Hypocrellin B-mediated sonodynamic action induces apoptosis of hepatocellular carcinoma cells

Objective

The present study aims to investigate apoptosis of hepatocellular carcinoma cells induced by hypocrellin B-mediated sonodynamic action.

Methods

The hypocrellin B concentration was kept constant at 2.5 μM and cells from the hepatocellular carcinoma HepG2 cell line were exposed to ultrasound with an intensity of 0.46 W/cm² for 8 s. Cell cytotoxicity was quantified using an MTT assay 24 h after sonodynamic therapy (SDT) of hypocrellin B. Apoptosis was investigated using a flow cytometry with Annexin V-FITC and propidium iodine staining. Intracellular reactive oxygen species (ROS) levels were detected using a flow cytometry with 2,7-dichlorodihydrofluorecein diacetate (DCFH-DA) staining.

Results

The cytotoxicity of hypocrellin B-mediated sonodynamic action on HepG2 cells was significantly higher than those of other treatments including ultrasound alone, hypocrellin B alone and sham treatment. Flow cytometry showed that hypocrellin B-induced sonodynamic action markedly enhanced the apoptotic rate of HepG2 cells. Increased ROS was observed in HepG2 cells after being treated with hypocrellin B-mediated sonodynamic action.

Conclusions

Our data demonstrated that hypocrellin B-mediated sonodynamic action remarkably induced apoptosis of HepG2 cells, suggesting that apoptosis is an important mechanism of cell death induced by hypocrellin B-mediated SDT.     

Sonodynamic action of pyropheophorbide-a methyl ester induces mitochondrial damage in liver cancer cells

Sonodynamic therapy with pyropheophorbide-a methyl ester (MPPa) presents a promising aspect in treating liver cancer. The present study aims to investigate the mitochondrial damage of liver cancer cells induced by MPPa-mediated sonodynamic action. Mouse hepatoma cell line H₂₂ cells were incubated with MPPa (2 μM) for 20 h and then exposed to ultrasound with an intensity of 0.97 W/cm² for 8 s. Cytotoxicity was investigated 24 h after sonodynamic action using MTT assay and light microscopy. Mitochondrial membrane potential (ΔΨm) was analyzed using flow cytometry with rhodamine 123 staining and ultrastructural changes were observed using transmission electron microscopy (TEM).The cytotoxicity of MPPa-mediated SDT on H₂₂ cell line was 73.00 ± 3.42%, greater than ultrasound treatment alone (28.12 ± 5.19%) significantly while MPPa treatment alone had no significant effect on H₂₂ cells. Moreover, after MPPa-mediated SDT cancer cells showed swollen mitochondria under TEM and a significant collapse of mitochondrial membrane potential. Our findings demonstrated that MPPa-mediated SDT could remarkably induce cell death of H₂₂ cells, and highlighted that mitochondrial damage might be an important cause of cell death induced by MPPa-mediated SDT.     

Impact of thermal effects induced by ultrasound on viability of rat C6 glioma cells

In order to have consistent and repeatable effects of sonodynamic therapy (SDT) on various cancer cells or tissue lesions we should be able to control a delivered ultrasound energy and thermal effects induced. The objective of this study was to investigate viability of rat C6 glioma cells in vitro depending on the intensity of ultrasound in the region of cells and to determine the exposure time inducing temperature rise above 43 °C, which is known to be toxic for cells. For measurements a planar piezoelectric transducer with a diameter of 20 mm and a resonance frequency of 1.06 MHz was used. The transducer generated tone bursts with 94 μs duration, 0.4 duty-cycle and initial intensity I_SATA (spatial averaged, temporal averaged) varied from 0.33 W/cm² to 8 W/cm² (average acoustic power varied from 1 W to 24 W). The rat C6 glioma cells were cultured on a bottom of wells in 12-well plates, incubated for 24 h and then exposed to ultrasound with measured acoustic properties, inducing or causing no thermal effects leading to cell death. Cell viability rate was determined by MTT assay (a standard colorimetric assay for assessing cell viability) as the ratio of the optical densities of the group treated by ultrasound to the control group. Structural cellular changes and apoptosis estimation were observed under a microscope. Quantitative analysis of the obtained results allowed to determine the maximal exposure time that does not lead to the thermal effects above 43 °C in the region of cells for each initial intensity of the tone bursts used as well as the threshold intensity causing cell death after 3 min exposure to ultrasound due to thermal effects. The averaged threshold intensity was found to be about 5.7 W/cm².     

Apoptosis of ovarian cancer cells induced by methylene blue-mediated sonodynamic action

Objective

The present study aims to investigate apoptosis of ovarian cancer cells induced by methylene blue (MB)-mediated sonodynamic therapy (SDT).

Methods

The MB concentration was kept constant at 100 μM and ovarian cancer HO-8910 cells were exposed to ultrasound therapy for 5 s with an intensity of 0.46 W/cm². The cytotoxicity was investigated 24 h after MB-mediated sonodynamic action. Apoptosis was analyzed using a flow cytometer with Annexin V-FITC and propidium iodine (PI) staining as well as fluorescence microscopy with Hoechst 33258 staining. Intracellular reactive oxygen species (ROS) level was measured by flow cytometer with 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA) staining.

Results

The cytotoxicity of MB-mediated SDT on HO-8910 cells after MB-mediated SDT was significantly higher than those of other treatments including ultrasound alone, MB alone and sham treatment. Flow cytometric analysis showed a significant increase in the early and late apoptotic cell populations by MB-mediated SDT of HO-8910 cells. Nuclear condensation and increased ROS levels were also found in HO-8910 cells treated by MB-mediated SDT.

Conclusions

Our findings demonstrated that MB-mediated sonodynamic action significantly induced apoptosis of HO-8910 cells and an increase in intracellular ROS level. This indicates that apoptosis is an important mechanism of cell death induced by MB-mediated SDT. Thus, MB-mediated SDT might be a potential therapeutic strategy for combating ovarian cancer.     

Ultrasound induces cellular destruction of nasopharyngeal carcinoma cells in the presence of curcumin

Objectives

Curcumin, a natural pigment from the traditional Chinese herb, has shown promise as an efficient enhancer of ultrasound. The present study aims to investigate ultrasound-induced cellular destruction of nasopharyngeal carcinoma cells in the presence of curcumin in vitro.

Methods

Nasopharyngeal carcinoma cell line CNE2 cells were incubated by 10 μm curcumin and then were treated by ultrasound for 8 s at the intensity of 0.46 W/cm². Cytotoxicity was evaluated using MTT assay and light microscopy. Mitochondrial damage was analyzed using a confocal laser scanning microcopy with Rhodamine 123 and ultrastructural changes were observed using a transmission electron microscopy (TEM).

Results

MTT assay showed that cytotoxicity induced by ultrasound treatment alone and curcumin treatment alone was 18.16 ± 2.37% and 24.93 ± 8.30%, respectively. The cytotoxicity induced by the combined treatment of ultrasound and curcumin significantly increased up to 86.67 ± 7.78%. TEM showed that microvillin disappearance, membrane blebbing, chromatin condensation, swollen mitochondria, and mitochondrial myelin-like body were observed in the cells treated by ultrasound and curcumin together. The significant collapse of mitochondrial membrane potential (MMP) was markedly observed in the CNE2 cells after the combined treatment of curcumin and ultrasound.

Conclusions

Our findings demonstrated that ultrasound sonication in the presence of curcumin significantly killed the CNE2 cells and induced ultrastructural damage and the dysfunction of mitochondria, suggesting that ultrasound treatment remarkably induced cellular destruction of nasopharyngeal carcinoma cells in the presence of curcumin.     

In vitro sonodynamic cytotoxicity in regulated cavitation conditions

Sonodynamic toxicity has always been linked to the cavitation phenomenon. In this work, sonodynamic effect with Photofrin^® was evaluated with a new ultrasound device: a regulated cavitation generator. In this way, acoustic intensity was substituted with cavitation level as ultrasound parameter. Photofrin^® potentiated significantly the cavitation cytotoxicity even for low setpoints where no inertial cavitation appeared. Therefore sonodynamic mechanism was principally mechanical, facilitated by the Photofrin^® insertion in cellular cytoplasmic membranes. This assertion was also supported by the fact that sonodynamic cytotoxicity was independent from the Photofrin^® presence or absence in the extracellular medium. Reproducible sonodynamic efficiency was perfectly obtained with this new regulated cavitation generator.     

Targeted sonodynamic therapy using protein-modified TiO2 nanoparticles

Our previous study suggested new sonodynamic therapy for cancer cells based on the delivery of titanium dioxide (TiO₂) nanoparticles (NPs) modified with a protein specifically recognizing target cells and subsequent generation of hydroxyl radicals from TiO₂ NPs activated by external ultrasound irradiation (called TiO₂/US treatment). The present study first examined the uptake behavior of TiO₂ NPs modified with pre-S1/S2 (model protein-recognizing hepatocytes) by HepG2 cells for 24 h. It took 6 h for sufficient uptake of the TiO₂ NPs by the cells. Next, the effect of the TiO₂/US treatment on HepG2 cell growth was examined for 96 h after the 1 MHz ultrasound was irradiated (0.1 W/cm², 30 s) to the cells which incorporated the TiO₂ NPs. Apoptosis was observed at 6 h after the TiO₂/US treatment. Although no apparent cell-injury was observed until 24 h after the treatment, the viable cell concentration had deteriorated to 46% of the control at 96 h. Finally, the TiO₂/US treatment was applied to a mouse xenograft model. The pre-S1/S2-immobilized TiO₂ (0.1 mg) was directly injected into tumors, followed by 1 MHz ultrasound irradiation at 1.0 W/cm² for 60 s. As a result of the treatment repeated five times within 13 days, tumor growth could be hampered up to 28 days compared with the control conditions.     

Application of ultrasound as pretreatment for extraction of podophyllotoxin from rhizomes of Podophyllum peltatum

The effect of high-power ultrasound pretreatment on the extraction of podophyllotoxin from Podophyllum peltatum was investigated. Direct sonication by an ultrasound probe horn was applied at 24 kHz and a number of factors were investigated: particle size (0.18-0.6 mm), type of solvent (0-100% aqueous ethanol), ultrasonic treatment time (2-40 min), and power of ultrasound (0-100% power intensity, maximum power: 78 W). The optimal condition of ultrasound was achieved with 0.425-0.6 mm particle size, 10 min sonication time, 35 W ultrasound power, and water as the medium. There was no obvious degradation of podophyllotoxin with ultrasound under the applied conditions, and an improvement in extractability was observed. The SEM microscopic structure change of treated samples disclosed the effect of ultrasound on the tissue cells. The increased pore volume and surface area after ultrasonic treatment also confirmed the positive effect of ultrasound pretreatment on the extraction yield of podophyllotoxin from the plant cells.     

The role of p53 in the response of tumor cells to sonodynamic therapy in vitro

p53 plays a pivotal role in apoptosis. In addition, p53 is currently extensively investigated as a promising strategy for highly specific anticancer therapy in chemotherapeutics and photodynamic therapy. However, the role of p53 in the response of tumor cells to sonodynamic therapy treatment is still unclear. In this study, we aim to investigate the activation of p53 in sonodynamic therapy. Three murine tumor models with distinct aggressiveness (S180, H-22 and EAC) were treated with 1.75 MHz continuous ultrasound at an acoustic intensity (I_SATA) of 1.4 W for 3 min in the presence of 20 μg/ml hematoporphyrin. The DNA fragment and nuclear damage were observed by TUNEL and single cell gel electrophoresis. Western blotting and RT-PCR were used to analyze the expression of p53, PUMA, Bax and Fas. Then we checked the translocation of p53 by confocal microscopy. DNA sequencing was used to determine the status of p53 gene in three tumor cell lines. Our results indicated that the level of p53 protein and mRNA increased significantly, and p53 activated the expression of its downstream pro-apoptosis gene PUMA, Bax and Fas in the S180 and H-22 cells. Meanwhile, p53 protein translocated onto mitochondria. In the EAC cells, expression and translocation of p53 was not found; the level of PUMA, Bax and Fas remained unaltered. The S180 cells showed most serious DNA fragment and nuclear damage with 77.43% TDNA; H-22 cells in the middle with 58.85% TDNA; whereas EAC cells appeared less nuclear material lost with just 15.82% TDNA. The results of DNA sequencing showed that the sequences of exons 5-8 of the p53 gene of S180, H-22 and EAC cells were the same with the sequences of wild-type p53 provided by NCBI. These results primarily demonstrated that: (1) p53 was activated to promote SDT-induced apoptosis through extrinsic and intrinsic signaling pathways in the S180 and H-22 cells; (2) cellular responses of different cells to SDT were distinct, the aggressive S180 cells were much more sensitive than H-22, whereas EAC cells were relatively less sensitive. The discrepancy among the cell lines may be due to different activation time of p53 protein.     

Sonodynamic therapy combined with novel anti-cancer agents,sanguinarine and ginger root extract: Synergistic increase in toxicity in the presence of PANC-1 cells in vitro

The presence of ultrasound-induced cavitation in sonodynamic therapy (SDT) treatments has previously enhanced the activity and delivery of certain sonosensitisers in biological systems. The purpose of this work was to investigate the potential for two novel anti-cancer agents from natural derivatives, sanguinarine and ginger root extract (GRE), as sonosensitisers in an SDT treatment with in vitro PANC-1 cells. Both anti-cancer compounds had a dose-dependent cytotoxicity in the presence of PANC-1 cells. A range of six discreet ultrasound power-frequency configurations were tested and it was found that the cell death caused directly by ultrasound was likely due to the sonomechanical effects of cavitation. Combined treatment used dosages of 100 μM sanguinarine or 1 mM of GRE with 15 s sonication at 500 kHz and 10 W. The sanguinarine-SDT and GRE-SDT treatments showed a 6% and 17% synergistic increase in observed cell death, respectively. Therefore both sanguinarine and GRE were found to be effective sonosensitisers and warrant further development for SDT, with a view to maximising the magnitude of synergistic increase in toxicity.     

Protoporphyrin IX-mediated sonodynamic action induces apoptosis of K562 cells

Objectives

The present study aims to investigate apoptosis of human leukemia K562 cells induced by protoporphyrin IX (PpIX)-mediated sonodynamic therapy (PpIX-SDT).

Methods

The uptakes of intracellular PpIX in K562 cells were detected by flow cytometry. The sub-cellular localization of PpIX was imaged by confocal microscope. The cytotoxic effect of PpIX-SDT was assessed by MTT (3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenylter-trazolium bromide tetrazolium) assay. Apoptosis was evaluated by chromatin condensation with DAPI (4′-6-diamidino-2-phenylindole) staining, decrease of mitochondria membrane potential (MMP), re-distribution of Bax, and the expression changes of the key apoptosis-associated protein (Caspase-3 and polypeptide poly (ADP-robose) polymerase). The possible mechanism of SDT-induced apoptosis was investigated by detecting by intracellular ROS (reactive oxygen species) generation and effect of ROS scavenger-NAC (N-acetylcysteine) on SDT induced apoptosis.

Results

The intracellular PpIX increased quickly within 2 h after PpIX administration and PpIX mainly localized in the mitochondria. Compared with PpIX alone and ultrasound alone groups, the synergistic cytotoxicity of PpIX plus ultrasound was significantly boosted. In addition, the ultrasound induced some extent of chromatin condensation and MMP loss was greatly enhanced by the presence of 2 μg/ml PpIX, where PpIX alone treatment showed no or only slight effect. Time-dependent Bax translocation, caspase-3 activation and PARP cleavage were detected in SDT treatment groups. Besides, intracellular ROS production was significantly enhanced after SDT, and the general ROS scavenger NAC could obviously alleviate the SDT-caused cell viability loss, MMP loss, Bax redistribution and nuclear changes.

Conclusions

These results indicated that PpIX-mediated sonodynamic action could induce apoptosis on K562 cells, and the intracellular ROS was involved in the PpIX-SDT induced apoptosis.     

In vitro activation of mitochondria-caspase signaling pathway in sonodynamic therapy-induced apoptosis in sarcoma 180 cells

Sonodynamic therapy (SDT) has been shown to mediate apoptosis in many experimental systems, but the detailed mechanism of this process is unclear. In this study, we aim to investigate the potential participation of the mitochondria-caspase signaling pathway in the SDT-induced apoptosis in isolated sarcoma 180 (S180) cells. The cell suspension was treated with 1.75 MHz continuous ultrasound (US) at an acoustic intensity (I_SATA) of 1.4 W for 3 min in the absence or presence of 20 μg/ml hematoporphyrin (Hp). At different times after the SDT-treatment, the apoptotic cells were identified under a scanning electron microscope, and the apoptosis index (AI) was determined by flow cytometry. In addition, the mitochondrial membrane potential, permeabilization of the inner mitochondrial membrane, and translocation of apoptosis-related proteins were assessed by confocal microscopy. Simultaneously, the activation of some special apoptosis-associated proteins [caspase-9, caspase-3, polypeptide poly (ADP-ribose) polymerase (PARP), and Bax] was evaluated by western blotting. Our results indicate that the ultrasonically activated Hp can cause obvious cell apoptosis (AI, 57.66%) at 3 h after treatment, and this effect can be significantly reduced by caspase-9 inhibitor (AI, 20.76%) and the oxygen scavenger NaN₃ (20.11%). However, the apoptosis induced by ultrasound alone was relatively lower (28.33%) and was not reduced by NaN₃. Further, SDT caused an 82.1% reduction in the mitochondrial membrane potential and a 70.7% reduction in the permeabilization of the inner mitochondrial membrane immediately after treatment, and these two effects were obviously prevented by NaN₃. In comparison with the control cells, the SDT-treated cells showed obvious cytochrome-c and Bax translocations, caspase activation, Bax expression, and PARP cleavage at 1 h after SDT-treatment. However, in the cells treated with ultrasound alone, these phenomena partially and weakly occurred 3 h after exposure. These results primarily showed that the mitochondria-caspase signaling pathway in S180 cells was activated in the US- and SDT-induced apoptosis. Moreover, Hp significantly accelerates the process of apoptosis and enhances the cytotoxic effect of ultrasonic treatment. Singlet oxygen may be responsible for the mitochondrial damage and the activation of the apoptotic signaling pathway.     

Sonodynamically induced anti-tumor effect with protoporphyrin IX on hepatoma-22 solid tumor

Objective

The purpose of this study was to evaluate sonodynamically induced anti-tumor effect of protoporphyrin IX (PPIX) in mice bearing hepatoma-22 (H-22) solid tumors, and the possible in vivo cell damage mechanism was also investigated.

Methods

The pharmacokinetics of PPIX was analyzed in plasma, skin, muscle and tumor of H-22 bearing mice. Tumors were irradiated with ultrasound (1.43 MHz, I_SATA 3 W/cm², 3 min) for three times at 8, 12 and 24 h after 5.0 mg/kg PPIX administration, respectively. The anti-tumor effects of sonodynamic therapy (SDT) were estimated by the tumor inhibition ratio (volume and weight). The bio-effects of SDT were evaluated by hematoxylin and eosin (H&E) staining, transmission electron microscope (TEM) observation, lipid peroxidation (LPO) measurement and anti-oxidative enzymes (glutathione peroxidase (GSH-PX), catalase (CAT) and superoxide dismutase (SOD)) assay.

Results

A significant anti-tumor effect was obtained by PPIX-mediated sonodynamic therapy (PPIX-SDT). At the fifteenth day after PPIX-SDT, the tumor growth and tumor weight inhibition ratios were 53.84% and 45.86%, respectively. In addition, the structure of tumor tissues and the anti-oxidative enzymes were obviously destroyed after SDT treatment.

Conclusions

A biochemical mechanism was involved in PPIX-SDT in vivo, and the free radicals produced by the synergistic treatment destroying the anti-oxidative system of tumor cells in vivo may play an important role in this action. Also, the thermal effect could not be excluded in inducing damage of cellular structures, like membrane disruption and chromatin condensation under current evaluation in this paper.     

Membrane fluidity altering and enzyme inactivating in sarcoma 180 cells post the exposure to sonoactivated hematoporphyrin in vitro

Sonodynamic therapy (SDT) is a novel tumor therapy method. We investigated membrane fluidity, activity of the enzymes and membrane morphology in vitro post hematoporphyrin-SDT treatment. Furthermore, the potential mechanisms behind the changes in membrane fluidity and enzymic activity were discussed. Tumor cells were exposed to ultrasound at 1.75 MHz for up to 3 min in the presence and absence of hematoporphyrin. Fluorescence polarization, contents of Malonaldehyde, and levels of free fatty acid were assessed. Activity of enzymes was checked by the plumbic nitrate detection method. For the morphologic study, a scanning electron microscope was used to observe the cellular surface. Ultrasonically induced cell damage increased in the presence of HPD (from 15% to 24%). Compared with ultrasound treatment alone, the fluidity decreased from 5.037 to 3.908, malonaldehyde content and free fatty acid level increased from 0.743 nmol/mL to 0.979 nmol/mL and from 237.180 μmol/L to 730.769 μmol/L, respectively, post ultrasound combined with HPD treatment. Inactivity of adenylate cyclase and guanylate cyclase and significant deformation of the cellular surface were also observed post SDT treatment. Our results suggested that alterations in membrane modality and lipid composition played important roles in SDT-mediated inhibition of tumor growth, even inducing tumor cell death, which might be attributed to a sono-chemical activation mechanism.     

Comparison of pharmacokinetics, intracellular localizations and sonodynamic efficacy of endogenous and exogenous protoporphyrin IX in sarcoma 180 cells

Purpose

The aim of the present study was to investigate the differences in pharmacokinetics, sub-cellular localizations and sonodynamic efficacy between endogenous and exogenous protoporphyrin IX (endo-PpIX and exo-PpIX) in sarcoma 180 (S180) cells.

Materials and methods

The 5-aminolevulinic acid (ALA)-derived endo-PpIX and exo-PpIX pharmacokinetic profiles were determined by the fluorescence intensity of cell extracts with a spectrophotometer based on a standard curve. The changes in their sub-cellular localization patterns over a prolonged incubation time were evaluated by laser scanning confocal microscopy. The cytotoxic effects of 5-ALA-mediated sonodynamic therapy (ALA-SDT) and exogenous PpIX-mediated sonodynamic therapy (PpIX-SDT) were also evaluated by the MTT assay.

Results

The exo-PpIX showed dose-dependent pharmacokinetics in which a plateau of intra- and extracellular content was observed 45 min after administration. However, the amount of ALA-derived endogenous intracellular PpIX, as well as extracellular PpIX in the same samples, showed linear accumulation with incubation time, which was independent of ALA concentration. Fluorescent imaging revealed that the exo-PpIX mainly accumulated at the plasma membrane in the early stage, whereas the ALA-derived PpIX initially localized in the mitochondria. Cells displayed sonodynamic damage by the synthesized endo-PpIX after addition of 1 mM ALA for 12 h, but the cytotoxicity induced by the equivalent amount of exo-PpIX was much more significant with increasing ultrasound intensities.

Conclusions

Our findings suggest that endo- and exo-PpIX in S180 cells differ not only in pharmacokinetics but also in sub-cellular localizations, which may affect their sonodynamic efficacy and mechanisms of inducing cell death.     

Effect of exposure parameters on cavitation induced by low-level dual-frequency ultrasound

In order to quantify the effects of exposure parameters under therapeutic conditions such as sonodynamic therapy, it is necessary initially to evaluate the inertial cavitation activity in vitro. In this study, the dependence of cavitation activity induced by the low-level dual-frequency ultrasound irradiation on exposure parameters has been studied. Experiments were performed in the near 150 kHz and 1 MHz fields in the progressive wave mode. It has been shown that at constant ultrasound energy the fluorescence intensity for continuous sonication is higher than for pulsed mode. With increasing the duty cycle of pulsed field, the inertial cavitation activity is increased. The activity of cavitation produced by simultaneous combined sonication by two ultrasound fields is remarkably higher than the algebraic sum of effects produced by fields separately (p-value < 0.05). This study shows that simultaneous combined dual-frequency ultrasound sonication in continuous mode is more effective in producing inertial cavitation activity at low-level intensity. Therefore, it is concluded that investigations in this combined ultrasound sonication can be useful in sonodynamic therapy for superficial tumors.     

Targeted sonocatalytic cancer cell injury using avidin-conjugated titanium dioxide nanoparticles

In this study, we applied sonodynamic therapy to cancer cells based on the delivery of titanium dioxide (TiO₂) nanoparticles (NPs) modified with avidin protein, which preferentially discriminated cancerous cells from healthy cells. Subsequently, hydroxyl radicals were generated from the TiO₂ NPs after activation by external ultrasound irradiation (TiO₂/US treatment). Although 30% of the normal breast cells (human mammary epithelial cells) exhibited the uptake of avidin-modified TiO₂ NPs, over 80% of the breast cancer cells (MCF-7) exhibited the uptake of avidin-TiO₂ NPs. Next the effect of the TiO₂/US treatment on MCF-7 cell growth was examined for up to 96 h after 1-MHz ultrasound was applied (0.1 W/cm², 30 s) to cells that incorporated the TiO₂ NPs. No apparent cell injury was observed until 24 h after the treatment, but the viable cell concentration declined to 68% compared with the control at 96 h.     

Fluorescence enhancement effect for the determination of curcumin with yttrium(III)—curcumin—sodium dodecyl benzene sulfonate system

It is found that the fluorescence of curcumin is greatly enhanced by yttrium(III) (Y³⁺) in the presence of sodium dodecyl benzene sulfonate. Based on this, a sensitive fluorimetric method for the determination of curcumin in aqueous solution is proposed. In the potassium hydrogen phthalate (KHP) buffer, the fluorescence intensity of curcumin is proportional to the concentration of curcumin in the range of 7.37×10⁻⁴-0.18, 0.18-2.95 μg mL⁻¹ and the detection limit is 0.1583 ng mL⁻¹. The actual samples are satisfactorily determined. In addition, the interaction mechanism is also studied.     

A study of ovarian cancer biomarker amplification using ultrasound for early stage detection

The application of serum biomarker to ovarian tumors for early stage detection and clinical diagnosis is a rapidly expanding research area. The problem with conventional markers is that they are often released too late or at too low a level to be detected in time to trigger effective treatment. Ultrasound has been used to influence bio-effects in living cells, but there is only one reported case of the use of ultrasound to enhance the release of a biomarker (Carcinoembryonic antigen CEA). In this study we report the use of ultrasound to enhance the release of a combination of ovarian cancer biomarkers (CA125 and CA19-9) to help in the diagnosis of ovarian cancer at an early stage. The results indicated that after 5 min sonication at a frequency of 1 MHz and intensity of 0.3 W cm⁻², the CA125 and CA19-9 levels were increased by 2.02 and 4.21-fold respectively. These findings suggest that ultrasonic treatment can be used to enhance the release of serum biomarkers from ovarian tumors.     

Sonodynamic antimicrobial chemotherapy: An emerging alternative strategy for microbial inactivation

Sonodynamic antimicrobial chemotherapy (SACT), which relies on a combination of low-intensity ultrasound and chemotherapeutic agents termed sonosensitizers, has been explored as a promising alternative for microbial inactivation. Such treatment has superior penetration ability, high target specificity, and can overcome resistance conferred by the local microenvironment. Taken of these advantages, SACT has been endowed with an extensive application prospect in the past decade and attracted more and more attention. This review focusses on the current understanding of the mechanism of SACT, the interaction of sonodynamic action on different microbes, the factors affecting the efficacy of SACT, discusses the findings of recent works on SACT, and explores further prospects for SACT. Thus, a better understanding of sonodynamic killing facilitates the scientific community and industry personnel to establish a novel strategy to combat microbial burden.