Shilajit/Fulvic Acid / Catalase Cancer Research Results

FulvicA, Shilajit/Fulvic Acid: Click to Expand ⟱
Features:
Fulvic acid is a naturally occurring compound found in soil, compost, and marine sediments. It is a complex mixture of many organic acids and has been studied for its antioxidant, anti-inflammatory, and immune-modulating properties.
Shilajit is a complex mineral–organic exudate found in mountainous regions (e.g., Himalayas). It contains fulvic acids, humic substances, dibenzo-α-pyrones (DBPs), trace minerals, and other low-molecular-weight compounds. Most standardized extracts are characterized by fulvic acid content (often 15–60%).

AD:
-Fulvic acid may help inhibit tau fibril formatio
-Antioxidant activity
-Anti-inflammatory effects

Cancer:
-Fulvic acid’s role in reducing drug resistance and improving drug absorption has been suggested
-Synergistic effects with chemotherapy

Fulvic Acid database results: Note how it is antioxidant for normal cells, but may produce ROS in cancer cells. (explains synergistic effect with chemo)
LeafSource Fulvic Acid note how they use Fulvic Acid to improve bioavailability of berberine.

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Mitochondrial function / electron transport support Bioenergetic modulation (context-dependent) ATP production support ↑ (reported) P, R Mitochondrial optimization Dibenzo-α-pyrones and fulvic acids are reported to support mitochondrial respiration in non-cancer models.
2 Nrf2 / antioxidant response Redox tone modulation (model-dependent) Nrf2 ↑; antioxidant enzymes ↑ R, G Redox buffering Commonly described as antioxidant; tumor-direction effects are not well established.
3 NF-κB inflammatory signaling NF-κB ↓ (reported; limited cancer data) Inflammation tone ↓ R, G Anti-inflammatory modulation Anti-inflammatory effects are better documented than direct tumor cytotoxicity.
4 ROS modulation ROS ↓ or stabilized (context-dependent) Oxidative stress ↓ P, R, G Antioxidant effect Acts primarily as redox stabilizer rather than ROS generator.
5 AMPK / metabolic stress pathways Metabolic modulation (limited direct tumor evidence) Energy homeostasis support ↑ R, G Metabolic adaptation Some reports suggest improved metabolic efficiency; not a primary oncologic mechanism.
6 Cell-cycle / apoptosis Apoptosis ↑ (reported in limited preclinical studies) G Conditional cytotoxicity Data are sparse and largely cell-line based; not a strong, consistent cytotoxic signature.
7 Immune modulation Immune tone modulation (context-dependent) Immune support ↑ R, G Adaptogenic effect Traditional use emphasizes immune and vitality support rather than direct anticancer activity.
8 Metal chelation / mineral transport Trace mineral transport effects (uncertain tumor relevance) Mineral absorption modulation P Biochemical modulation Fulvic acid has chelation properties; relevance to oncology unclear.
9 Quality / contamination risk Variable depending on preparation Heavy metal exposure risk if unrefined Safety constraint Crude shilajit may contain heavy metals; purified standardized extracts preferred.
10 Bioavailability variability Systemic exposure varies by extraction/purification Translation constraint Composition varies widely; standardization typically based on fulvic acid content.

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

  • P: 0–30 min (rapid mitochondrial/redox interactions)
  • R: 30 min–3 hr (acute signaling and metabolic shifts)
  • G: >3 hr (gene-regulatory adaptation and phenotype outcomes)


Catalase, Catalase: Click to Expand ⟱
Source:
Type:
Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases.
Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer.
Catalase is an enzyme found in nearly all living cells exposed to oxygen. Its primary role is to protect cells from oxidative damage by catalyzing the conversion of hydrogen peroxide (H₂O₂), a potentially damaging byproduct of metabolism, into water (H₂O) and oxygen (O₂). This detoxification process is crucial because excess H₂O₂ can lead to the formation of reactive oxygen species (ROS) that damage proteins, lipids, and DNA.

Catalase and Cancer
Oxidative Stress and Cancer:
Cancer cells often experience increased levels of oxidative stress due to rapid proliferation and metabolic changes. This stress can lead to DNA damage, promoting tumorigenesis.
Catalase helps mitigate oxidative stress, and its expression can influence the survival and proliferation of cancer cells.
Expression Levels in Different Cancers:
Overexpression: In some cancers, such as breast cancer and certain types of leukemia, catalase may be overexpressed. This overexpression can help cancer cells survive in oxidative environments, potentially leading to more aggressive tumor behavior.
Downregulation: Conversely, in other cancers, such as colorectal cancer, reduced catalase expression has been observed. This downregulation can lead to increased oxidative stress, contributing to tumor progression and metastasis.
Prognostic Implications:
Survival Rates: Studies have shown that high levels of catalase expression can be associated with poor prognosis in certain cancers, as it may enable cancer cells to resist apoptosis (programmed cell death) induced by oxidative stress.

Some types of cancer cells have been reported to exhibit lower catalase activity, possibly increasing their vulnerability to oxidative damage under certain conditions. This vulnerability has even been exploited in some therapeutic strategies (for example, approaches that generate excess H₂O₂ or other ROS specifically targeting cancer cells have been researched).


Scientific Papers found: Click to Expand⟱
4028- FulvicA,    Mineral pitch induces apoptosis and inhibits proliferation via modulating reactive oxygen species in hepatic cancer cells
- in-vitro, Liver, HUH7
Apoptosis↑, TumCP↓, ROS↑, NO↑, Dose↝, MMP↓, Cyt‑c↑, SOD↓, Catalase↓, GSH↑, lipid-P↑, miR-21↓, miR-22↑,
4030- FulvicA,    Therapeutic Potential of Fulvic Acid in Chronic Inflammatory Diseases and Diabetes
- Review, NA, NA
*Inflam↓, TNF-α↓, *COX2↓, *PGE2↓, *ROS↓, *GutMicro↑, *BioEnh↑, *BioEnh↑, *SOD↑, *Catalase↑, *GPx↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Catalase↓, 1,   GSH↑, 1,   lipid-P↑, 1,   ROS↑, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics

MMP↓, 1,  

Cell Death

Apoptosis↑, 1,   Cyt‑c↑, 1,  

Transcription & Epigenetics

miR-21↓, 1,  

Migration

miR-22↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature

NO↑, 1,  

Immune & Inflammatory Signaling

TNF-α↓, 1,  

Drug Metabolism & Resistance

Dose↝, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

Catalase↑, 1,   GPx↑, 1,   ROS↓, 1,   SOD↑, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,   Inflam↓, 1,   PGE2↓, 1,  

Drug Metabolism & Resistance

BioEnh↑, 2,  

Clinical Biomarkers

GutMicro↑, 1,  
Total Targets: 9

Scientific Paper Hit Count for: Catalase, Catalase
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#:358  Target#:46  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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