Photophysical properties of rose bengal and its derivatives (XII)

Pączkowski, Jerzy; Lamberts, Joseph J. M.; Pączkowska, Bożena; Neckers, Douglas C.

doi:10.1016/0748-5514(85)90146-1

Cited by 74 publications

(27 citation statements)

References 23 publications

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“…6, the triplet state lifetime and the rate constant for intersystem crossing of rhodamine 6G and rose bengal is given. In the present paper rose bengal as an established 1 O 2 generator [61,62] is applied as reference dye. We measure a striking low triplet quantum yield of about 40% in acetonitrile, which is consistent to the relatively high fluorescence quantum yield (36%) of rose bengal in this solvent.…”

Section: Resultsmentioning

confidence: 99%

Singlet molecular oxygen photosensitized by Rhodamine dyes: correlation with photophysical properties of the sensitizers

Stracke

Heupel

Thiel

1999

Journal of Photochemistry and Photobiology A: Chemistry

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By measuring its IR phosphorescence the formation of singlet molecular oxygen 1 O 2 photosensitized by rhodamine dyes is directly proved. The 1 O 2 formation rate is compared with that expected from the low probability (≈1%) of intersystem crossing of the photosensitizers. The quantum yield for triplet population and the triplet lifetime of the investigated dyes is measured by using a laser-scanning-microscopy technique. The influence of quenching agents (nitrobenzene and COT) is discussed. It results that the formation of 1 O 2 can be prevented effectively by quenching of the S 1 or T state of the photosensitizer. The influence of the molecular ground-state oxygen 3 O 2 concentration [ 3 O 2 ] is investigated. The presence of the paramagnetic 3 O 2 leads to an increased S 1 →T intersystem crossing rate of the photosensitizers and therefore to a reinforced formation of singlet molecular oxygen. It is found for rhodamine 6G as well as for rose bengal that in air-saturated acetonitrile nearly the half of the excited dye triplets are quenched by molecular oxygen. The 1 O 2 concentration can be significantly reduced by decreasing the 3 O 2 concentration below its air saturated level.

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Section: Resultsmentioning

confidence: 99%

Singlet molecular oxygen photosensitized by Rhodamine dyes: correlation with photophysical properties of the sensitizers

Stracke

Heupel

Thiel

1999

Journal of Photochemistry and Photobiology A: Chemistry

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“…Although the rose bengal-induced coronary vasoconstriction is unlikely to account for the initiation of arrhythmias, there seems little doubt that, after extended periods of photoactivation, this factor can exacerbate the vulnerability of the heart to arrhythmias or support their maintenance. This was demonstrated ( Figure 11) in studies in which we subjected hearts to 6 minutes of illumination followed by 14 minutes of perfusion in the dark. In comparison to hearts that were continuously illuminated (in all of which coronary flow fell and severe arrhythmias developed), coronary flow recovered to its control value, and vulnerability to arrhythmias declined.…”

Section: Rapidity Of Injurymentioning

confidence: 96%

“…This suggests that some degree of electrophysiologic "recovery" may be occurring because at the end of 6-minute illumination, more than 80% of hearts were arrhythmic, but in the succeeding 14 15 minutes after the end of illumination, sometimes after a relatively long period of stable rhythm. Metabolic Studies The protocols used for these studies are depicted in Figure 2.…”

Section: B and 6b And Open Boxes Inmentioning

confidence: 99%

“…In further studies in which rose bengal was washed out for 10 minutes before photoactivation, several arrhythmias still developed, indicating that rose bengal binds strongly to tissue and acts as a cellular level rather than in the vascular compartment. To assess the reversibility of rose bengal-induced effects, hearts (n=6/group) were perfused with rose bengal (250 nmol/1) for 1, 2, 4, 6, and 20 minutes followed by perfusion in the dark for 19,18,16,14, and 0 minutes, respectively. During dark perfusion, the incidence of arrhythmias declined and any decrease in coronary flow was reversed.…”

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confidence: 99%

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Singlet oxygen-induced arrhythmias. Dose- and light-response studies for photoactivation of rose bengal in the rat heart.

1989

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In a study of aerobically perfused rat hearts, the in situ photoactivation (530-590 nm) of rose bengal (a process that leads to the production of singlet oxygen and superoxide) has been shown to lead to the rapid development of electrocardiographic abnormalities and arrhythmias. With rose bengal concentrations of 1,000, 500, 250, 100, and 50 nmol/l (n =6/group), photoactivation (3,600 lx) led to electrocardiographic changes (inversion of the T wave, Q-T prolongation, or both) after 3.8±0.9, 4.5±0.7, 11.8+2.1, 24.8+3.9, and 65.3+6.0 seconds), respectively; ventricular premature beats occurred in 100% of hearts after 0.5+0.2, 1.1±0.3, 2.2±0.7, 4.4±0.8, and 6.6±+1.2 minutes, respectively. Ventricular tachycardia occurred in 83%, 83%, 83%, 67%, and 50% of hearts after 2.1±0.2, 2.1±0.4, 2.8+0.7, 5.7±2.0, and 11.2+1.9 minutes, respectively, and complete atrioventricular block in 100%, 100%, 100%, 100%, and 67% of hearts after 3.8±0.7, 6.5± 1.0, 5.5+0.9, 13.8± 1.0, and 14.1±0.9 minutes, respectively. With a fixed concentration (250 nmol/l) of rose bengal, similar light-response relations were observed. Photoactivation of rose bengal had no eifect on heart rate but caused a transient (0-4 minutes) vasodilation followed by a progressive vasoconstriction. In further studies in which rose bengal was washed out for 10 minutes before photoactivation, several arrhythmias still developed, indicating that rose bengal binds strongly to tissue and acts as a cellular level rather than in the vascular compartment. To assess the reversibility of rose bengal-induced effects, hearts (n=6/group) were perfused with rose bengal (250 nmol/1) for 1, 2, 4, 6, and 20 minutes followed by perfusion in the dark for 19, 18, 16, 14, and 0 minutes, respectively. During dark perfusion, the incidence of arrhythmias declined and any decrease in coronary flow was reversed. However, analysis of contents of adenosine triphosphate, creatine phosphate, lactate, and creatine kinase leakage indicated the occurrence of severe injury that did not abate on termination of photoactivation. Finally, although many arrhythmias developed before the onset of vasoconstriction, the reduction in flow with consequent ischemia was shown to exacerbate vulnerability to arrhythmias. In conclusion, short-lived reactive oxygen intermediates such as singlet oxygen and superoxide, which are produced during the photoactivation of rose bengal, can cause rapid and major damage to the heart and its function. (Circulation 1989;80:1432-1448 Kusama et al Singlet Oxygen-Induced Arrhythmias 1433 radicals) produced in "bursts"8 during ischemia and reperfusion may cause membrane injury9 that can lead to the genesis of severe arrhythmias. Our initial observationsl2 with rose bengal would lend further support to this concept. In consequence, we have now undertaken detailed dose-response and light-response studies with rose bengal in the isolated aerobically perfused rat heart to learn more about the novel effects of this fluorescein derivative. We also investigated whether the injury induced...

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“…Singlet oxygen produced from rose benfal-oxygen uptake measurements Singlet oxygen ( 02) is produced from the photo-illumination of rose bengal [14]. Rose bengal (0.125 mM) was added to 2.0 ml pre-warmed buffer with 0.5 mm captopril or 0.5 mM MPG or buffer alone at 370 C. The mixture was then photo-illuminated with a tungsten lamp whilst oxygen uptake was recorded for 30 min at 370 C. Oxygen uptake was expressed as nmol ml-.…”

Section: Methodsmentioning

confidence: 99%

Effect of captopril, enalaprilat and mercaptopropionyl glycine (MPG) on the oxidative activity of human isolated neutrophils.

Clapperton

Abdullah

et al. 1995

Brit J Clinical Pharma

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1. Neutrophil NADPH oxidase produces the superoxide anion (O2‐) anion radical from oxygen. The thiol containing ACE inhibitor, captopril has been reported to inhibit isolated NADPH oxidase. The above effect of captopril, if present in intact cells, could contribute to the ability of this drug to alleviate neutrophil‐mediated tissue damage. We have, therefore, investigated the effect of captopril on the oxidative activity of intact human isolated neutrophils. 2. The effects of captopril on neutrophil oxidative activity were compared with those of enalaprilat (a non‐thiol ACE inhibitor) and N‐mercaptopropionyl glycine (MPG) (a simple thiol). 3. The oxidative response of PMA‐stimulated neutrophils measured by lucigenin chemiluminescence was not affected by any of these test agents. The thiol captopril and MPG (but not enalaprilat) caused an initial delay in luminol chemiluminescence production by PMA‐stimulated neutrophils. 4. Captopril and MPG (but not enalaprilat) increased, rather than decreased oxygen uptake, when added to PMA‐stimulated neutrophils. Thiol oxidation was determined to be, at least partly, responsible for the excess oxygen uptake observed. 5. NADPH oxidase activity in intact neutrophils was not affected by captopril, MPG or enalaprilat. The inhibition of NADPH oxidase activity is unlikely to contribute to the therapeutic effects of captopril and other thiols.

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Photophysical properties of rose bengal and its derivatives (XII)

Cited by 74 publications

References 23 publications

Singlet molecular oxygen photosensitized by Rhodamine dyes: correlation with photophysical properties of the sensitizers

Singlet molecular oxygen photosensitized by Rhodamine dyes: correlation with photophysical properties of the sensitizers

Singlet oxygen-induced arrhythmias. Dose- and light-response studies for photoactivation of rose bengal in the rat heart.

Effect of captopril, enalaprilat and mercaptopropionyl glycine (MPG) on the oxidative activity of human isolated neutrophils.

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