Database Query Results : SonoDynamic Therapy UltraSound, ,

SDT, SonoDynamic Therapy UltraSound: Click to Expand ⟱

Features:

Sonodynamic therapy (SDT) is an emerging, non-invasive treatment modality that employs ultrasound energy in conjunction with sonosensitizers to induce cytotoxicity in target tissues. A key mechanism by which SDT exerts its therapeutic effects is through the generation of reactive oxygen species (ROS).
Also known as high-intensity focused ultrasound (HIFU)

SDT relies on the ultrasound-triggered activation of sonosensitizers (similar in concept to photosensitizers used in photodynamic therapy). When activated by ultrasound, these compounds undergo energy transitions that lead to the production of ROS, such as singlet oxygen and free radicals.

-Advantages of SDT include its non-invasive nature, deep tissue penetration of ultrasound, and the ability to target localized areas with high precision.
-Challenges remain in precisely controlling ROS production and ensuring that the resulting oxidative stress is sufficient to induce cell death in tumor cells without overwhelming damage to surrounding normal tissues.

Sonosensitizers:
– Hematoporphyrin Derivative (HPD) and Photofrin
– Protoporphyrin IX (PpIX)
– Chlorin e6 (Ce6)
– Phthalocyanine compounds
– Titanium Dioxide (TiO2) Nanoparticles
– Other metallic or semiconductor nanoparticles, sometimes functionalized or loaded with traditional sensitizer molecules (e.g., gold nanoparticles, copper-cysteamine), have been explored to enhance ROS production and improve tumor targeting.
– Curcumin, derived from turmeric, has been shown in several studies to exhibit sonosensitizing properties.
– Under ultrasound activation, quercetin may act as a sonosensitizer, increasing ROS generation and contributing to cancer cell apoptosis.

US frequency range of 150 kHz–3 MHz, irradiation dose of 2–3 W cm−2, and the actuation duration range of 1–20 min are used for SDT research

https://can-amhifu.com/

https://canadaclinicsupply.com/product/soundcare-plus-professional-dual-ultrasound-device-by-roscoe/
https://physiostore.ca/product-category/therapeutic-modalities/therapeutic-ultrasound/clinical-ultrasound-systems/
https://physiostore.ca/richmar-home-ultrasound-2000-2nd-edition/

-SDT is a pro-oxidant modality → strong antioxidants could theoretically reduce efficacy if present at high tissue levels (same logic as PDT), but this is highly protocol- and sensitizer-dependent.
-Hypoxia can blunt ROS-based killing; strategies sometimes include oxygenation, microbubbles, or vascular modulation.

Rank	Pathway / Axis	Cancer / Tumor Context	Normal Tissue Context	TSF	Primary Effect	Notes / Interpretation
1	ROS burst (sonosensitizer activation)	ROS ↑↑ (local); oxidative damage ↑	Collateral ROS possible depending on targeting	P	Primary cytotoxic driver	Core SDT mechanism: ultrasound-activated sensitizers generate ROS; effectiveness depends on oxygenation and sensitizer localization.
2	Mitochondrial dysfunction (ΔΨm loss) → intrinsic apoptosis	ΔΨm ↓; cyt-c ↑; caspase-9/3 ↑ (reported)	↔ / injury possible at high exposures	R, G	Apoptosis execution	Often downstream of ROS; magnitude depends on dose and cell redox fragility.
3	Lipid peroxidation / membrane damage	Membrane integrity ↓; lipid peroxidation ↑	Off-target membrane injury possible	P, R	Cell damage / necrotic pressure	ROS and mechanical effects can destabilize membranes; can contribute to necrosis-like death if severe.
4	ER stress / UPR activation	ER stress ↑; CHOP ↑; UPR ↑ (reported)	↔ / stress response possible	R, G	Stress overload	ROS-triggered protein misfolding and calcium dysregulation can drive UPR and pro-death signaling.
5	DNA damage response (DDR)	DNA oxidation / breaks ↑; γH2AX ↑ (reported)	↔ / injury possible	R, G	Replication stress / apoptosis support	DNA damage is typically secondary to ROS; relevance depends on tumor proliferation state.
6	Ferroptosis-like signaling (context-dependent)	Lipid ROS ↑; GPX4 pressure ↑ (reported in some SDT papers)	↔	R, G	Non-apoptotic oxidative death	Some SDT systems push lipid peroxidation strongly enough to resemble ferroptosis; not universal.
7	Autophagy response	Autophagy ↑ (adaptive) or contributes to death (context)	↔	G	Stress adaptation	Autophagy can be protective or pro-death depending on magnitude of SDT stress and sensitizer localization.
8	Microenvironment effects (vascular permeability / perfusion)	Local perfusion changes; permeability ↑ (reported)	Potential local vascular injury	P, R	Delivery modulation	Ultrasound can increase permeability (esp. with microbubbles); may enhance drug delivery in some protocols.
9	Immune activation (DAMPs / ICD-like signals)	Immunogenic cell death signals ↑ (reported)	—	G	Anti-tumor immunity support	Cell stress/death can release DAMPs and promote antigen presentation; data vary by model and sensitizer.
10	Parameter dependence / safety constraints	Effect varies with sensitizer + ultrasound settings + oxygenation	Heating / cavitation injury risk if misapplied	—	Translation constraint	SDT outcomes depend heavily on ultrasound frequency/intensity/duty cycle and sensitizer biodistribution; not “plug-and-play.”

Time-Scale Flag (TSF): P / R / G

P: 0–30 min (ROS burst; immediate membrane/vascular effects)
R: 30 min–3 hr (stress pathways: ER/DDR; apoptosis initiation)
G: >3 hr (cell death execution; immune/phenotype outcomes)

Sonodynamic Therapy — Common Sonosensitizer Classes

Sensitizer Class	Examples	Primary Mechanistic Bias	Dominant Death Pathways (Reported)	Notes / Interpretation
Porphyrins / Hematoporphyrin derivatives	Hematoporphyrin, Protoporphyrin IX, Photofrin-like agents	ROS generation (Type I/II-like chemistry under ultrasound)	Intrinsic apoptosis (ΔΨm ↓, cyt-c ↑), caspases ↑	Most classical SDT sensitizers; strong mitochondrial localization; mechanistically closest to PDT analogs.
Chlorins / Phthalocyanines	Chlorin e6 (Ce6), phthalocyanine derivatives	High ROS yield	Apoptosis ↑; lipid peroxidation ↑; ER stress ↑	Often used in nanoformulations to improve tumor accumulation and ultrasound activation efficiency.
Xanthene dyes	Eosin Y, Rose Bengal	ROS burst + membrane effects	Apoptosis ↑; necrotic pressure (dose-dependent)	Some studies show strong oxidative burst; selectivity depends on uptake and targeting.
Repurposed chemotherapeutics	Doxorubicin, 5-ALA (via PpIX accumulation)	Combined ROS + intrinsic drug mechanism	Apoptosis ↑; DDR ↑	Dual-mechanism systems: drug effect plus ultrasound-enhanced ROS; schedule-dependent outcomes.
Metal-based nanoparticles	TiO2, ZnO, MnO2-based systems	ROS catalysis; Fenton-like chemistry	Lipid peroxidation ↑; ferroptosis-like signaling (reported)	Often engineered to amplify ROS via catalytic surfaces; ferroptosis signatures reported in some platforms.
Organic nano-sonosensitizers	Polymeric micelles, liposome-loaded sensitizers	Targeted ROS release	Apoptosis ↑; immune activation (DAMPs ↑)	Improved tumor delivery; often combined with immune checkpoint therapy in preclinical systems.
Gas-generating / microbubble-assisted systems	O2-loaded microbubbles, perfluorocarbon systems	Cavitation + oxygenation enhancement	Enhanced ROS; vascular disruption	Used to overcome hypoxia and improve ROS yield; parameter-sensitive.
Natural compound–based sensitizers (experimental)	Curcumin, certain flavins (reported)	ROS generation (lower potency vs porphyrins)	Apoptosis ↑ (reported)	Less standardized; ROS yield and ultrasound responsiveness vary widely.

Scientific Papers found: Click to Expand⟱

2538-

AgNPs,

SDT,

Dual-functional silver nanoparticle-enhanced ZnO nanorods for improved reactive oxygen species generation and cancer treatment

Study,

Var,

vitro+vivo,

NA,

mice

ROS↑, This study introduces zinc oxide (ZnO) nanorods (NRs) in situ loaded with silver nanoparticles (ZnO@Ag NRs), designed to optimize ROS production under ultrasound irradiation and offer significant advantages in tumor specificity and biosafety
eff↑, In conclusion, our findings confirmed that the ROS production ability of ZnO@Ag exceeded that of ZnO and is highly depended on the duration of US treatment in this study.
eff↑, The ZnO@Ag group had the most effective cell-killing effects under ultrasound (1.5 W/cm2, 50% duty cycle, 1 MHz, 5 min) than any of the other five groups
TumCP↓, ZnO@Ag significantly inhibited tumor cell proliferation, consistent with earlier tumor growth curve findings
toxicity↓, None of the intervention groups showed significant organ toxicity

2539-

AgNPs,

SDT,

Combined effect of silver nanoparticles and therapeutical ultrasound on ovarian carcinoma cells A2780

in-vitro,

Melanoma,

A2780S

tumCV↓, Experimental results indicate a significant decrease of viability of cell, which was affected by the combined action of ultrasound field and silver nanoparticles, compared to the separate exposure of silver nanoparticles or ultrasonic field.
sonoP↑, One of the characteristic effects of sonodynamic therapy is the loosening of cell membranes, thus causing their increased porosity
BioEnh↑,

4415-

AgNPs,

SDT,

CUR,

Examining the Impact of Sonodynamic Therapy With Ultrasound Wave in the Presence of Curcumin-Coated Silver Nanoparticles on the Apoptosis of MCF7 Breast Cancer Cells

in-vitro,

BC,

MCF-7

29.3 ± 5.6 nm

 48.23 µg/ml

SDT was performed using an US frequency of 1 MHz, intensity of 2 W/cm2, and a distance of 2 cm.

tumCV↓, Curcumin-coated silver nanoparticles (Cur@AgNPs) have shown potential as a sensitizer, demonstrating adverse effects on cancer cell survival.
BAX↑, proapoptotic genes, such as Bax and Caspase-3, increased, while the expression of the antiapoptotic gene Bcl-2 decreased in MCF7 cells treated with the SDT.
Casp3↑,
Bcl-2↓,
eff↑, effect of SDT in the presence of Cur@AgNPs decreases cell viability dependence on US mode
ROS↑, Combined treatment increased the amount of ROS induction
sonoS↑, Higher concentrations of AgNPs (100 μg/ml) acted as acoustic sensitizers and enhanced ROS production
eff↑, Using curcumin as a biological coating reduced the toxicity of AgNPs and improved their significant effects with SDT
MMP↓, reduction in mitochondrial membrane potential (MMP) and the opening of mitochondrial permeability transition pores (mPTPs)
Cyt‑c↑, ultimately facilitating the release of cytochrome c from the mitochondria into the cytosol.

1603-

Cu,

BP,

SDT,

Glutathione Depletion-Induced ROS/NO Generation for Cascade Breast Cancer Therapy and Enhanced Anti-Tumor Immune Response

in-vitro,

BC,

4T1

in-vivo,

NA,

mice

GSH↓, Cu2O was incorporated into BP(black phosphorus) to exhaust the overexpressed intracellular GSH
Fenton↑, However, the Cu+-catalyzed Fenton reaction converts H2O2 into OH at a high reaction rate, even in a neutral environment (160 times than that of Fe2+)
ROS↑, BCL nanoparticles exhibited multifunctional characteristics for GSH depletion-induced ROS/NO generation,
NO↑,
sonoS↑, Numerous studies have confirmed that BP, as a sonosensitizer, can induce ROS generation in cancer therapy
eff↑, These results indicated that an acidic environment can effectively promote Cu release.
NO↑, massive NO production
*toxicity∅, Additionally, no significant body weight loss or apparent histological abnormalities of the major organs (heart, liver, spleen, lungs, and kidneys) were observed, indicating the negligible organ toxicity
eff?, In vivo studies demonstrated that BCL plus US treatment could significantly inhibit tumor growth

2535-

M-Blu,

SDT,

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

in-vitro,

Ovarian,

HO-8910

tumCV↓, 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.
ROS↑, Nuclear condensation and increased ROS levels were also found in HO-8910 cells treated by MB-mediated SDT.

2546-

M-Blu,

SDT,

The sonodynamic antitumor effect of methylene blue on sarcoma180 cells in vitro

in-vitro,

sarcoma,

S180

1,10,100uM  0.24 W/cm(2) for 30 seconds

TumCD↑, After ultrasound (US) exposure at 0.24 W/cm(2) for 30 seconds, survival rates of S180 cells in the presence of 10 and 100 microM MB were significantly lower than that of the control group

2547-

M-Blu,

SDT,

The effect of dual-frequency ultrasound waves on B16F10 melanoma cells: Sonodynamic therapy using nanoliposomes containing methylene blue

in-vitro,

Melanoma,

B16-BL6

tumCV↓, The dual-frequency protocols caused higher viability losses compared to the kHz and MHz sonications (P < .05).
ROS↑, SDT takes advantage of both physical effects (such as mechanical stress and cavitation) and biochemical effects (such as ROS) to cause cell damage and apoptosis and also to inhibit tumor growth
mtDam↑, MB-mediated SDT could obviously cause the cell death of ovarian cancer cells probably by inducing mitochondrial damage

1674-

PBG,

SDT,

HPT,

Study on the effect of a triple cancer treatment of propolis, thermal cycling-hyperthermia, and low-intensity ultrasound on PANC-1 cells

in-vitro,

PC,

PANC1

in-vitro,

Nor,

H6c7

tumCV↓, cell viability of a human cancer cell line PANC-1 decreased to a level 80% less than the control
ROS↑, triple treatment showed a significant accumulation of the intracellular ROS (up to a 2.1-fold increase)
eff↑, combination of TC-HT and US also promotes the anticancer effect of the heat-sensitive chemotherapy drug cisplatin on PANC-1 cells
Dose∅, moderate propolis concentration 0.3%, 10-cycles TC-HT and 2.25 MHz US with intensity 0.3 W/cm2 and duration 30 minutes were chosen to avoid the thermotoxicity on PANC-1 cells
selectivity↑, Moreover, normal cells such as the human skin cells Detroit 551 (Figure 1D) and human pancreatic duct cells H6c7 (Figure 1E) were not significantly affected by the triple treatment as well as all the other treatments.
MMP↓, ratio of the cells exhibiting MMP loss was significantly promoted to 23.3% after the double treatment of propolis + TC-HT, and it was further elevated significantly to 34.7% by employing the triple treatment.
mtDam↑, hence caused more mitochondrial dysfunction
cl‑PARP↑, PARP cleavage was further promoted significantly to a 6.2-fold increase by US in the triple treatment
p‑ERK↓, the p-ERK level was suppressed by propolis + TC-HT treatment (0.30-fold decrease), and was further down-regulated when US was introduced in the triple treatment (0.15-fold decrease)
p‑JNK↑, p-JNK and p-p38 levels both exhibited a reverse performance, which were promoted the most in the triple treatment (8.7-fold and 9.2-fold increase, respectively)
p‑p38↑,
eff↓, inhibitory effect of the triple treatment was restored by NAC
ChemoSen↑, cisplatin + TC-HT treatment significantly elevated PARP cleavage to a 3.20-fold increase. This elevation was further increased with the help of US (5.82-fold increase).

1403-

SDT,

BBR,

From 2D to 3D In Vitro World: Sonodynamically-Induced Prooxidant Proapoptotic Effects of C60-Berberine Nanocomplex on Cancer Cells

in-vitro,

Cerv,

HeLa

 1 MHz, 1 W/cm2 US and  20 µM C60-Ber for 24 h

in-vitro,

Lung,

LLC1

eff↑, revealed that US irradiation alone had negligible effects on LLC and HeLa cancer cells. However, both monolayers and spheroids irradiated with US in the presence of the C60-Ber exhibited a significant decrease in viability
tumCV↓,
ATP↓,
ROS↑,
Casp3↑,
Casp7↑,
mtDam↑,

2536-

SDT,

Sonodynamic Therapy: Rapid Progress and New Opportunities for Non-Invasive Tumor Cell Killing with Sound

Review,

Var,

ROS↑, [i.e. focused ultrasound (FUS)] to drive highly localized formation of tumor cell-killing reactive oxygen species (ROS).
eff↑, FUS activates “sonosensitizers”, which like photosensitizers, selectively accumulate in tumor cells and generate ROS.
Dose?, typically 1W/cm2 and up

2537-

SDT,

Design and Challenges of Sonodynamic Therapy System for Cancer Theranostics: From Equipment to Sensitizers

Review,

Var,

Dose↝, US frequency range of 150 kHz–3 MHz, irradiation dose of 2–3 W cm−2, and the actuation duration range of 1–20 min are used for SDT research
eff↑, found that the dual‐frequency ultrasound treatment in mouse breast cancer had the apparent SDT effect, while single‐frequency ultrasound treatment did not.
eff↑, Compared with single irradiation, the same dose of US fractionation exhibited better suppression of tumor growth since US dose fractionation gave rise to higher ROS concentration
eff↑, Moreover, the induced nanomaterials enhanced the cavitation and ROS yield to provide the augmented therapeutic efficiency.
eff↑, Black phosphorus (BP) as a representative semiconductor, exhibited SDT optimized with high ROS production.

2548-

SDT,

Sonoporation, a Novel Frontier for Cancer Treatment: A Review of the Literature

Review,

Var,

sonoP↑, Sonoporation has garnered significant attention for its potential to temporarily permeabilize cell membranes through the application of ultrasound waves, thus enabling an efficient cellular uptake of molecules
Dose↝, When, however, the acoustic intensity (ISATA) exceeds a certain threshold, typically 5 W/cm2 [8,9], the microbubble collapses forcefully, mechanically breaking the membrane;
eff↓, very low-intensity ultrasound (VLIUS) to tumor and normal cells, revealing that a specific VLIUS intensity (120 mW/cm2) significantly enhanced the uptake of nanoparticles and improved the delivery of the chemotherapy drug trabectedin in cancer cells
Dose↝, nanoparticles were combined with low-intensity focused ultrasound with a frequency of 1.0 MHz, a duty cycle of 50%, and an acoustic intensity of 2000, 2400, and 2800 mW/cm2
BioEnh↑,
toxicity↝, Ultrasound, especially at high acoustic intensities, can induce collateral damages that are not easy to predict; this is why low-intensity applications must be promoted.

2549-

SDT,

Landscape of Cellular Bioeffects Triggered by Ultrasound-Induced Sonoporation

Review,

Var,

sonoP↑, Numerous studies have provided us with firm evidence that sonoporation may assist cancer treatment through effective drug and gene delivery. provide greater drug distribution within tissues.
tumCV↓, Until now, numerous studies have reported various cellular alterations caused by US, e.g., a decreased viability [23], disrupted cell membrane potential [24,25], altered calcium signalling [26,27], production of reactive oxygen species
MMP↓,
ROS↑, When the gas pressure increases significantly or the temperature rapidly rises during the collapse of MBs, such extreme conditions can generate reactive oxygen species (ROS) as well as electromagnetic waves
Ca+2↑, an increased intracellular concentration of Ca2+ ions is known to induce the production of free radicals by mitochondria.
eff↝, US, microbubble responds in a wide range of behaviours that cause acoustic cavitation
eff↑, Several studies have shown that the higher the concentration of MBs, the more intensified the sonoporation and the bigger the pores in the cell membrane
selectivity↑, Interestingly, they found that MCF-7/ADR cells displayed a higher sensitivity to sonoporation
Half-Life↝, discovered that the size of the generated pore determined the reversibility of the sonoporation: membrane perforations smaller than 30 μm2 disappeared within 1 min after US treatment, whereas pores >100 μm2 were still open within half an hour.
Dose↝, Whereas US exposure at 0.75 W/cm2 provided the highest level of methane dicarboxylic aldehyde (MDA) in doxorubicin resisted cells
P-gp↓, Microbubble-based sonoporation has been shown to reduce the expression of Pgp in the blood-brain barrier in rats. Aryal et al. [136] observed a suppression of Pgp that lasted more than 72 h.
ER Stress↑, Zhong et al. revealed that sonoporation is not only capable of ER stress induction but also that these signals can be transduced to mitochondria and guide US-treated cells toward apoptosis.
other↑, This review has clearly highlighted that ultrasound (US)-triggered bioeffects are not limited to the cell membrane, but they also alter cell functioning at diverse levels.

2550-

SDT,

Intracellular Delivery and Calcium Transients Generated in Sonoporation Facilitated by Microbubbles

in-vitro,

Nor,

Rat cardiomyoblast (H9c2) cells

*Ca+2↑, Only cells adjacent to the ultrasound-driven microbubble exhibited propidium iodide (PI) uptake with simultaneous [Ca2+]i increase and fura-2 dye loss.
sonoP↑, Sonoporation has the ability to enhance the delivery of large-molecular weight drugs, genes, and proteins to cells,
BioEnh↑,

2551-

SDT,

Sonoporation: Past, Present, and Future

Review,

Var,

other↝, several novel non-bubble-based sonoporation mechanisms are under development
sonoP↑, This review will cover both the bubble-based and non-bubble-based sonoporation mechanisms being employed for intracellular delivery,
Dose↝, Sonoporation enhances the intracellular delivery of cargos into cells by employing acoustic waves to disrupt their membranes.

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

toxicity↓, 1, toxicity↝, 1,
Total Targets: 39

Pathway results for Effect on Normal Cells:

Migration ⓘ

Ca+2↑, 1,

Functional Outcomes ⓘ

toxicity∅, 1,
Total Targets: 2

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:267  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Database Query Results : SonoDynamic Therapy UltraSound, ,

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Migration ⓘ

Functional Outcomes ⓘ

Home Page