Rewiring Cellular Fate – The 2012 Bonavida & Baritaki Study on Stable Water Clusters and Melanoma Cell Dynamics

PLEASE REFER TO GLOSSARY OF TECHNICAL TERMS AT BOTTOM OF ARTICLE

Article 2 in a series of 2: Orchestrating Immune Harmony – The 1998 Bonavida & Gan Study on Stable Water Clusters and Cytokine Modulation in Human BloodRewiring Cellular Fate – The 2012 Bonavida & Baritaki Study on Stable Water Clusters and Melanoma Cell Dynamics

FOR A MORE SCIENTIFIC BREAKDOWN OF THE STUDY SCROLL FURTHER DOWN

After seeing how Stable Water Clusters can influence immune signaling in blood, a natural follow-up question arises for practitioners: Can the same preparations also affect processes inside individual cells, particularly those involved in growth control and orderly cell removal?

The 2012 study by Dr. Benjamin Bonavida and Dr. Stavroula Baritaki directly addresses this. Published in Forum on Immunopathological Diseases and Therapeutics under the title “Stable Water Clusters–Mediated Molecular Alterations in Human Melanoma Cell Lines,” the work used the exact same cluster preparations tested in the 1998 cytokine study. 

This shared material allows us to connect the two investigations in a concrete way.

The body maintains tissue balance partly through apoptosis, an organized process in which a cell breaks itself down when it is damaged or no longer needed. Many abnormal cells show reduced sensitivity to these natural signals. 

The researchers asked a focused question: If laboratory-grown human melanoma cells are exposed to the cluster preparations, do they show changes in proliferation or in their readiness to undergo apoptosis?

They selected two cell lines—A375, which responds more readily to signals, and M233, which is more resistant—and grew them in culture dishes. Cells received either the active cluster preparation (Prep B) or a matched control without clusters (Prep A), along with plain laboratory water as an additional reference. 

The samples were coded so that measurements were performed without knowledge of which contained the clusters, and independent chemical analysis confirmed that both preparations were identical in composition except for the presence of clusters in Prep B.

One question that immediately comes to mind is whether any effects on cell growth are consistent across different cell types. The results were cell-line specific.

In the more resistant M233 line, neither preparation altered proliferation rates across the concentrations and time points tested. In the A375 line, however, Prep B produced a clear dose-dependent slowing of proliferation, most noticeable after 48 hours.

The control preparation showed no effect. The change reflected reduced cell division rather than direct damage to the cells.

Practitioners often ask how such preparations might influence the apoptosis process itself. The study examined sensitivity to a natural signaling molecule called FasL, which binds to Fas receptors on the cell surface and initiates the apoptosis sequence. Cells treated with Prep B displayed increased numbers of Fas receptors. 

When FasL was added afterward, a higher proportion of A375 cells entered apoptosis, as measured by activation of caspase-3, an enzyme that carries out key steps in the breakdown process. 

Prep A produced none of these changes.

A further question concerns the level at which these changes occur: Are they limited to surface receptors, or do they extend deeper into the cell’s internal instructions? 

To explore this, the researchers measured the activity of 84 genes associated with apoptosis regulation. Only a small number showed meaningful shifts after exposure to Prep B. 

DP5/Harakiri increased approximately 2.7-fold; this protein interferes with protective mechanisms that prevent cell death. 

APO2L/TRAIL rose approximately 2.2-fold and supports death-receptor signaling. 

Several additional genes linked to cleanup pathways also moved in directions consistent with greater readiness for apoptosis. The overall pattern was selective and measured.

These cellular observations connect directly to the 1998 findings. Cytokines such as IFN-γ and TNF-α, which increased in the blood samples, are established regulators of Fas receptor expression and apoptosis sensitivity. 

The 1998 study documented changes at the level of immune communication within whole blood. The 2012 study documented changes at the level of receptors and gene activity inside isolated cells. Viewed together, the two investigations show that the same preparations can influence related aspects of the body’s regulatory systems: coordinated signaling between immune cells on the one hand, and appropriate responses within individual cells on the other.

The difference in response between the two cell lines raises a point familiar to every practitioner: outcomes can vary according to baseline characteristics, much as they do among patients. Both studies were conducted under controlled laboratory conditions and do not demonstrate therapeutic effects in people. They do, however, provide clear evidence of specific biological activities that may be useful when considering Double Helix Water as part of a comprehensive care plan.

A final practical question many practitioners ask is how these timing patterns might translate into daily use.

 The 1998 study showed cytokine shifts within 8 to 24 hours, while the 2012 study noted cellular effects most evident at 48 hours. 

This suggests that consistent daily exposure at intervals that maintain steady levels may align with the observed windows of activity. 

Individual responses can be followed through patient-reported symptoms and routine laboratory indicators such as measures of inflammation.

Taken as a pair, the 1998 and 2012 studies describe a consistent pattern for Stable Water Clusters: measurable effects on immune messengers in blood and on proliferation and death pathways in cultured cells. 

The work used the same source material and careful controls. It gives practitioners in the Double Helix Water program a factual basis for ongoing clinical observation. Patterns noted in individual cases, when shared within program channels, help build collective understanding.

A MORE IN-DEPTH REVIEW OF THE PUBLISHED PAPER FOR OUR SCIENTIFICALLY INCLINED READERS:

Building on the immune orchestration detailed in the previous article, we turn to a complementary investigation that probes SWC’s direct influence at the cellular and molecular level. What if the same structured water preparation that modulates cytokine language in blood could also reprogram proliferation control and apoptotic competence in abnormal cells?

The 2012 study by Drs. Benjamin Bonavida and Stavroula Baritaki, “Stable Water Clusters–Mediated Molecular Alterations in Human Melanoma Cell Lines,” published in Forum on Immunopathological Diseases and Therapeutics, delivers intriguing in-vitro data that extends the 1998 findings into cancer biology.

Using two human melanoma lines—A375 (moderately sensitive) and M233 (more resistant)—as models, the team tested blinded preparations from Dr. Shui Yin Lo: Prep B (active SWC) versus Prep A (control), plus laboratory water. 

Chemical validation via GC/MS by an independent UCLA professor confirmed identical composition and zero organic contaminants, eliminating artifact concerns. 

Cells were cultured in media with 0–10% final concentrations of each preparation, with analyses spanning viability, proliferation (XTT assay for metabolic activity), death receptor expression (Western blot for Fas protein), apoptosis sensitization (flow cytometry for cleaved caspase-3 after FasL exposure), and gene profiling (RT-Profiler PCR array of 84 apoptosis-related genes).

The findings are selective and cell-line specific—mirroring clinical heterogeneity we encounter daily. In the more resistant M233 line, neither preparation altered proliferation or viability across concentrations or time points (24–48 hours). 

But in A375 cells, Prep B produced significant, dose-dependent inhibition of proliferation, most pronounced at 48 hours. 

Higher SWC percentages yielded greater reductions in viable cell numbers, while Prep A and controls showed no effect. 

This was not overt cytotoxicity but a measured restraint on growth—precisely the kind of gentle influence practitioners seek in terrain support.

Apoptosis pathways proved equally responsive. A375 cells pretreated with Prep B became markedly more sensitive to recombinant FasL (0–50 ng/mL), with increased frequencies of cleaved caspase-3-positive cells at higher FasL doses. Western blots confirmed Prep B upregulated total Fas receptor protein in a concentration-dependent manner (effective at 5–7.5% ranges); Prep A did not. 

More “death receptors” on the surface translated directly into amplified extrinsic apoptotic signaling—the FasL/Fas/caspase-8/3 cascade used by NK cells and CTLs.

Gene expression profiling after 48 hours of Prep B treatment revealed highly selective modulation among the 84 apoptosis regulators. Only a small subset shifted meaningfully:

• DP5/Harakiri (pro-apoptotic Bcl-2 family antagonist) rose ~2.7-fold, binding and inhibiting anti-apoptotic Bcl-2/Bcl-xL to promote mitochondrial outer-membrane permeabilization.

• APO2L/TRAIL ligand increased ~2.2-fold, further enhancing death-receptor signaling and potentially curbing invasion.

• ICE/caspase-1 (linking inflammation to pyroptosis) climbed ~1.73-fold, ASC/CARD5 (inflammasome adaptor) ~1.7-fold, and NIP1/SEC20 ~1.52-fold.

• BCL-B showed a mixed +2.2-fold shift.  The net profile favored pro-apoptotic balance—subtle transcriptional reprogramming without a nonspecific gene storm or broad toxicity.

These molecular shifts echo the 1998 cytokine data with remarkable convergence. There, SWC elevated IFN-γ and TNF-α—cytokines known to transcriptionally induce Fas and TRAIL receptors while priming cytotoxic effectors. 

Here, SWC directly supplies those receptors and sensitizes cells to ligand-triggered death. 

IL-12’s role in 1998 further amplifies this: enhanced TH1 priming meets more responsive targets. The shared researcher, identical SWC source, and blinded controls strengthen the link—immune-level modulation (blood) and cellular-level fine-tuning (tumor models) appear as two sides of the same biophysical coin.

For practitioners focused on oncology terrain or chronic proliferative concerns, this duality holds practical promise. A patient with immune evasion and apoptosis resistance might benefit simultaneously from restored cytokine dialogue (1998) and direct reprogramming toward natural cell turnover (2012). 

The 48-hour peak effects align with dosing intervals suggested by cytokine kinetics, inviting protocols that titrate concentration based on individual response. 

Cell-line variability (A375 responsive, M233 less so) reminds us that terrain matters—baseline signaling thresholds influence outcomes, much as patient-specific factors do in clinic.

Importantly, no gross cytotoxicity occurred; changes were selective and reversible in character. This positions SWC as a potential low-risk adjunct alongside detoxification, nutrition, and conventional care—never a standalone therapy. 

Monitoring via inflammatory markers, imaging, or symptom logs becomes essential.

Taken together, the two studies illuminate SWC’s multi-level subtlety: rapid cytokine recalibration in complex blood milieu pairs with targeted gene and receptor shifts in isolated cancer cells. Both demonstrate dose- and time-dependence without contaminants or overt harm. 

These insights empower terrain-based strategies for infections, autoimmunity, or supportive oncology care. We encourage you to integrate thoughtfully, document observations, and share within our community.

The biophysical elegance—structured water influencing hydration shells, signaling interfaces, or proton dynamics—challenges conventional views of water as inert. 

These preliminary yet rigorously controlled findings open doors to deeper inquiry, inviting clinicians to witness real-world resonance.

GLOSSARY OF TECHNICAL TERMS:

Any word within a definition that appears in bold is also defined in this glossary.

Abnormal cells: Cells that are not healthy or normal. They may be damaged, growing too fast, ignoring signals to stop multiplying, or failing to die when they should. In this study, the term usually refers to cancer cells or other problem cells that the body would normally remove through apoptosis.

Amino acids: Small building blocks that link together like beads on a string to form proteins.

Antagonist: Something that opposes or blocks the action of another substance. In the study, DP5/Harakiri is called a pro-apoptotic antagonist because it actively blocks (opposes) the protective Bcl-2 proteins that would otherwise keep the cell alive. By blocking these protectors, it helps push the cell toward apoptosis (orderly self-destruction).

APO2L/TRAIL: A signaling molecule that supports death-receptor pathways and helps trigger apoptosis, especially in abnormal cells.

APO2L/TRAIL ligand: A signaling molecule that attaches to “death receptors” on cells and helps trigger apoptosis, especially in abnormal or cancerous cells. See Abnormal Cells and Cancer Cells in this glossary.

Apoptosis: The body’s natural, orderly process in which a cell breaks itself down and dies when it is damaged or no longer needed, without causing harm to surrounding tissue.

ASC/CARD5: A protein that helps assemble complexes inside cells that can trigger inflammation or cell death as part of the body’s cleanup system.

BCL-B/Boo: A member of the Bcl-2 family of proteins that can influence whether a cell survives or undergoes apoptosis; its exact role can vary depending on the cell type.

Bcl-2 family: A group of proteins that act like switches controlling whether a cell lives or dies; some protect cells from death, while others promote it.

Biophysical elegance: The idea that a simple physical property of water (its structured clusters) can influence complex biological processes in a precise, non-chemical way.

Cancer Cells: Cells that have changed in a way that makes them grow and divide much faster than normal cells. They often ignore the body’s signals to stop multiplying or to undergo apoptosis. In this study, the researchers used melanoma cancer cells to test how Stable Water Clusters might affect them.

Caspase: A family of special enzymes inside cells that act like tiny molecular scissors. During apoptosis, caspases cut up important cell parts in a neat, controlled way so the cell can break down and die cleanly without harming nearby cells.

Caspase-3 (cleaved caspase-3): An enzyme that acts as one of the final “executioners” in the apoptosis process; when it is “cleaved” (activated), it carries out the orderly dismantling of the cell.

Cell: The smallest living unit that can carry out all the basic functions of life on its own. Your body is made of trillions of these tiny units — skin cells, blood cells, muscle cells, and every other kind. Each cell is like a miniature factory surrounded by a thin outer wall (membrane) that controls what enters and leaves. Inside, cells use molecules as their building materials and tools to make energy, send signals, grow, repair themselves, and decide when it is time to die through apoptosis. In short, cells are built from and run by molecules, while molecules are the actual working parts that allow cells to stay alive and do their jobs.

Cell-line specific: An effect that shows up strongly in one particular laboratory-grown cell type but not in others—reflecting how real patients can respond differently based on their individual biology.

Clinical heterogeneity: The natural differences we see from one patient to another in real-world practice — even when they have the same condition. People can show different symptoms, different severity, or different responses to treatment. This is exactly what the study mirrored when one melanoma cell line responded to the Stable Water Clusters while the other did not.

Complexes: Groups of proteins that join together inside a cell to form a team. These teams can start inflammation or cell death as part of the body’s cleanup system.

Curbing invasion: Reducing or limiting the ability of cancer cells to spread into surrounding healthy tissue or to other parts of the body. In the study, the increase in APO2L/TRAIL was noted as potentially helping to curb invasion by making the cancer cells less able to move into and damage nearby tissues.

Cytokine kinetics: The timing and pattern of how cytokine levels rise, reach their peak, and then fall back down after a trigger. It shows how quickly the immune messages appear and how long they last. In the 1998 study, cytokine kinetics showed rapid increases within about 8 hours, followed by balancing signals appearing around 24 hours. Death receptors: Special proteins on the surface of cells that act like receiving stations or locks (that needs the right key or signal to activate). When signaling molecules such as FasL or APO2L/TRAIL attach to them, they trigger apoptosis, starting the orderly process of cell self-destruction.

Death-receptor pathways: The chain of signals that travel inside the cell after a signaling molecule attaches to death receptors. These pathways carry the message deeper into the cell and eventually trigger apoptosis, causing the cell to break down in an orderly way.

DNA: The long, spiral-shaped molecule that carries the complete set of genetic instructions for building and running a living thing. It is like the master blueprint or recipe book stored inside almost every cell. Genes (also, see Gene in this glossary) are specific sections of DNA that contain the instructions for making particular proteins.

DP5/Harakiri: A pro-apoptotic protein that blocks the action of protective Bcl-2 proteins, making it easier for the cell to undergo self-destruction.

Enzyme: A special kind of protein that acts like a helper or tool inside cells. It speeds up chemical reactions so the cell can do its jobs faster, such as breaking down food for energy or helping to trigger apoptosis. The enzyme itself is not used up and can be used again.

Extrinsic: Coming from outside. In the term “extrinsic apoptotic signaling,” it means the cell death signal starts from outside the cell (for example, a signaling molecule attaching to a death receptor on the cell surface) rather than from something happening inside the cell itself.

Extrinsic apoptotic signaling: The pathway of cell death that starts when an outside signal (such as FasL) binds to a receptor on the cell surface and triggers the suicide program. Also see Extrinsic in this Glossary.

Fas receptor: A protein on the outside of cells that acts like a “kill switch” button. When activated by its partner (FasL), it triggers the cell to undergo apoptosis.

Fas receptors: Proteins on the surface of cells that act like locks. When the right key (FasL) fits into them, they start the apoptosis process.

FasL (Fas ligand): A molecule that binds to the Fas receptor on a cell’s surface, flipping the “kill switch” that leads to apoptosis.

Fold shift (also commonly called fold change): A simple way to describe how much a measurement has increased or decreased compared to its original or control level.

For example:

• A 2-fold increase means the amount has doubled (it is now twice as high).

• A 2.7-fold increase (as seen with DP5/Harakiri in the study) means the level rose to 2.7 times the original amount.

This is a standard way scientists report changes in gene activity or protein levels. Gene: A section of DNA that works like a detailed instruction manual. It tells the cell how to make a specific protein or carry out a particular job. Genes control things such as cell growth, repair, or when a cell should undergo apoptosis.

Gene activity: The process of certain genes being turned “on” so the cell makes specific proteins according to the instructions stored in those genes.

Gene expression: The process in which a gene is turned on so the cell can read the instructions inside that gene and make the specific protein the gene is responsible for. This is how genes control what the cell does — for example, growing, repairing itself, or undergoing apoptosis.

Gene expression profiling: A lab technique that measures which genes are turned “on” or “off” in a cell after a treatment, giving a readout of how the cell is changing at the molecular level.

ICE/IL1BC (caspase-1): An enzyme that can trigger inflammation or a form of cell death called pyroptosis; it also helps process certain immune signals.

Immune evasion: The ability of cancer cells or abnormal cells to avoid detection and destruction by the immune system. They may hide their identifying markers, suppress immune cell activity, or block normal immune signals so the body does not recognize or attack them.

Immune Signals: Messages sent between immune cells (also, see Immune System in this glossary) using signaling molecules. These messages coordinate the body’s defense by telling immune cells when to attack germs or abnormal cells, when to calm down, or when to clean up

Immune System: The body’s natural defense network made up of special cells and signals that work together to protect against germs, viruses, bacteria, and anything else that does not belong inside the body. It helps fight infections and keep the body in balance.

Inflammasome adaptor: A special protein that acts like a connector or helper inside the cell. It brings together other proteins to build a larger team (called the inflammasome). Once the team is assembled, it can trigger inflammation or cell death as part of the body’s natural cleanup system. ASC/CARD5 is an example of an inflammasome adaptor.

Inflammatory markers: Simple blood tests that show whether there is ongoing inflammation in the body. They help practitioners track how the body is responding and whether inflammation is increasing, decreasing, or staying the same.

Ligand: A molecule that fits perfectly into a receptor on the surface of a cell, like a key sliding into a lock. When it attaches, it delivers a message telling the cell what to do — for example, to start apoptosis, to grow, or to stop growing. Many signaling molecules are ligands.

Melanoma Cancer Cells: A specific type of cancer cells that begin in the skin’s pigment-making cells. They grow and divide very quickly and often ignore normal signals to stop multiplying or to undergo apoptosis. In this study, the researchers used laboratory-grown melanoma cancer cells to test the effects of Stable Water Clusters.

Melanoma cell lines (A375 and M233): Specific strains of human melanoma (skin cancer) cells that have been grown continuously in the lab for research; each line behaves slightly differently, mimicking how real tumors can vary.

Mitochondria: The tiny power plants inside almost every cell. They turn the food you eat and the oxygen you breathe into energy the cell can use to live and work.

Mitochondrial outer-membrane permeabilization: The step in apoptosis where the outer covering of the cell’s energy-producing mitochondria develops holes, releasing substances that help finish the cell’s self-destruction.

Modulation: A gentle, fine-tuning adjustment of a biological process. Instead of forcing a strong or sudden change, modulation means making small, balanced shifts to help the system work more smoothly — for example, the way Stable Water Clusters modulate cytokine levels or apoptosis signals without causing strong or disruptive effects.

Molecule: The smallest complete unit of any substance that still has all the properties of that substance. Molecules are made by joining atoms (the tiniest building blocks of matter) together. For example, water, proteins, and signaling molecules are all made of molecules.

NIP1/SEC20: A protein that interacts with Bcl-2 family members and helps regulate whether apoptosis occurs.

NK cells and CTLs: Two important types of immune cells that act as the body’s assassins.

NK cells (Natural Killer cells) are fast-acting defenders that can quickly recognize and kill virus-infected or abnormal cells without needing special training.

CTLs (Cytotoxic T Lymphocytes, also called cytotoxic T cells) are trained killers that learn to spot specific threats and destroy them using signals such as FasL.

Oncology: The branch of medicine that studies cancer (also, see Cancer Cells in this glossary) and how to treat it. It includes understanding how cancer starts and grows, and finding ways to support the body against it.

Oncology terrain: In integrative medicine, the overall internal environment (terrain) of a patient dealing with cancer—focusing on supporting the body’s natural balance rather than only targeting the tumor itself.

Overt cytotoxicity: Clear, obvious, and direct killing or severe damage to cells. It is the kind of harm you can easily see in lab tests — the cells are poisoned or destroyed outright rather than gently slowed down. In the 2012 study, the Stable Water Clusters did not cause overt cytotoxicity. They only slowed cancer-cell growth in a measured way without killing the cells.

PCR: Stands for Polymerase Chain Reaction. It is a laboratory technique that makes millions of copies of a specific piece of DNA so scientists can measure or study it more easily.

Polymerase: A special enzyme that builds long chains of DNA or RNA by linking together smaller building blocks. It is the key tool used in PCR to copy DNA so scientists can study it.

Prep A: The control preparation used in the study. It looked exactly like the test sample but did not contain Stable Water Clusters.

Prep B: The active preparation used in the study. It contained the Stable Water Clusters and was the real test material.

Pro-apoptotic: Describes something that promotes or helps start apoptosis. It pushes the cell toward orderly self-destruction.

Proliferation: The process by which cells grow and multiply; in cancer research, it is often measured to see whether something slows down unwanted cell growth.

Protein: Large molecules made from chains of smaller building blocks called amino acids. Proteins do most of the important work in the body, including sending signals, fighting infections, and controlling cell processes.

Proton dynamics: The movement and behavior of tiny positively charged particles (protons) within and around molecules, which can affect how cells send signals or maintain their internal balance.

Pyroptosis: A form of inflammatory cell death (different from quiet apoptosis) that releases signals to alert the immune system.

Receptor: A special protein on the surface or inside a cell that works exactly like a lock on a door. Only the correct key (a signaling molecule or ligand) can fit into it perfectly. When the right key slides in, the receptor “unlocks” and immediately starts a chain of signals inside the cell, telling the cell what to do — for example, to start apoptosis, to grow, or to stop growing.

Recombinant: Made in a laboratory using genetic engineering. Scientists take the gene for a natural substance (such as FasL) and insert it into bacteria or other cells so those cells produce large amounts of the substance. In the study, recombinant FasL is a lab-made version of the natural signaling molecule FasL used for experiments. It works exactly like the natural version but is pure and available in controlled amounts.

RNA: A molecule very similar to DNA but usually single-stranded instead of double-stranded. While DNA is the long-term master blueprint stored in the cell, RNA acts like a temporary working copy or messenger. It carries instructions from a gene (DNA) to the parts of the cell that actually build proteins.

RT-Profiler: The brand name of a specialized lab tool (a PCR array) that lets scientists quickly measure the activity of dozens of genes at once. It is used for gene expression profiling.

RT (Real Time)-Profiler PCR Array: A specialized lab tool that uses the PCR technique to measure the activity of dozens of genes related to apoptosis all at once. In RT-Profiler PCR Array, an “array” is an organized grid of many small test spots set up together on one plate. Each spot tests the activity of a different gene, letting scientists measure dozens of genes at the same time in a single experiment.

Signaling interfaces: The places on or inside cells where messages are received and passed along, much like junctions where different communication pathways meet.

Signaling molecules: Small substances (often proteins) that cells use to send messages to each other or within the same cell. They act like chemical keys or instructions that attach to receptors on cell surfaces and tell the cell what to do — for example, to grow, stop growing, or start apoptosis.

Stable Water Clusters: Groups of water molecules arranged in a stable, organized pattern that holds together under normal room temperature and pressure.

Upregulated: When the amount or activity of a gene or protein is increased inside a cell. In the study, Prep B upregulated Fas receptor protein, meaning the cells produced more of these death receptors on their surface.

Western blot: A common lab method used to detect and measure specific proteins inside cells, similar to a highly sensitive fingerprint test for proteins.

Quiet apoptosis: The normal, calm, and orderly type of apoptosis. In quiet apoptosis the cell neatly breaks itself down and disappears without causing inflammation or sending alarm signals to the immune system. This is the most common and “silent” form of programmed cell death. It is called “quiet” because it happens without disturbing nearby cells or attracting attention. It is different from pyroptosis, which is a more inflammatory (“loud”) form of cell death that alerts the immune system. Pyroptosis may occur during serious infections, for example when a cell is heavily infected by certain bacteria (like those that cause food poisoning) or viruses (such as in severe flu), or when there is serious injury or toxin damage that requires a strong warning signal to the body’s defense system.

XTT assay: A laboratory test (an “assay” is simply a lab measurement or experiment designed to check something specific). It uses a special dye called XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide). Living cells turn this dye into a colored substance. The more color produced, the more actively the cells are using energy. Lower color means fewer living or dividing cells. In the study, this test showed how well the Stable Water Cluster preparation slowed cancer-cell growth.

ORIGINAL STUDY

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