Sonodynamic therapy induces oxidative stress, DNA damage and apoptosis in glioma cells

Sun, Yue; Wang, Haiping; Zhang, Kun; Liu, Jingfei; Wang, Pan; Wang, Xiaobing; Liu, Quanhong

doi:10.1039/c8ra07099g

Cited by 19 publications

(8 citation statements)

References 46 publications

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“…Literature data state that 260 nm is the characteristic wavelength of DNA due to π → π* transition of DNA bases and that DNA double-strand breaks provide an increase in absorption at 260 nm, i.e., a hyperchromic effect that can be used to evaluate the level of DNA damage. In our study, an increase in absorbance values at 260 nm was observed in the spectrum obtained after the interaction of dsDNA with Cu(II) (Figure ), confirming that the DNA was damaged and underwent fragmentation and degradation …”

Section: Resultssupporting

confidence: 75%

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Voltammetric Measurement of Antioxidant Activity by Prevention of Cu(II)-Induced Oxidative Damage on DNA Bases Using a Modified Electrode

2023

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The protective effect of antioxidants using electrochemical techniques can be evaluated by examining the oxidative changes in deoxyribonucleic acid (DNA) nucleobases. In this study, a gold nanoparticle (AuNP)-decorated and multiwalled carbon nanotube (MWCNT)-Nafion-modified glassy carbon electrode (GCE/AuNP/MWCNT-Nafion) was developed to evaluate the preventive ability of antioxidants on oxidative DNA damage. A modified working electrode was prepared and characterized by cyclic voltammetry, electrochemical impedance spectroscopy, and scanning electron microscopy. The developed electrochemical method relies on two phenomena: (i) reactive species (RS) produced by dissolved oxygen in the presence of copper(II) partially damage the DNA immobilized on the electrode surface and (ii) antioxidant compounds prevent this damage by scavenging the formed RS. Changes in guanine, adenine, and cytosine oxidation signals resulting from DNA damage were measured using differential pulse stripping voltammetry before/after the interaction of dsDNA with Cu(II) while antioxidants were absent or present. The DNA protective ability of antioxidants was assessed for a number of antioxidant compounds (i.e., ascorbic acid, gallic acid, epicatechin, catechin, epicatechin gallate, glutathione, chlorogenic acid, N-acetyl cysteine, rosmarinic acid, quercetin, and rutin). Quercetin was found to show the highest antioxidant effect, and its limit of detection was determined as 1 μM. The manufactured biosensor was put in an application for the determination of antioxidant activity of herbal teas.

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Section: Resultssupporting

confidence: 75%

“…In our study, an increase in absorbance values at 260 nm was observed in the spectrum obtained after the interaction of dsDNA with Cu(II) (Figure 6), confirming that the DNA was damaged and underwent fragmentation and degradation. 42 3.5. Electrochemical Detection of DNA Damage in the Copper-Catalyzed System.…”

Section: Optimization Of the Experimental Conditionsmentioning

confidence: 99%

Voltammetric Measurement of Antioxidant Activity by Prevention of Cu(II)-Induced Oxidative Damage on DNA Bases Using a Modified Electrode

2023

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“…The majority of the cell-damaging effects induced by PDT and SDT are generally attributed to ROS. Sun et al (41) found that ROS were major triggering intermediates during the DVDMS-SDT treatment of human glioma U-373 MG cells, and that the increase in apoptosis was accompanied by an increase in cleaved-caspase 3 level and DNA fragmentation. Our study indicated that DVDMS-mediated PDT and SDT significantly inhibited the expression levels of PCNA and Bcl-xL, and enhanced cleaved-caspase 3.…”

Section: Discussionmentioning

confidence: 99%

Sinoporphyrin sodium is a promising sensitizer for photodynamic and sonodynamic therapy in glioma

Liu

Zhou

et al. 2020

Oncol Rep

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The aim of the present study was to explore the antitumor effects of sinoporphyrin sodium (DVDMS)-mediated photodynamic therapy (PDT) and sonodynamic therapy (SDT) in glioma, and to reveal the underlying mechanisms. The uptake of DVDMS by U-118 MG cells was detected by flow cytometry (FCM). A 630-nm semiconductor laser and 1-MHz ultrasound were used to perform PDT and SDT, respectively. Cell proliferation and apoptosis were evaluated using the Cell Counting Kit-8 assay, FCM and Hoechst 33258 staining, respectively. Western blot analysis was used to detect protein expression and phosphorylation levels. BALB/c nude mice were used to establish a xenograft model of U-118 MG cells. DVDMS was injected intravenously and PDT and SDT were performed 24 h later. An in vivo imaging system was used to evaluate the fluorescence of DVDMS, to measure tumor sizes, and to evaluate the therapeutic effects. The uptake of DVDMS by U-118 MG cells was optimal after 4 h. PDT and SDT following DVDMS injection significantly inhibited the proliferation and increased apoptosis of glioma cells in vitro (P<0.05, P<0.01) respectively. In vivo, the fluorescence intensity of DVDMS was lower in the PDT and SDT groups compared with the DVDMS group, while tumor cell proliferation and weight were lower in the PDT and SDT groups than in the control group (P<0.05, P<0.01). However, there was no significant difference when laser, ultrasound or DVDMS were applied individually, compared with the control group. Hematoxylin and eosin staining suggested that both PDT and SDT induced significant apoptosis and vascular obstruction in cancer tissues. DVDMS-mediated PDT and SDT inhibited the expression levels of proliferating cell nuclear antigen (PCNA) and Bcl-xL, increased cleaved-caspase 3 levels, and decreased the protein phosphorylation of the PI3K/AKT/mTOR signaling pathway. Changes in the expression of PCNA, and Bcl-xL and in the levels of cleaved-caspase 3 were partly reversed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger. Similar results were obtained with FCM. DVDMS-mediated PDT and SDT inhibited glioma cell proliferation and induced cell apoptosis in vitro and in vivo, potentially by increasing the generation of ROS and affecting protein expression and phosphorylation levels.

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“…Several studies have explored the molecular mechanisms of SDT for GBM treatment through in vitro and in vivo experiments. Many drugs, including 5-ALA [ 44 – 52 ], fluorescein [ 53 ], rose Bengal [ 54 ], hematoporphyrin mono-methyl ether (HMME) [ 38 , 55 – 60 ], sino-porphyrin [ 61 – 63 ], photofrin [ 64 , 65 ], photolon [ 66 , 67 ], protoporphyrin IX (ppIX) [ 52 ], talaporfin sodium [ 52 ], aluminum phthalocyanine disulfonate (AlPcS 2a ) [ 68 , 69 ], and titanium dioxide (TiO 2 ), have been used as sonosensitizers [ 70 , 71 ], which mainly accumulate in the mitochondria (Table 1 ).…”

Section: Killing Mechanisms Of Sdtmentioning

confidence: 99%

“…Upon activation by US, ROS generation can result in a decrease in mitochondrial membrane potential (MMP) as well as mitochondrial swelling [ 46 , 48 , 54 , 56 – 58 , 61 , 63 ]. Meanwhile, the degradation of the sarcoplasmic/endoplasmic reticulum Ca 2+ ATPase (SERCA 2 ) in the endoplasmic reticular can lead to elevation of cytoplasmic Ca 2+ levels [ 56 , 58 ].…”

Section: Killing Mechanisms Of Sdtmentioning

confidence: 99%

Nanosensitizers for sonodynamic therapy for glioblastoma multiforme: current progress and future perspectives

et al. 2022

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Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor, and it is associated with poor prognosis. Its characteristics of being highly invasive and undergoing heterogeneous genetic mutation, as well as the presence of the blood–brain barrier (BBB), have reduced the efficacy of GBM treatment. The emergence of a novel therapeutic method, namely, sonodynamic therapy (SDT), provides a promising strategy for eradicating tumors via activated sonosensitizers coupled with low-intensity ultrasound. SDT can provide tumor killing effects for deep-seated tumors, such as brain tumors. However, conventional sonosensitizers cannot effectively reach the tumor region and kill additional tumor cells, especially brain tumor cells. Efforts should be made to develop a method to help therapeutic agents pass through the BBB and accumulate in brain tumors. With the development of novel multifunctional nanosensitizers and newly emerging combination strategies, the killing ability and selectivity of SDT have greatly improved and are accompanied with fewer side effects. In this review, we systematically summarize the findings of previous studies on SDT for GBM, with a focus on recent developments and promising directions for future research.

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Sonodynamic therapy induces oxidative stress, DNA damage and apoptosis in glioma cells

Abstract: Malignant glioma remains one of the most challenging diseases to treat because of the invasive growth of glioma cells and the existence of the blood–brain barrier (BBB), which blocks drug delivery to the brain.

Cited by 19 publications

References 46 publications

Voltammetric Measurement of Antioxidant Activity by Prevention of Cu(II)-Induced Oxidative Damage on DNA Bases Using a Modified Electrode

Voltammetric Measurement of Antioxidant Activity by Prevention of Cu(II)-Induced Oxidative Damage on DNA Bases Using a Modified Electrode

Sinoporphyrin sodium is a promising sensitizer for photodynamic and sonodynamic therapy in glioma

Nanosensitizers for sonodynamic therapy for glioblastoma multiforme: current progress and future perspectives

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