DEFINITION OF TYPE I and TYPE II PHOTOSENSITIZED OXIDATION

Foote, Christopher S.

doi:10.1111/j.1751-1097.1991.tb02071.x

Cited by 1,131 publications

(792 citation statements)

References 6 publications

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“…ROS interact with substrates to cause biological damage. [8][9][10] The photosensitizer triplet may react directly with a biological substrate under hypoxic conditions. In type II interactions, the excited triplet will transfer energy to 3 O 2 to produce excited-state singlet oxygen ( 1 O 2 ), the major cytotoxic species causing biological damage.…”

Section: Introductionmentioning

confidence: 99%

Macroscopic singlet oxygen modeling for dosimetry of Photofrin-mediated photodynamic therapy: an in-vivo study

et al. 2016

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, "Macroscopic singlet oxygen modeling for dosimetry of Photofrin-mediated photodynamic therapy: an in-vivo study," J. Biomed. Opt. Abstract. Although photodynamic therapy (PDT) is an established modality for cancer treatment, current dosimetric quantities, such as light fluence and PDT dose, do not account for the differences in PDT oxygen consumption for different fluence rates (ϕ). A macroscopic model was adopted to evaluate using calculated reacted singlet oxygen concentration (½ 1 O 2 rx ) to predict Photofrin-PDT outcome in mice bearing radiationinduced fibrosarcoma tumors, as singlet oxygen is the primary cytotoxic species responsible for cell death in type II PDT. Using a combination of fluences (50, 135, 200, and 250 J∕cm 2 ) and ϕ (50, 75, and 150 mW∕cm 2 ), tumor regrowth rate, k, was determined for each condition. A tumor cure index, CI ¼ 1 − k ∕k control , was calculated based on the k between PDT-treated groups and that of the control, k control . The measured Photofrin concentration and light dose for each mouse were used to calculate PDT dose and ½ 1 O 2 rx , while mean optical properties (μ a ¼ 0.9 cm −1 , μ 0 s ¼ 8.4 cm −1 ) were used to calculate ϕ for all mice. CI was correlated to the fluence, PDT dose, and ½ 1 O 2 rx with R 2 ¼ 0.35, 0.79, and 0.93, respectively. These results suggest that ½ 1 O 2 rx serves as a better dosimetric quantity for predicting PDT outcome.

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Section: Introductionmentioning

confidence: 99%

Macroscopic singlet oxygen modeling for dosimetry of Photofrin-mediated photodynamic therapy: an in-vivo study

et al. 2016

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“…Photons excite the PS to the highly unstable singlet state, which then shifts to the long-lived triplet state before transferring electrons to organic molecules or energy to molecular oxygen, respectively producing free radicals (type I mechanism) or singlet oxygen ( 1 O 2 -type II mechanism) [2][3][4]. These highly reactive species are antibacterial because they irreversibly damage proteins, membrane lipids and DNA [1].…”

Section: Introductionmentioning

confidence: 99%

Rose bengal uptake by E. faecalis and F. nucleatum and light-mediated antibacterial activity measured by flow cytometry

Manoil

Filieri

Schrenzel

et al. 2016

Journal of Photochemistry and Photobiology B: Biology

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Rose bengal uptake by E. faecalis and F. nucleatum and light-mediated antibacterial activity measured by flow cytometry Antibacterial photodynamic therapy (aPDT) using rose bengal (RB) and blue-light kills bacteria through the production of reactive oxygen derivates. However, the interaction mechanism of RB with bacterial cells remains unclear. This study investigated the uptake efficiency and the antibacterial activity of blue light-activated RB against Enterococcus faecalis and Fusobacterium nucleatum. Spectrophotometry and epifluorescence microscopy were used to evaluate binding of RB to bacteria. The antibacterial activity of RB after various irradiation times was assessed by flow cytometry in combination with cell sorting. Uptake of RB increased in a concentration dependent manner in both strains although E. faecalis displayed higher uptake values. RB appeared to bind specific sites located at the cellular poles of E. faecalis and at regular intervals along F. nucleatum. Blue-light irradiation of samples incubated with RB significantly reduced bacterial viability. After incubation with 10 μM RB and 240 s irradiation, only 0.01% (± 0.01%) of E. faecalis cells and 0.03% (±0.03%) of F. nucleatum survived after treatment. This study indicated that RB can bind to E. faecalis and F. nucleatum in a sufficient amount to elicit effective aPDT. Epifluorescence microscopy showed a yet-unreported property of RB binding to bacterial membranes. Flow cytometry allowed the detection of bacteria with damaged membranes that were unable to form colonies on agars after cell sorting.

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“…In biological systems, 1 O 2 is generated by absorption of incident light of specific wavelengths by excitable endogenous or exogenous molecules known as photosensitizers. This type of photosensitization is known as type II (46,47). A large number of sensitizers occur naturally in organisms (riboflavin, 4-thiouridine and 2-thiouracil, bilirubin, etc.…”

Section: Uvb Uvamentioning

confidence: 99%

Photochemistry and photobiology of actinic erythema: defensive and reparative cutaneous mechanisms

Tedesco¹,

Martínez²,

González³

1997

Braz J Med Biol Res

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Sunlight is part of our everyday life and most people accept it as beneficial to our health. With the advance of our knowledge in cutaneous photochemistry, photobiology and photomedicine over the past four decades, the terrestrial solar radiation has become a concern of dermatologists and is considered to be a major damaging environmental factor for our skin. Most photobiological effects (e.g., sunburn, suntanning, local and systemic immunosuppression, photoaging or dermatoheliosis, skin cancer and precancer, etc.) are attributed to ultraviolet radiation (UVR) and more particularly to UVB radiation (290-320 nm). UVA radiation (320-400 nm) also plays an important role in the induction of erythema by the photosensitized generation of reactive oxygen species (singlet oxygen OH)) that damage DNA and cellular membranes, and promote carcinogenesis and the changes associated with photoaging. Therefore, research efforts have been directed at a better photochemical and photobiological understanding of the so-called sunburn reaction, actinic or solar erythema. To survive the insults of actinic damage, the skin appears to have different intrinsic defensive mechanisms, among which antioxidants (enzymatic and non-enzymatic systems) play a pivotal role. In this paper, we will review the basic aspects of the action of UVR on the skin: a) photochemical reactions resulting from photon absorption by endogenous chromophores; b) the lipid peroxidation phenomenon, and c) intrinsic defensive cutaneous mechanisms (antioxidant systems). The last section will cover the inflammatory response including mediator release after cutaneous UVR exposure and adhesion molecule expression.Correspondence

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DEFINITION OF TYPE I and TYPE II PHOTOSENSITIZED OXIDATION

Cited by 1,131 publications

References 6 publications

Macroscopic singlet oxygen modeling for dosimetry of Photofrin-mediated photodynamic therapy: an in-vivo study

Macroscopic singlet oxygen modeling for dosimetry of Photofrin-mediated photodynamic therapy: an in-vivo study

Rose bengal uptake by E. faecalis and F. nucleatum and light-mediated antibacterial activity measured by flow cytometry

Photochemistry and photobiology of actinic erythema: defensive and reparative cutaneous mechanisms

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