Hydrogen Gas / ROS Cancer Research Results

H2, Hydrogen Gas: Click to Expand ⟱
Features:
Hydrogen Gas, Powerful Antioxidant
Mechanistically, H₂ is most defensibly framed as a selective antioxidant + anti-inflammatory signaling modulator (often via Nrf2↑ and NF-κB↓ / NLRP3↓), with strongest clinical relevance in oncology being reduction of treatment toxicities (radiation/CCRT side-effects), with mixed/early evidence for direct anticancer effects.

1.Antioxidant and Nrf2/ARE Pathway: activate Nrf2, which induces antioxidant enzymes.
2.NF-κB Pathway: reported to inhibit NF-κB activation, thereby reducing inflammatory cytokine production
3.Mitochondrial Apoptosis Pathway
4.MAPK (Mitogen-Activated Protein Kinases) Pathway
5.PI3K/Akt/mTOR Pathway
6.Inflammatory Cytokine Signaling: Reducing cytokines (such as IL-6, TNF-α)
7.p53 Pathway
8.Autophagy Pathways: might regulate autophagy, (dual roles in cancer)

Example unit sometimes used in studies
Example Canadian Supplier

Hydrogen gas can be generated in small amount by hydrogenase of certain members of the human gastrointestinal tract microbiota from unabsorbed carbohydrates in the intestine through degradation and metabolism, which then is partially diffused into blood flow and released and detected in exhaled breath, indicating its potential to serve as a biomarker.

Many studies have shown that H2 therapy can reduce oxidative stress. This, however, contradicts radiation therapy and chemotherapy, in which ROS are required to induce apoptosis and combat cancer. Yet many studies show chemoprotective and radioprotective and some even show chemosentizing
Nevertheless there are some papers claiming ROS ↑ for cancer cells

Hydrogen Gas in Water is also used.
- the amount of H2 dissolved in solutions is limited: up to 0.8 mM (1.6 mg/L) H2 can be dissolved in water under atmospheric pressure at room temperature

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Selective ROS/RNS buffering (•OH, ONOO− emphasis) Oxidative damage tone ↓ (context-dependent) Radiation/chemo oxidative injury ↓ P, R Rapid cytoprotection Landmark work proposes H2 selectively reduces highly reactive species (e.g., hydroxyl radical) rather than globally suppressing signaling ROS. Treat as "selective antioxidant" rather than broad ROS quencher.
2 Nrf2 antioxidant response (Keap1/Nrf2; SOD/GPx/GSH systems) Stress adaptation modulation (context-dependent) Nrf2 ↑; endogenous antioxidant enzymes ↑ R, G Endogenous antioxidant upshift Multiple reviews describe H2 as engaging Nrf2-linked programs and increasing antioxidant enzyme activity; direction in tumors is model-specific and should not be oversold as uniformly anti-tumor.
3 NF-κB inflammatory transcription Inflammatory/pro-survival transcription ↓ (context) Inflammation ↓ (tissue protective) R, G Anti-inflammatory signaling Commonly reported downstream of redox modulation: reduced NF-κB activity and reduced inflammatory cytokine outputs.
4 NLRP3 inflammasome (priming/activation) Inflammasome signaling ↓ (context) NLRP3 activation ↓; tissue injury signaling ↓ R, G Inflammasome dampening Often described as part of an antioxidant–anti-inflammatory synergy (Nrf2↑ with NF-κB/NLRP3↓). Use "reported" language.
5 Mitochondrial protection / mitochondrial ROS Mito-stress tone ↓ (context) Mitochondrial function preserved; oxidative injury ↓ R, G Bioenergetic stabilization Frequently reported as reduced mitochondrial oxidative injury and improved cellular resilience in injury/inflammation models.
6 Radiation/CCRT toxicity mitigation (clinical relevance) Adjunct use: may reduce acute radiation toxicities without obvious loss of tumor control (early evidence) Mucositis/dermatitis/inflammation severity ↓ (reported) G Supportive care Clinical studies report feasibility/safety and reduced radiotherapy-related toxicities in selected settings; treat as supportive/adjunct, not standalone anti-cancer therapy.
7 Apoptosis / proliferation control Mixed reports: apoptosis ↑ or neutral depending on model Often anti-apoptotic in injury models G Context-dependent cell fate shift Unlike classic cytotoxins, H2 effects on apoptosis/proliferation are not uniform; keep as model-dependent and secondary.
8 Clinical safety signal (inhalation studies) — Generally well tolerated at low concentrations in studied settings — Translation constraint / safety framing Human safety studies exist for low-concentration inhalation; practical use must be medical-grade and safety-controlled due to flammability risk.

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

  • P: 0–30 min (direct chemical/rapid signaling effects)
  • R: 30 min–3 hr (acute redox + inflammatory signaling shifts)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
3762- H2,    Effects of Molecular Hydrogen Assessed by an Animal Model and a Randomized Clinical Study on Mild Cognitive Impairment
- in-vivo, AD, NA
*ROS↓, *memory↑, *neuroP↑, *cognitive↑, *OS↑,
3764- H2,    Therapeutic Effects of Hydrogen Gas Inhalation on Trimethyltin-Induced Neurotoxicity and Cognitive Impairment in the C57BL/6 Mice Model
- in-vivo, AD, NA
*memory↑, *Aβ↓, *p‑tau↓, *BAX↓, *ROS↓, *NO↓, *Ca+2↓, *MDA↓, *Catalase↓, *GPx↓, *TNF-α↓, *Bcl-2↑, *VEGF↑, *Inflam↓, *cognitive↑,
3766- H2,    The role of hydrogen in Alzheimer′s disease
- Review, AD, NA
*antiOx↑, *Inflam↓, *AMPK↑, *SIRT1↑, *FOXO↑, *mtDam↓, *neuroP↑, *ROS↓, *p38↓, *cognitive↑, *BDNF↑, *memory↑, *lipid-P↓, *IL6↓, *TNF-α↓, *JNK↓, *NF-kB↓, *NLRP3↓,
3767- H2,    The role of hydrogen therapy in Alzheimer's disease management: Insights into mechanisms, administration routes, and future challenges
- Review, AD, NA
*Inflam↓, *neuroP↑, *toxicity↓, *antiOx↑, *ROS↓, *NLRP3↓, *IL1β↓, *mtDam↓, *ATP↑, *AMPK↑, *FOXO3↑, *SOD1↑, *Catalase↑, *NRF2↑, *NO↓, *MDA↓, *lipid-P↓, *memory↑, *ER(estro)↓, *BDNF↑, *cognitive↑, *APP↓, *BACE↓, *Aβ↓, *BP∅, *BBB↑,
3768- H2,    Effects of Hydrogen Gas Inhalation on Community-Dwelling Adults of Various Ages: A Single-Arm, Open-Label, Prospective Clinical Trial
- Trial, AD, NA
*ROS↓, *NO↓, *BACE↓, *BDNF↑, *VEGF↑, *p‑tau↓, *MCP1↓, *IL6↓, *cognitive↑, *toxicity∅,
3770- H2,    Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases
- Review, AD, NA - Review, Park, NA
*antiOx↑, *NRF2↑, *HO-1↑, *Inflam↓, *neuroP↑, *cardioP↑, *other↓, *ROS↓, *NADPH↓, *Catalase↑, *GPx1↑, *NO↓, *mt-ROS↓, *SIRT3↑, *SIRT1↑, *TLR4↓, *mTOR↓, *cognitive↑, *Sepsis↓, *PTEN↓, *Akt↓, *NLRP3↓, *AntiAg↑, *IL6↓, *TNF-α↓, *IL1β↓, *MDA↓, *memory↑, *FOXO3↑, TumCG↓, *LDL↓,
3771- H2,    Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation—Fantasy or Reality?
- Review, AD, NA - Review, Stroke, NA
*cognitive↑, AntiCan↑, *Inflam↓, *antiOx↑, *ROS↓, *neuroP↑, *SOD↑, *GPx↑, *MDA↑, *BBB↑, *OS↑, *Ca+2↓, *APP↓, *p‑tau↓,
3772- H2,    Therapeutic potential of hydrogen-rich water in zebrafish model of Alzheimer’s disease: targeting oxidative stress, inflammation, and the gut-brain axis
- in-vivo, AD, NA
*cognitive↑, *Aβ↓, *Inflam↓, *ROS↓, *GutMicro↑, *TNF-α↓, *IL6↓, *IL1β↓, *IL10↓, *Catalase↑, *GSH↑,
3773- H2,    Role and mechanism of molecular hydrogen in the treatment of Parkinson’s diseases
- Review, Park, NA
*neuroP↑, *antiOx↑, *Inflam↓, *ROS↓, *NADPH↓, *NRF2↑, *BBB↑, *IL1β↓, *IL6↓, *TNF-α↓, *NF-kB↓, *NLRP3↓, *Sepsis↓, *p‑mTOR↓, *AMPK↑, *SIRT1↑, *HO-1↑,
3774- H2,    The role of hydrogen in Alzheimer’s disease
- Review, AD, NA
*Inflam↓, *antiOx↑, *NLRP3↓, *memory↑, *Aβ↓, *AMPK↑, *SIRT1↑, *FOXO3↑, *p‑p38↓, *JNK↓, *ROS↓, *cognitive↑, *ER(estro)↑, *BDNF↑,
3776- H2,    The role of hydrogen in Alzheimer's disease
- Review, AD, NA
*antiOx↑, *Inflam↓, *NLRP3↓, *AMPK↑, *SIRT1↑, *FOXO3↑, *ROS↓, *BDNF↑,
3761- H2,    Therapeutic Inhalation of Hydrogen Gas for Alzheimer's Disease Patients and Subsequent Long-Term Follow-Up as a Disease-Modifying Treatment: An Open Label Pilot Study
- Human, AD, NA
*cognitive↑, *BBB↑, *ROS↓, *NRF2↑, *Inflam↓, *NFAT↓, *FAO↓, *4-HNE↓, *PGC-1α↑, *Ferroptosis↓,
3787- H2,    Hydrogen, a Novel Therapeutic Molecule, Regulates Oxidative Stress, Inflammation, and Apoptosis
- Review, AD, NA
*Inflam↓, *antiOx↑, *ROS↓, *other↝, *NF-kB↓, *IL2↓, *IL6↓, *TNF-α↓, *HO-1↑, Apoptosis↑, TumAuto↑, *Sepsis↓, *NLRP3↓, Pyro↑,
4237- H2,    Hydrogen-Rich Saline Protects Against Spinal Cord Injury in Rats
- in-vitro, NA, NA
*Apoptosis↓, *ROS↓, *motorD↑, *BDNF↑,
4306- H2,    Molecular Hydrogen as an Emerging Candidate for Preventing Alzheimer’s Disease
- Review, AD, NA
*ROS↓, *memory↑, *neuroP↑, *OS↑, *Inflam↓,
4307- H2,    Hydrogen Gas Attenuates Toxic Metabolites and Oxidative Stress-Mediated Signaling to Inhibit Neurodegeneration and Enhance Memory in Alzheimer’s Disease Models
- in-vivo, AD, NA
*cognitive↑, *Inflam↓, *ROS↓, *neuroP↑, *memory↑, *BBB↑, *BDNF↑, *TNF-α↓, *Catalase↑, *IL6↓, *Aβ↓, *GABA↓, *Dose↝,
4308- H2,    A biomimetic upconversion nanoreactors for near-infrared driven H2 release to inhibit tauopathy in Alzheimer's disease therapy
- in-vivo, AD, NA
*BioAv↝, *ROS↓, *p‑tau↓, *Dose↝, *cognitive↑,
4345- H2,    The Benefit of Hydrogen Gas as an Adjunctive Therapy for Chronic Obstructive Pulmonary Disease
- Human, NA, NA
*Inflam↓, *antiOx↑, *ROS↓, *NLRP3↑, *NF-kB↓, *SOD↑, *Catalase↑, *AntiAg↑,
2507- H2,    Hydrogen protects against chronic intermittent hypoxia induced renal dysfunction by promoting autophagy and alleviating apoptosis
- in-vivo, NA, NA
*RenoP↑, *ROS↓, *Apoptosis↓, *ER Stress↓, *CHOP↓, *Casp12↓, *GRP78/BiP↓, *LC3‑Ⅱ/LC3‑Ⅰ↑, *Beclin-1↑, *p62↓, *mTOR↓,
2508- H2,    Molecular hydrogen is a promising therapeutic agent for pulmonary disease
- Review, Var, NA - Review, Sepsis, NA
*ROS↓, eff↝, *Inflam↓, *NRF2↑, *HO-1↑, *SOD↑, *Catalase↑, *MPO↑, *ASK1↓, *NADPH↓, *Sepsis↓, *HMGB1↓, ROS↑, NLRP3↑, GSDMD↑, chemoP↑, eff↑,
2510- H2,    Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals
- in-vivo, Stroke, NA
*ROS↓, *antiOx↑,
2514- H2,    Hydrogen: A Novel Option in Human Disease Treatment
- Review, NA, NA
*Inflam↓, *IL1β↓, *IL6↓, *IL8↓, *IL10↓, *TNF-α↓, *ROS↓, *HO-1↓, *NRF2↑, *ER Stress↓, H2O2↑,
2515- H2,    Recent Advances in Studies of Molecular Hydrogen against Sepsis
- Review, Sepsis, NA
*Sepsis↓, *Inflam↓, *antiOx↑, *ROS↓, *NADPH↓,
2516- H2,    Hydrogen Gas in Cancer Treatment
- Review, Var, NA
*Half-Life↓, *ROS↓, *selectivity↑, *SOD↑, *HO-1↑, *NRF2↑, *chemoP↑, *radioP↑, ROS↑, *Inflam↓, eff↑, *TNF-α↓, *IL6↓, *cl‑Casp8↑, *Bax:Bcl2↓, *Apoptosis↓, *cardioP↑, *hepatoP↑, *RenoP↑, *chemoP↑, eff↝, chemoP↑, radioP↑, eff↑, TumCG↓, Ki-67↓, VEGF↓, selectivity↑,
2518- H2,    Hydrogen Therapy Reverses Cancer-Associated Fibroblasts Phenotypes and Remodels Stromal Microenvironment to Stimulate Systematic Anti-Tumor Immunity
- in-vitro, BC, 4T1 - in-vitro, Nor, 3T3
TumCD↑, CD4+↑, ROS↓,
2520- H2,    The Impact of Molecular Hydrogen on Mitochondrial ROS and Apoptosis in Colorectal Cancer Cells
- in-vitro, CRC, NA
mt-ROS↓, ChemoSen↑, other↝,
2521- H2,    Oxyhydrogen Gas: A Promising Therapeutic Approach for Lung, Breast and Colorectal Cancer
- Review, CRC, NA - Review, Lung, NA - Review, BC, NA
Inflam↑, ROS↓, ChemoSen↑, p‑PI3K↓, p‑Akt↓, QoL↑, GutMicro↑, chemoP↑, radioP↑, *NRF2↑, *Catalase↑, *GPx↑, *HO-1↑, *SOD↑, *TNF-α↓, *IL4↓, *IL6↓, ChemoSen↑, Appetite↑, cognitive↑, Pain↓, Sleep↑, other?,
2523- H2,    Prospects of molecular hydrogen in cancer prevention and treatment
- Review, Var, NA
ROS↓, TumCP↓, TumMeta↓, AntiTum↑, GutMicro↑, Inflam↓, OS↑, radioP↑, selectivity↑, SOD↑, IL1β↑, IL8↑, TNF-α↑, neuroP↑,
2525- H2,    Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis
- in-vivo, NA, NA
OS↓, cardioP↑, *AST↓, ALAT↓, *ROS↓, *MDA↓, *hepatoP↑, *Inflam↓, chemoP↑,
2526- H2,    Influence of hydrogen-occluding-silica on migration and apoptosis in human esophageal cells in vitro
- in-vitro, ESCC, KYSE-510
*ROS↓, selectivity↑, ROS↓,
2528- H2,    Local generation of hydrogen for enhanced photothermal therapy
- in-vitro, Var, NA
eff↑, ROS↓, selectivity↑, ROS↑, other↝, ROS↑,
4126- Silicon,  H2,    Oral Administration of Si-Based Agent Attenuates Oxidative Stress and Ischemia-Reperfusion Injury in a Rat Model: A Novel Hydrogen Administration Method
- in-vivo, NA, NA
*creat↓, *ROS↓, *other↑, *MDA↓, *other↑, *Inflam↓,

Showing Research Papers: 1 to 32 of 32

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 32

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↑, 1,   ROS↓, 5,   ROS↑, 4,   mt-ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   GSDMD↑, 1,   Pyro↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other?, 1,   other↝, 2,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑PI3K↓, 1,   TumCG↓, 2,  

Migration ⓘ

Ki-67↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   IL1β↑, 1,   IL8↑, 1,   Inflam↓, 1,   Inflam↑, 1,   TNF-α↑, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   eff↑, 4,   eff↝, 2,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   GutMicro↑, 2,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   Appetite↑, 1,   cardioP↑, 1,   chemoP↑, 4,   cognitive↑, 1,   neuroP↑, 1,   OS↓, 1,   OS↑, 1,   Pain↓, 1,   QoL↑, 1,   radioP↑, 3,   Sleep↑, 1,  
Total Targets: 47

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

4-HNE↓, 1,   antiOx↑, 11,   Catalase↓, 1,   Catalase↑, 7,   Ferroptosis↓, 1,   GPx↓, 1,   GPx↑, 2,   GPx1↑, 1,   GSH↑, 1,   HO-1↓, 1,   HO-1↑, 6,   lipid-P↓, 2,   MDA↓, 5,   MDA↑, 1,   MPO↑, 1,   NRF2↑, 8,   ROS↓, 27,   mt-ROS↓, 1,   SIRT3↑, 1,   SOD↑, 5,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   mtDam↓, 2,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 5,   FAO↓, 1,   LDL↓, 1,   NADPH↓, 4,   SIRT1↑, 5,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 3,   ASK1↓, 1,   BAX↓, 1,   Bax:Bcl2↓, 1,   Bcl-2↑, 1,   Casp12↓, 1,   cl‑Casp8↑, 1,   Ferroptosis↓, 1,   JNK↓, 2,   p38↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↑, 2,   other↝, 1,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   ER Stress↓, 2,   GRP78/BiP↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO↑, 1,   FOXO3↑, 4,   mTOR↓, 2,   p‑mTOR↓, 1,   PTEN↓, 1,  

Migration ⓘ

AntiAg↑, 2,   APP↓, 2,   Ca+2↓, 2,   NFAT↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 4,   VEGF↑, 2,  

Barriers & Transport ⓘ

BBB↑, 5,  

Immune & Inflammatory Signaling ⓘ

HMGB1↓, 1,   IL10↓, 2,   IL1β↓, 5,   IL2↓, 1,   IL4↓, 1,   IL6↓, 10,   IL8↓, 1,   Inflam↓, 20,   MCP1↓, 1,   NF-kB↓, 4,   TLR4↓, 1,   TNF-α↓, 10,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 7,   GABA↓, 1,   p‑tau↓, 4,  

Protein Aggregation ⓘ

Aβ↓, 5,   BACE↓, 2,   NLRP3↓, 7,   NLRP3↑, 1,  

Hormonal & Nuclear Receptors ⓘ

ER(estro)↓, 1,   ER(estro)↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   Dose↝, 2,   Half-Life↓, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,   BP∅, 1,   creat↓, 1,   GutMicro↑, 1,   IL6↓, 10,  

Functional Outcomes ⓘ

cardioP↑, 2,   chemoP↑, 2,   cognitive↑, 12,   hepatoP↑, 2,   memory↑, 8,   motorD↑, 1,   neuroP↑, 8,   OS↑, 3,   radioP↑, 1,   RenoP↑, 2,   toxicity↓, 1,   toxicity∅, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 5,  
Total Targets: 105

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
32 Hydrogen Gas
1 Silicic Acid
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#:295  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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