Ultrafast formation of nonemissive species via intermolecular interaction in single crystals of conjugated molecules.

We investigate the influence of interchain interactions on the photoluminescence processes in a sexithiophene single crystal by applying hydrostatic pressure. We perform transient photoluminescence spectroscopy in the time domain of 100 fs for pressures up to 60 kbar. The combined use of steady-state and time-resolved optical spectroscopies allows us to show that the pressure-induced quenching of the photoluminescence is caused by an ultrafast (approximately 100 fs) formation of intermolecular species.

The influence of self-absorption on the photoluminescence of thin film CdS demonstrated by two-photon absorption.

By means of two-photon excited photoluminescence, we demonstrate the influence of self-absorption on the emission properties of thin (1.5 microm) film CdS formed by laser ablation. The excitation of the sample is performed with 200 fs pulses at 804 nm (1.54 eV). The photoluminescence spectrum takes the form of a single peak centered at 510 nm (2.43 eV) at 300 K. The spectrum is shifted about 45 meV to lower energies with respect to the photoluminescence excited by one photon absorption. By fitting the photoluminescence spectra with the Roosbroeck-Shockley relation and Urbach's rule, it is shown by Beer's law that the shift is caused by self-absorption. The results further provide evidence of low impurity concentration and excellent surface quality. They also confirm the outstanding optical properties of thin film CdS formed by pulsed-laser deposition and suggest the application of the films for effective up-conversation materials in ultra-fast experiments.

Geometry-dependent electronic properties of highly fluorescent conjugated molecules

We present a combined experimental/theoretical study of the electronic properties of conjugated para-phenylene type molecules under high pressure up to 80 kbar. Pressure is used as a tool to vary the molecular geometry and intermolecular interaction. The influence of the latter two on singlet and triplet excitons as well as polarons is monitored via optical spectroscopy. We have performed band structure calculations for the planar poly(para-phenylene) and calculated the dielectric function. By varying the intermolecular distances and the length of the polymer repeat unit the observed pressure effects can be explained.

Prostacyclin elevation following glutathione depletion in vivo. Possible threshold dependency in liver and lung.

The major objective of this study was to determine if a threshold level of glutathione (GSH) depletion is required to elevate plasma prostacyclin (6-ketoPGF1 alpha) in male Sprague-Dawley rats. Rats were treated i.p. with various doses of phorone, diethyl maleate (DEM), or GSH with and without DEM. Similar maximal depletions of hepatic GSH (to 10% of control) and renal GSH (to 50% of control) were observed with DEM and phorone, but lung GSH was depleted maximally by only 30% with phorone compared with a 70% depletion by DEM. Changes in lung GSH, but not kidney GSH, were closely correlated with changes in hepatic GSH 6-KetoPGF1 alpha levels in the lung were 10- to 30-fold higher than in kidney or liver, and there was a stronger correlation between lung and plasma 6-ketoPGF1 alpha than with the other two tissues. The increase in lung 6-ketoPGF1 alpha following GSH depletion did not appear to be due to a shift in prostaglandin metabolite synthesis since reciprocal changes in PGE2 were not observed; lung PGE2 levels were largely unaffected by DEM or phorone. Both DEM and phorone elevated plasma 6-ketoPGF1 alpha but the magnitude of increase for DEM (5- to 6-fold) was much greater than the 2-fold increase for phorone. The increase in plasma 6-ketoPGF1 alpha by 1.0 mL DEM/kg was attenuated by simultaneous administration of 2 mmol GSH/kg. The results indicate that the lung may be responsible for increases in plasma 6-ketoPGF1 alpha following GSH depletion and that a critical level of GSH depletion in the liver and/or lung may be necessary to elevate plasma 6-ketoPGF1 alpha levels.

Effect of glutathione depletion on tissue and plasma prostacyclin and thromboxane in rats.

Experiments were designed to determine the effects of glutathione (GSH) depletion with L-buthionine sulfoximine (BSO) or diethyl maleate (DEM) on tissue and plasma prostacyclin (6-keto-PGF1 alpha) and thromboxane (TxB2) levels in male Sprague-Dawley rats. Despite depleting hepatic GSH to as much as 34% of control, BSO at various levels (0.4, 0.8 and 1.2 g/kg body wt) had no effect on hepatic, renal, pulmonary or cardiac tissue levels of 6-keto-PGF1 alpha and TxB2 or circulating levels of 6-keto-PGF1 alpha in portal or arterial plasma. When rats were pretreated with 3-methylcholanthrene (3-MC) to induce cytochrome P450, BSO (0.8 g/kg body wt) also had no effect on tissue or plasma prostanoid levels with the exception of a slight, but significant, increase in hepatic 6-keto-PGF1 alpha in non-induced rats. In contrast, depletions of hepatic, renal and pulmonary tissue GSH by DEM (1 mL/kg body wt) to 12, 50 and 30% of control, respectively, were associated with elevations of 6-keto-PGF1 alpha in these tissues and in plasma obtained by right ventricular heart puncture. Pretreatment of rats with 3-MC had no significant effect on tissue GSH or prostanoid levels in controls or DEM-treated rats but plasma levels of 6-keto-PGF1 alpha were lower in comparison to non-induced rats. DEM with or without 3-MC pretreatment was associated with increased TxB2 in renal tissue, whereas DEM elevated TxB2 only in pulmonary tissue from non-induced rats. It appears that factors besides GSH depletion may be required to raise plasma and/or tissue 6-keto-PGF1 alpha levels in vivo.

Indomethacin attenuation of hepatic perfusion and plasma 6-ketoPGF1 alpha elevations following glutathione depletion in rabbits.

Glutathione (GSH) is important in detoxification and regulating cyclooxygenase activity. Since the liver has high levels of GSH, xenobiotic-induced changes in hepatic GSH could affect hepatic tissue blood perfusion (HP) via alterations in prostaglandin synthesis. In anesthetized male New Zealand rabbits, elevating GSH with GSH monoethyl ester had no affect on HP. Treatment of rabbits with diethyl maleate to deplete GSH also had no affect on HP in animals previously given GSH monoethyl ester. However, HP increased within 20 min in rabbits treated with diethyl maleate prior to GSH monoethyl ester. In another experiment, a similar rise in HP following GSH depletion was accompanied by arterial plasma 6-ketoPGF1 alpha (the stable metabolite of prostacyclin) levels that were 4-times higher than in the controls. Plasma TxB2 (the stable metabolite of thromboxane) also increased following diethyl maleate, but only to levels that were 25-times lower than for 6-ketoPGF1 alpha. Since indomethacin blocked the rise in HP, as well as the increases in 6-ketoPGF1 alpha and TxB2, these results indicate changes in HP may occur following GSH depletion as a result of increased synthesis of one or more arachidonic acid metabolites and implicate prostacyclin as a possible mediator of this phenomenon.