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O HECHTER

Publications and source records attributed to O HECHTER.

At least 19 recordsLinked to original sources

Permeability and metabolism of lactose in Neurospora crassa.

Lester, G. (Worcester Foundation for Experimental Biology, Shrewsbury, Mass.), D. Azzena, and O. Hechter. Permeability and metabolism of lactose in Neurospora crassa. J. Bacteriol. 84:217-227. 1962.-Germinated conidia of Neurospora crassa suspended in buffer take up lactose, and this uptake can be attributed to the intracellular accumulation and to the metabolism of lactose. The former process predominates initially, and the latter after a few hours of incubation. The accumulation of lactose appears to be mediated by a very specific transport system, which can bring about intracellular concentrations that greatly exceed the external concentration of lactose. Both the influx and efflux of lactose appear to be dependent on metabolic energy, since azide and low temperature inhibit these events. The steroid hormone 11-deoxycorticosterone also reduces the uptake and prevents the accumulation of lactose. The metabolism of lactose was clearly demonstrated, but the pathway(s) of metabolism was not defined. The amount of beta-galactosidase activity extractable from the cells was insufficient to be solely responsible for the initial step in lactose metabolism. The present studies are discussed in relationship to ion permeability and lactose metabolism in N. crassa, and to galactoside permeability in Escherichia coli.

Biological Transport↗

Effect of inhibitors on D-xylose permeability in rat diaphragm muscle.

The influence of metabolic inhibitors and low temperatures upon D-xylose transfer has been studied in rat diaphragm muscle preparations in vitro. Using intact fiber preparations, it has been confirmed that at body temperature metabolic inhibitors like DNP have an insulin-like action in that they permit D-xylose to distribute into previously unavailable intracellular aqueous regions; inhibitors, unlike insulin, disturb cation distribution in association with increased sugar penetration. Although the studies with inhibitors suggest an energy requirement for maintenance of D-xylose exclusion, the D-xylose exclusion mechanism is effectively maintained at 0 degrees for many hours, and under these conditions, inhibitors have little or no effect on D-xylose distribution, though they do produce potassium loss. In cut muscle fiber preparations, in which insulin significantly increases the rate at which D-xylose equilibrates between cell water and external medium, DNP does not increase the rate of D-xylose entry, but does abolish the effect of insulin in this preparation. The results suggest that insulin action upon sugar permeability in muscle involves two barrier systems; some of the characteristics of these systems have been defined.

Animals↗

Insulin-induced accumulation of D-xylose against an apparent concentration gradient in diaphragm muscle. in vivo.

The effect of insulin administration upon D-xylose-1-C(14) penetration into the diaphragm and gastrocnemius muscles of functionally nephrectomized normal, hypophysectomized, and adrenalectomized rats has been examined. It was found in all groups that after the administration of tracer amounts of D-xylose, this sugar enters the cell water of diaphragm to a greater extent than in gastrocnemius muscle, both in the presence and absence of exogenous insulin. Insulin increases the apparent intracellular distribution of D-xylose in both muscles in all three types of rats. After insulin administration, the intracellular concentration of D-xylose in diaphragm muscle was estimated to be about two times greater than D-xylose concentration in plasma; D-xylose accumulation was not observed in gastrocnemius muscle of insulin-treated rats. Intracellular accumulation of D-xylose occurs in diaphragm of insulin-treated rats at plasma concentrations of D-xylose ranging from 4 to 2200 microg/ml; however, a "saturation" phenomenon appears to be operative, since intracellular distribution declines as plasma D-xylose concentration is increased within this range. A decline in intracellular D-xylose distribution also occurs in gastrocnemius as plasma D-xylose is increased, suggesting that entry into this muscle as well does not exhibit the characteristics of a simple diffusion process. The significance of these in vivo observations is briefly discussed in relation to widely accepted assumptions concerning sugar permeability in muscle.

Animals↗

Effects of insulin on the permeability of D- and L-xylose and D- and L-arabinose in rat diaphragm muscle.

The permeability characteristics of D- and L-xylose and D- and L-arabinose have been compared in isolated intact rat diaphragm muscle preparations, in the absence and presence of exogenous insulin. In the absence of added insulin, these pentoses distribute in less than a third of the total cell water. In the presence of added insulin, intracellular distribution of all these pentoses is increased. L-Xylose and D-arabinose distribute in 50 per cent of the intracellular water, whereas D-xylose and L-arabinose distribute in 80 per cent of the cell water. A significant lag period was observed before the insulin effect upon the penetration of L-xylose and D-arabinose was evident whereas the effect upon D-xylose and L-arabinose was rapid. The lag period with L-xylose could be abolished by pretreating the tissues with insulin for 1 hour, but such pretreatment had little effect on D-xylose. These results indicate that insulin has a biphasic effect upon the monosaccharide exclusion system in diaphragm muscle. In dinitrophenol-treated tissues, in which all permeability processes are irreversibly damaged and in which sucrose and pentoses penetrate into most of the cell water, the entry rate of pentoses and sucrose is initially similar but subsequently D-xylose and L-arabinose penetrate more rapidly than their corresponding optical isomers.

Animals↗