insulin. This means that the stimulatory action on glycogenolysis that was seen as a net effect under the specific conditions of the present work could be counterbalancing inhibitory effects in vivo. This combination of events could eventually diminish the effectiveness of the drug as a hypoglycemic agent in the fed state.
Asunto(s)
Gliburida/farmacología , Glucólisis/efectos de los fármacos , Hipoglucemiantes/farmacología , Glucógeno Hepático/metabolismo , Hígado/metabolismo , Animales , Relación Dosis-Respuesta a Droga , Gluconeogénesis , Glucosa/metabolismo , Cinética , Lactatos/metabolismo , Masculino , Consumo de Oxígeno , Perfusión , Piruvatos/metabolismo , Ratas , Ratas Wistar , Ácido Úrico/metabolismoRESUMEN
The action of extracellular ATP on organic anion transport in the bivascularly perfused rat liver was investigated, using bromosulfophthalein as a model substance. Transport was measured by means of the multiple-indicator dilution technique. The action of portal 100 microM ATP presented the following characteristics: (a) inhibition of bromosulfophthalein single pass extraction; the inhibition degree decreased with increasing bromosulfophthalein doses; (b) diminution of the influx rate coefficients; (c) 86.7% decrease of the maximal activity of the saturable component for bromosulfophthalein transport, but 100% increase of the non-saturable component; (d) diminution of the bromosulfophthalein flow-limited distribution space; (e) no significant alteration of the rate coefficients for metabolic sequestration. The action of ATP on organic anion transport in the intact liver occurred at much lower concentrations (10x) than those previously reported for isolated hepatocytes. This reinforces the suggestion that inhibition of organic anion transport could be a physiologically relevant effect of extracellular ATP.