"Competitive quenching": a mechanism by which perihydroxylated perylenequinone photosensitizers can prevent adverse phototoxic damage caused by verteporfin during photodynamic therapy.

"Competitive quenching": a mechanism by which perihydroxylated perylenequinone photosensitizers can prevent adverse phototoxic damage caused by verteporfin during photodynamic therapy. Research Abstract Details 

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"Competitive quenching": a mechanism by which perihydroxylated perylenequinone photosensitizers can prevent adverse phototoxic damage caused by verteporfin during photodynamic therapy. Abstract Text:

Gad Lavie,Tilda Barliya,Mathilda Mandel,Michael Blank,Yonina Ron,Arie Orenstein,Tami Livnat,Noga Friedman,Lev Weiner,Mordechai Sheves,Dov Weinberger,Gad Lavie,Tilda Barliya,Mathilda Mandel,Michael Blank,Yonina Ron,Arie Orenstein,Tami Livnat,Noga Friedman,Lev Weiner,Mordechai Sheves,Dov Weinberger,

Incorporation of photodynamic therapy into clinical practice for induction of vascular photo-occlusion highlights the need to prevent adverse phototoxicity to sensitive juxtaposed tissues, particularly in the retina. We developed a system termed "competitive quenching" to prevent adverse phototoxic damage. It involves differential compartmentalization of a photoactivator to the intravascular compartment for photoexcitation and delivery of phototoxicity to targeted vessels. A different photodynamic agent is partitioned to the extravascular retinal space to quench reactive oxygen species generated by photosensitization, thereby protecting the adjacent retinal tissues from adverse phototoxicity. The absorption spectra of quenchers must span wavelengths that are shorter and excluded from the spectral range of photoexcitation light to prevent photoactivation of the quencher. Perihydroxylated perylenequinones were found to be suitable to function as "competitive quenchers" with the prototype hypericin identified as a potent quencher. Here we examined the mechanisms operative in competitive quenching and suggest that hypericin forms a complex with verteporfin, thereby quenching singlet oxygen formation. Furthermore, we show that hypericin, with six phenolic hydroxyls, protects retinal and endothelial hybridoma cells from phototoxicity more effectively than the dimethyl tetrahydroxy helianthrone structural analog with only four such phenolic hydroxyls. The findings suggest that hydroxyl numbers contribute to the efficacy of competitive quenching.

"Competitive quenching": a mechanism by which perihydroxylated perylenequinone photosensitizers can prevent adverse phototoxic damage caused by verteporfin during photodynamic therapy. Publishing Authors By Initials

G Lavie,T Barliya,M Mandel,M Blank,Y Ron,A Orenstein,T Livnat,N Friedman,L Weiner,M Sheves,D Weinberger,G Lavie,T Barliya,M Mandel,M Blank,Y Ron,A Orenstein,T Livnat,N Friedman,L Weiner,M Sheves,D Weinberger,

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PUBMED ID PMID:

MEDLINE DATE: 2007 Sep-Oct

"Competitive quenching": a mechanism by which perihydroxylated perylenequinone photosensitizers can prevent adverse phototoxic damage caused by verteporfin during photodynamic therapy. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Photochemistry and photobiology

VOLUME: 83

Page Numbers: 1270-7

Journal Abbreviation: Photochem. Photobiol.

ISSN: 0031-8655

DAY: 20

MONTH: 09

YEAR: 2007

"Competitive quenching": a mechanism by which perihydroxylated perylenequinone photosensitizers can prevent adverse phototoxic damage caused by verteporfin during photodynamic therapy. Information

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LANGUAGE: eng

NlmUniqueID: 376425

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AFFILIATION: Institute of Hematology & Blood Center, Sheba Medical Center, Tel-Hashomer, Israel. gad.lavie@sheba.health.gov.il

Country: United States

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MEDLINETA: Photochem Photobiol

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