Photomechanical effects: experimental studies of pigment granule absorption, cavitation, and cell damage

Roegener, Jan; Lin, Charles P.

doi:10.1117/12.379339

Cited by 16 publications

(17 citation statements)

References 7 publications

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“…It was recently established that laser-induced local heating of cellular structures (through photothermal (PT) mechanisms), using either pulsed or continuous laser radiation and mediated by light-absorbing nanoparticles and microparticles, may provide precisely localized damage that can be limited to single cells [9,[13][14][15][16][17][18][19]. Accumulation of light-absorbing nanoparticles in relatively transparent cells may enhance their optical absorption up to several orders of magnitude [20,21].…”

Section: Introductionmentioning

confidence: 99%

Selective laser nano‐thermolysis of human leukemia cells with microbubbles generated around clusters of gold nanoparticles

2006

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Section: Introductionmentioning

confidence: 99%

Selective laser nano‐thermolysis of human leukemia cells with microbubbles generated around clusters of gold nanoparticles

2006

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“…2 3 4 The Roegener/Lin ex vivo study used an irradiation beam at 532 nm, 100 ps, and had a top-hat beam profile. 1 We expected the Roegener/Lin study data to fall well below our data on the logarithmic plot as infrared laser exposures have a higher damage threshold than their visible counterparts due to reduced melanin absorption at the longer wavelengths. 13 In addition, longer pulse durations have a higher damage threshold than shorter pulses.…”

Section: Resultsmentioning

confidence: 85%

“…8 Roegener and Lin identified intracellular microcavitation as the damage mechanism for RPE cells when exposed to pulsed radiation in the visible spectrum. 1 Their study used RPE explants from calf eyes (ex vivo) and exposed them to 532 nm laser irradiation pulsed at 100 ps with a top hat beam profile. They irradiated the RPE cells at various spot sizes and found the fluence required to cause cellular release of calcein dye 50% of the time (ED 50 ) to be nearly constant at 0.043 J/cm 2 for all spot sizes-20, 40, 100, and 200 µm.…”

Section: Introductionmentioning

confidence: 99%

Microcavitation and spot size dependence for damage of artificially pigmented hTERT-RPE1 cells

et al. 2004

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We performed measurements to validate damage threshold trends in minimum visible lesion (MVL) studies as a function of spot size for nanosecond laser pulses. At threshold levels, nanosecond pulses produce microcavitation bubbles that expand and collapse around individual melanosomes. This microcavitation process damages the membranes of retinal pigment epithelium (RPE) cells. A spot size study on retinal explants 1 found cell damage fluence (energy/area) thresholds were independent of spot size when microcavitation caused the damage, contradicting past in vivo retinal spot size experiments. 2 3 4 The explant study (ex vivo) used a top-hat beam profile, whereas the in vivo studies used Gaussian beams. The difference in spot size trends for damage in vivo versus ex vivo may be attributed to the optics of the eye but this has not been validated. In this study, we exposed artificially pigmented human RPE cells (hTERT-RPE1)-in vitro-to 7 ns pulsed irradiation from a Ti:Sa TSA-02 regenerative amplifier (1055 nm) with beam diameters of 44, 86, and 273 µm (Gaussian beam profiles). We detected the microcavitation event with strobe illumination and time-resolved imaging. We used the fluorescent indicator dye calcein-AM, with excitation by an Argon laser (488 nm), to assess cell damage. Our current results follow trends found in the in vivo studies.

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“…In the late 1990s Kelly 12,13 , Lin 14 , and others [15][16][17] reported the induction of cell death by microcavitation (bubbles) around melanin granules heated by incident laser irradiation. Cell death almost always followed the induction of a bubble in the cell.…”

Section: Discussionmentioning

confidence: 99%

Repetitive pulses and laser-induced retinal injury thresholds

Lund

2007

SPIE Proceedings

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Experimental studies with repetitively pulsed lasers show that the ED 50 , expressed as energy per pulse, varies as the inverse fourth power of the number of pulses in the exposure, relatively independently of the wavelength, pulse duration, or pulse repetition frequency of the laser. Models based on a thermal damage mechanism cannot readily explain this result. Menendez et al. proposed a probability-summation model for predicting the threshold for a train of pulses based on the probit statistics for a single pulse. The model assumed that each pulse is an independent trial, unaffected by any other pulse in the train of pulses and assumes that the probability of damage for a single pulse is adequately described by the logistic curve. The requirement that the effect of each pulse in the pulse train be unaffected by the effects of other pulses in the train is a showstopper when the end effect is viewed as a thermal effect with each pulse in the train contributing to the end temperature of the target tissue.There is evidence that the induction of cell death by microcavitation bubbles around melanin granules heated by incident laser irradiation can satisfy the condition of pulse independence as required by the probability summation model. This paper will summarize the experimental data and discuss the relevance of the probability summation model given microcavitation as a damage mechanism.

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Photomechanical effects: experimental studies of pigment granule absorption, cavitation, and cell damage

Cited by 16 publications

References 7 publications

Selective laser nano‐thermolysis of human leukemia cells with microbubbles generated around clusters of gold nanoparticles

Selective laser nano‐thermolysis of human leukemia cells with microbubbles generated around clusters of gold nanoparticles

Microcavitation and spot size dependence for damage of artificially pigmented hTERT-RPE1 cells

Repetitive pulses and laser-induced retinal injury thresholds

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