Study of cell killing effect on S180 by ultrasound activating protoporphyrin IX

Wang, Xiao-Bing; Liu, Quan Hong; Wang, Pan; Tang, Wei; Hao, Qiao

doi:10.1016/j.ultras.2007.11.001

Cited by 26 publications

(13 citation statements)

References 21 publications

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“…It has been reported that, with the systemic administration of exogenous ALA, PpIX can be produced and accumulated in cancer cells and inflammatory cells because of their limited capacity of porphobilinogen deaminase and ferrochelatase. 9,10 Moreover, PpIX is mainly accumulated in the mitochondria where the PpIX is produced from ALA. 11 The generation of reactive oxygen species (ROS) from the ultrasonic-activated PpIX leads to an attack on the cell mitochondria and inactivation of key antioxidant enzymes, 12,13 which are considered to be responsible for the sonodynamic damage of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Effects of 5-aminolevulinic acid-mediated sonodynamic therapy on macrophages

Cheng¹,

Sun²,

Guo³

et al. 2013

IJN

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Background: Inflammatory cells exhibit an elevated level of protoporphyrin IX (PpIX) after the administration of 5-aminolevulinic acid (ALA). Here, we investigate the sonodynamic effects of ALA-derived PpIX (ALA-PpIX) on macrophages, which are the pivotal inflammatory cells in atherosclerosis. Methods and results: Cultured THP-1 macrophages were incubated with ALA. Fluorescence microscope and fluorescence spectrometer detection showed that intracellular PpIX increased with the concentration of ALA in the incubation solution in a time dependent manner; the highest level of intracellular PpIX was observed after 3-hour incubation. 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assays demonstrated that lower concentrations (less than 2 mM) of ALA have no influence on cell viability (more than 90% of cells survived), but sonodynamic therapy (SDT) with a low concentration of ALA significantly decreased the survival rate of cells, and the effect was increased with both ALA concentration and ultrasound exposure time. Cell apoptosis and necrosis induced by ALA-mediated SDT (ALA-SDT) were measured using Hoechst 33258 and propidium iodide assay. ALA-SDT induced both cell apoptosis and necrosis, and the maximum apoptosis/necrosis ratio was observed at 6 hours after SDT with 1 mM of ALA and 5 minutes of ultrasound exposure. Flow cytometry analysis showed that ALA-SDT significantly increased late stage apoptotic cells (about 10-fold control). Furthermore, ALA-SDT induced reactive oxygen species generation in THP-1 macrophages immediately after the treatment and a conspicuous loss of mitochondrial membrane potential (MMP) at 6 hours compared with that of the control, ALA alone, and ultrasound alone groups. Conclusion: ALA-SDT exhibited synergistic apoptotic effects on THP-1 macrophages, involving excessive intracellular reactive oxygen species generation and MMP loss. Therefore, ALA-SDT is a potential treatment for atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

Effects of 5-aminolevulinic acid-mediated sonodynamic therapy on macrophages

Cheng¹,

Sun²,

Guo³

et al. 2013

IJN

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“…Many studies show that these energies, resulting from ultrasonic cavitation, are sufficient to activate the photosensitive compounds such as porphyrins and anthracyclines inducing significant cell damage [18][19][20][21]. Therefore, the photosensitive compounds reveal potential acting as the sonosensitizers that are used in SDT [22,23]. Toluidine blue (TB, the structure is shown in Scheme 1) is one kind of the chemical synthetic dye.…”

Section: Introductionmentioning

confidence: 99%

Spectroscopic analyses on interaction of bovine serum albumin (BSA) with toluidine blue (TB) and its sonodynamic damage under ultrasonic irradiation

Wang

Guo

Liu

et al. 2011

Journal of Luminescence

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“…In this manner, the enzyme activity and nucleic acid structure were affected, contributing to tumor cell death (Mates, 2000;Kinoshita and Hynynen, 2006;Wang et al, 2008Wang et al, , 2010Li et al, 2012). Additionally, high levels of oxygen free radicals were produced because of ultrasonic cavitation kill tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of rat osteosarcoma cell apoptosis induced by a combination of low-intensity ultrasound and 5-aminolevulinic acid in vitro

Zhou

Yang

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We investigated the killing effect of low-intensity ultrasound combined with 5-aminolevulinic acid (5-ALA) on the rat osteosarcoma cell line UMR-106. Logarithmic-phase UMR-106 cells were divided into a control group, ultrasound group and 5-ALA group. The cell apoptotic rate, production of reactive oxygen species, and the change in mitochondrial membrane potential were analyzed by flow cytometry; ultrastructural changes were observed by transmission electron microscopy. Using low-intensity ultrasound at 1.0 MHz and 2.0 W/cm 2 plus 5-ALA at a concentration of 2 mM, the apoptotic rate of the sonodynamic therapy group was 27.2 ± 3.4% which was significantly higher than that of the control group, ultrasound group, and 5-ALA group (P < 0.05). The production of reactive oxygen species was 32.6 ± 2.2% and the decrease in mitochondrial membrane potential was 39.5 ± 2.5%. The 33342 staining showed nuclear condensation and fragmentation in the ultrasound group and 5-ALA group. Structural changes in the cell membrane, mitochondria, Golgi apparatus, and other organelles observed by transmission electron microscopy included formation of apoptotic bodies. The killing effect of low-intensity ultrasound combined with 5-ALA on UMR-106 cells was significant. Cell apoptosis played a vital role in the killing effect, and the mitochondria pathway contributed to the apoptosis of UMR-106 cells.

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Study of cell killing effect on S180 by ultrasound activating protoporphyrin IX

Cited by 26 publications

References 21 publications

Effects of 5-aminolevulinic acid-mediated sonodynamic therapy on macrophages

Effects of 5-aminolevulinic acid-mediated sonodynamic therapy on macrophages

Spectroscopic analyses on interaction of bovine serum albumin (BSA) with toluidine blue (TB) and its sonodynamic damage under ultrasonic irradiation

Mechanism of rat osteosarcoma cell apoptosis induced by a combination of low-intensity ultrasound and 5-aminolevulinic acid in vitro

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