Mitochondrial Mechanisms of Rejuvenation

  The Cell: Fundamental Architecture and Homeostasis.
The cell represents a fundamental structural and functional unit of a living organism. It is a dynamic system where every component participates in maintaining internal homeostasis, ensuring constancy of composition, energetics, and signaling. To understand the effect of plasma ionization products on the cell, it is necessary to identify the key structures providing barrier, transport, and energetic functions.
Let’s start with its external barrier—the membrane lipid bilayer.
The plasma membrane is a semipermeable barrier about 5 nm thick, constructed from phospholipids, cholesterol, and proteins. Two oppositely oriented lipid monolayers form the bilipid layer, where hydrophilic “heads” face outwards and hydrophobic “tails” face inwards. This structure specifically determines the membrane’s selective permeability: small nonpolar molecules ($O₂, CO₂, H₂O₂$) can diffuse, whereas ions and large polar molecules require special transporters or channels. The membrane is not static—it is characterized by fluidity and the presence of lipid rafts—microdomains enriched with cholesterol and sphingolipids that serve as platforms for membrane receptors and signaling complexes. Damage or oxidation of raft components, including under the influence of reactive oxygen species (ROS), leads to changes in the cell’s signaling architecture, which plays a significant role in the mechanisms of aging.

In addition to this external barrier, membrane transport systems play a key role.
The cell’s ionic equilibrium and resting potential are maintained through the coordinated function of several key transport proteins. The first and foremost is Na⁺/K⁺-ATPase—the main “energy pump” of the plasma membrane. It pumps three Na ions out of the cell in exchange for two K+ ions, using the energy of ATP hydrolysis. This mechanism forms the membrane potential and is critically important for maintaining osmotic balance. Next are the potassium channels —they regulate membrane conductance and are responsible for repolarization after depolarization events. Potassium flux is crucial for cell volume homeostasis and mitochondrial function. And finally, Ca²⁺-channels and exchangers (Na+, Ca2+}, SERCA,  MCU in mitochondria)—these structures coordinate intracellular signals, apoptosis, and metabolic processes.
Continuing the study of membrane structures, attention should be paid to membrane-associated signaling complexes. In addition to transport systems, numerous receptors (TGF-βR, EGFR, GPCR, Toll-like-receptors, etc.)  are located in the membrane, which initiate intracellular signaling cascades. They coordinate cell proliferation, apoptosis, autophagy, and the antioxidant response. The interaction of reactive plasma metabolites with these proteins can alter their conformation through redox modification of cysteine residues, which is one of the central mechanisms of the plasma-induced biological effect.
Cell viability is ensured by the coordinated work of specialized organelles. Among these, three structures are of paramount importance for understanding the mechanisms of plasma influence: lysosomes, mitochondria, and the nucleus. Each performs key functions directly related to the cell’s energetic, signaling, and regenerative homeostasis.
One such key structure is the Lysosome—the center of cellular catabolism and autophagy. Lysosomes are membrane-bound organelles 0.2–0.5 µm in diameter, containing over 60 hydrolases (proteases, lipases, nucleases), optimally active at an acidic pH 4.5–5.0, which is maintained by the V-ATPase proton pump. Their function is the breakdown and reuse of macromolecules, defective proteins, and organelles. In the context of cellular aging and oxidative stress, lysosomes play a key role in the quality control system. They are the endpoint of the autophagy pathway, where the degradation of the autophagosome’s contents occurs. The accumulation of “lysosomal debris” (lipofuscin, peroxidized lipids, iron) is one of the characteristic signs of cellular senescence. Consequently, the normal function of lysosomes is critically important for preventing age-related dysfunctions.
Equally important in this process are the Mitochondria—the energetic center and stress sensor. Mitochondria are double-membrane organelles that provide most of the cellular ATP through oxidative phosphorylation OXPHOS. The inner membrane forms cristae, where the complexes I–V of the respiratory chain are located. They transfer electrons from NADH and FADH₂ к O₂, forming an electrochemical proton gradient (Δψm), which drives ATP-synthase.   However, mitochondria are not only energy stations but also centers for redox signaling and apoptosis. They are sensitive to changes in membrane composition, Ca²⁺ concentration, and ROS. An excess of reactive oxygen species can lead to the opening of the mitochondrial permeability transition pore (mPTP), loss of Δψm, and release of cytochrome c, which triggers the caspase cascade and apoptosis. At the same time, moderate RONS stress stimulates adaptation mechanisms: mitophagy, activation of antioxidant genes, and the restoration of energetic balance. Thus, mitochondria act as bioenergetic sensors, determining the cell’s fate—survival or death—depending on the level of oxidative load.

Concluding the overview, we move to the nucleus—the coordinator of the stress response and regeneration. The nucleus is the central regulator of transcriptional processes. It integrates signals received from the cytoplasm into the genetic program of the stress response. One of the key mechanisms is the Nrf2/KEAP1/ARE pathway, which is activated by moderate oxidative irritation, including that caused by RONS generated by plasma. Under normal conditions, the transcription factor Nrf2 is bound to the cytosolic inhibitor KEAP1. When reactive species oxidize the cysteine residues of KEAP1, Nrf2 is released and translocates to the nucleus, where it binds to the antioxidant response elements (ARE), activating the expression of genes encoding antioxidant defense enzymes (HO-1, NQO1, GCLM) and DNA repair. The result is the strengthening of internal defense, stimulation of restorative protein synthesis, and cell proliferation, which creates the molecular basis for tissue regeneration after controlled plasma exposure. Thus, the nucleus ensures the genetic integration of the plasma-induced signal, transforming temporary oxidative stress into a program of cytoprotection and restoration.
Finally, we should consider the logical outcome of this dynamic—the Accumulation of defective organelles, which underlies systemic aging. With age, organelles that have lost their functionality gradually accumulate in cells and tissues—damaged mitochondria, lysosomes with low enzymatic activity, fragmented endoplasmic reticulum (ER). Such structures not only cease to perform their functions but also become a source of constant oxidative stress.   Deficient mitochondria produce an excess of superoxide instead of efficient ATP synthesis; old lysosomes lose the ability to break down damaged proteins, and their contents can leak into the cytosol, activating inflammation. Disruption of inter-organelle interaction—between mitochondria, lysosomes, the nucleus, and the ER—leads to cellular metabolism disorder, failure of intercellular communication, and loss of tissue integrity. The body, attempting to compensate for this dysfunction, engages adaptation or compensatory mechanisms: activation of survival signaling pathways, enhancement of glycolysis, organelle hyperplasia. However, these mechanisms only temporarily maintain balance while simultaneously exacerbating energetic deficit and a chronic oxidative background, which ultimately forms the molecular basis of aging.
  Mitochondrial Dysfunction and Tissue Aging. Let’s consider how changes in energy metabolism occur with age. In a healthy cell, energy is produced through the tricarboxylic acid cycle (Krebs cycle), where organic compounds are oxidized to form reduced coenzymes (NADH, FADH2). They supply electrons to the mitochondrial electron transport chain (ETC), where the electron flux generates the proton gradient necessary for ATP synthesis. But with age, the efficiency of this process decreases. Complexes I and III become the main sources of excess reactive oxygen species (ROS), which damage mitochondrial DNA, proteins, and lipids. This creates a vicious cycle: damage – decreased energetic efficiency – increased ROS production – even more damage. As a result, the cell gradually switches to a less efficient pathway—glycolysis, even in the presence of oxygen (Warburg effect), which reduces the energetic autonomy of tissues.
The decrease in energetic efficiency immediately leads to the disruption of redox homeostasis and metabolic balance. The accumulation of ROS, caused by mitochondrial dysfunction, changes the cell’s redox state, causing the oxidation of proteins, enzymes, and DNA. Under these conditions, stress signaling pathways are activated—NF-κB, p38 MAPK, JNK—which stimulate inflammatory reactions and apoptosis. Metabolic disruption leads to the failure of intercellular communication: cells cease to respond adequately to hormones, cytokines, and growth factors, which contributes to tissue degradation. Gradually, cells with reduced energetic potential accumulate in tissues, being in a state of senescence—metabolically active but non-functional. They release SASP-factors (senescence-associated secretory phenotype)—inflammatory cytokines, metalloproteinases, and oxidized lipids, which exacerbate inflammation and the aging of surrounding cells.
It is not surprising that defective mitochondria become triggers of systemic aging. Studies show that the accumulation of defective mitochondria is a key mechanism of biological aging. Such mitochondria consume substrates but do not form sufficient ATP, instead releasing superoxide and peroxides, disrupting cellular homeostasis. Their excessive accumulation activates secondary oxidative stress, inflammation, calcium imbalance, and ultimately, tissue degeneration. The loss of mitochondrial quality control is a consequence of the decrease in the activity of autophagic mechanisms, particularly mitophagy—a process in which damaged organelles are recognized by the proteins PINK 1 and Parkin, encapsulated in autophagosomes, and destroyed in lysosomes. Without this clearance, the cell loses the ability to renew its energetic pool, which gradually leads to metabolic exhaustion and tissue aging.
All these processes have systemic consequences of mitochondrial dysfunction. At the organism level, the consequence is the disruption of metabolism and inter-tissue regulation. Muscles lose strength, skin loses elasticity, and the immune system loses reactivity. The liver and heart experience an energy deficit, while the brain suffers from oxidative stress and inflammation. Thus, mitochondrial dysfunction becomes the universal denominator of aging, regardless of the organ or system.
The Final Conclusion is self-evident. Aging can be viewed as the accumulation of errors in the cell’s quality control system. When the mechanisms of autophagy, mitophagy, and apoptosis function inadequately, the body accumulates “broken” cells and organelles, creating a chronic oxidative background and metabolic chaos. Therefore, maintaining health and slowing aging requires periodic clearing of the cellular environment: either by restoring the functions of damaged organelles (through the activation of mitophagy, antioxidant signaling pathways Nrf2, optimization of the redox state), or by eliminating irreparably defective cells through controlled apoptosis. It is the balance between restoration and self-destruction that determines the body’s ability to maintain youth, structural integrity, and functional energy.
  Interaction of Plasma Metabolites (RONS) with Cellular Structures and their Role in Regeneration. First, let’s define the source of active agents during gas ionization. When plasma forms as the 4-th state of matter, partial ionization of molecules occurs in the air or a mixture of inert gases. This results in the formation of reactive oxygen and nitrogen species (RONS), such as hydrogen peroxide, nitrogen dioxide, peroxynitrite, and others. These particles have an extremely short lifetime but sufficient reactivity to engage in biochemical interaction with cell membranes, proteins, and lipids. It is important to note that besides RONS, an electric field and weak ultraviolet (UV) radiation are generated during the gas ionization process, which enhance the biological effect of plasma metabolites, particularly by increasing membrane permeability—a phenomenon known as plasmaporation.
The first stage of effect is the interaction of RONS with the cell membrane. The first barrier for active species is the plasma membrane bilipid layer. RONS are capable of oxidizing unsaturated fatty acids that are part of phospholipids, forming peroxidative chain reactions. This leads to a local disruption of membrane structure, the formation of micropores, and a temporary increase in its permeability for ions and signaling molecules. For example, H₂O₂ easily diffuses across the membrane via aquaporins, acting as a secondary messenger. NO•  modulates the function of ion channels and affects vascular tone and cellular respiration. Short-lived radicals (•OH, O₂•⁻) act primarily locally, initiating damage signals that activate protective pathways (Nrf2, MAPK, PI3K/Akt). The point is that in high doses, this process can cause apoptosis, but in controlled concentrations,RONS act as an “update signal,” initiating the clearance of defective components from the cell.
Next, let’s consider the influence of gas ionization technology on mitochondria and the initiation of controlled stress. RONS generated by plasma are capable of penetrating the cytoplasm and affecting mitochondrial dynamics. Moderate ROS increase in mitochondria activates the sensor protein PINK1, which accumulates on the outer membrane of damaged mitochondria. This, in turn, leads to the recruitment of Parkin—a ubiquitin ligase—which marks dysfunctional mitochondria for mitophagy. Thus, a controlled dose of plasma stress does not destroy the cell but “compels” it to clear itself of energetically deficient organelles. Mitochondrial pool remodeling occurs—damaged structures are eliminated, and healthy ones proliferate. This leads to the improvement of respiratory chain efficiency, reduction of basal ROS level, and restoration of the cell’s energetic balance.
This process is inextricably linked to the activation of autophagy and the involvement of lysosomes. After marking the damaged organelles, an autophagosome is formed, which fuses with the lysosome—an organelle rich in degradative enzymes. The metabolite-induced oxidative signal activates the key regulators of autophagy—AMPK and Beclin-1, which initiate the formation of the autophagic membrane. The lysosome, in turn, is activated due to the increased expression of proton pumps (V-ATPase), which lowers its pH and makes the enzymes maximally active. Ultimately, RONS serve as a trigger for controlled autophagy, during which the cell eliminates not only defective mitochondria but also other damaged structures, ensuring internal “cleanup” and cytoplasm rejuvenation.
The activation of clearance is not the only effect; simultaneously, we see what happens to the nucleus under the action of gas ionization products on the cell, namely—the activation of regeneration genes. When the RONS concentration reaches a certain hormetic threshold, oxidation of cysteine residues of the inhibitor KEAP occurs in the cytoplasm, which releases the transcription factor Nrf2. Nrf2 translocates to the nucleus and binds to antioxidant response elements (ARE), activating the expression of genes encoding antioxidant defense enzymes  and DNA repair. The result is the strengthening of internal defense, stimulation of restorative protein synthesis, and cell proliferation, which creates the molecular basis for tissue regeneration after controlled plasma exposure.
In addition to the chemical signal, the plasma electromagnetic field plays a role. Besides chemical metabolites, plasma generates a low-amplitude electromagnetic field, which affects the cell membrane potential. Due to this, ion channels are activated (especially calcium channels), leading to a short-term increase in intracellular Ca²⁺—a powerful signal for exocytosis, migration, differentiation, and cytoskeletal remodeling. This effect synergizes with RONS-dependent signaling cascades and can contribute to the activation of tissue proliferation and restoration programs.
As a final conclusion, the following can be stated. Thus, gas ionization products—plasma metabolites—act not only as oxidizers but as signaling molecules of regeneration. In a controlled dose, they: increase membrane permeability and trigger protective signals, stimulate mitophagy and autophagy, activate restorative transcription factors (Nrf2), and harmonize ion exchange through the influence of the electromagnetic field. It is precisely these mechanisms that create conditions for self-cleansing, restoration, and cell rejuvenation, making cold atmospheric plasma a promising tool in the fight against aging at the cellular level.
  Apoptosis, Autophagy, and Homeostasis: Plasma as a Regulator of the Cell Life Cycle. Let’s start with the understanding of cellular homeostasis as dynamic equilibrium. Every cell is in a state of constant balance between synthesis and degradation, damage and restoration, life and death. This dynamic equilibrium is determined by the coordination of three main processes: autophagy—internal clearing of defective components; apoptosis—programmed cell death without inflammation; and regeneration—replacement of cells that have completed their life cycle. Disruption of this triad, particularly the suppression of autophagy or defective apoptosis, leads to the accumulation of non-functional cells and organelles, which is the central pathogenetic mechanism of aging.
  The basis of this equilibrium is Autophagy—a mechanism for restoring homeostasis. Autophagy is a controlled process by which the cell recycles damaged or old proteins and organelles, breaking them down in lysosomes. It is activated during energetic deficit, oxidative stress, or mechanical damage. Under the action of RONS created by cold plasma, there is moderate activation of AMPK (the cell’s energy sensor) and suppression of mTOR, which triggers the autophagosome formation cascade. This process is not destructive—on the contrary, it ensures the selective removal of defective structures and cytoplasm renewal, thereby preventing apoptosis. After the completion of clearance, the cell restores energetic stability and transitions to a state of functional renewal, which is the basis of its long-term survival.
When restoration is impossible, Apoptosis—the natural mechanism of cellular “selection”—comes into effect. When cell damage becomes irreversible, the apoptosis program is activated—a safe self-destructive reaction. Apoptosis is controlled by mitochondria: the release of cytochrome c leads to the activation of caspases-9, -3, -7, which cleave the cell’s protein scaffold, without inducing inflammation. The apoptosis process can be initiated by the intrinsic, mitochondrially-mediated pathway of pore formation in the mitochondrial outer membrane. These pores allow cytochrome c to leave the intermembrane space and enter the cytosol, where it activates the family of proteolytic enzymes (caspases), causing morphological and biochemical changes characteristic of apoptosis. It is important to emphasize that cold atmospheric plasma in moderate doses does not cause mass apoptosis but can selectively initiate the death of cells that have lost control over division or have critical DNA damage. This is particularly important in the context of oncoprevention and the restoration of tissue homeostasis, where plasma helps to “clear” cells threatening the system. Thus, plasma metabolites act as a signaling filter, promoting the survival of healthy cells and eliminating defective ones.
It is obvious that both processes require clear coordination between autophagy and apoptosis. Both processes—autophagy and apoptosis—are closely interconnected. RONS can act as regulatory molecules that determine the direction of the reaction: at low concentrations, they stimulate repair and clearance (Nrf2, AMPK, PINK1, Parkin), and at high concentrations—they activate the death program (JNK, p53, caspases). That is, the action of plasma depends on the dose and duration of exposure: a short impulse causes “mild stress” and stimulates regeneration, while excessive exposure causes the death of out-of-control cells.
All this brings us to the homeostatic function of gas ionization technology. Cold atmospheric plasma within controlled parameters acts as a physiological regulator, not a destructive agent. It creates temporary, dosed instability that mobilizes cellular self-regulation mechanisms: RONS act as triggers for adaptive reactions and clearance; the plasma electric field is a stimulator of ion exchange and intracellular signaling; and short impulses act as factors of hormetic training, increasing cell resistance to future stresses. As a result, the cell not only restores its structure but also updates its survival program, which increases the duration of its functional life.
As a concluding statement, the following can be said. Cell life is a continuous cycle of birth, function, clearance, and completion. With age, the effectiveness of filtering defective structures decreases in this system, and it is here that controlled plasma intervention can restore equilibrium. Cold atmospheric plasma, thanks to the combination of RONS and the electromagnetic field: restores cellular quality control, initiates autophagy and mitophagy, promotes selective apoptosis of “broken” cells, and reactivates regeneration signaling pathways. Thus, gas ionization technology does not just affect individual cells—it maintains homeostasis at the tissue scale, helping the body preserve youth, adaptability, and structural integrity.
  Plasma Therapy as an Anti-Aging Intervention Strategy. First, let’s consider the biological logic of plasma intervention. Aging is not only the accumulation of damage but also the loss of efficiency in self-restoration mechanisms. Plasma therapy acts precisely on these mechanisms, serving as a mild stimulator of cellular “repair”. Its effect is not limited to an antibacterial effect or surface coagulation: it penetrates deep into cellular processes, modulating redox signaling, mitophagy, autophagy, and gene-transcriptional responses. The controlled introduction of RONS creates a hormetic stimulus—a short-term oxidative stress that activates adaptive systems without a destructive effect. Thus, the cell receives a “training signal,” which increases its resistance to subsequent stresses and restores internal equilibrium.
This leads us to the molecular pathways involved in the anti-aging effect of GIT (Gas Ionization Technology). The biological effect of plasma is mediated through several key signaling pathways. Nrf2/KEAP1/ARE activation occurs, leading to an increase in the expression of antioxidant enzymes (HO-1, NQO1, GPx, SOD) and strengthened cytoprotection. Simultaneously, AMPK stimulation and mTOR inhibition are observed, which initiates autophagy and clears the cell of defective organelles. Furthermore, PINK1, Parkin-dependent mitophagy is activated for the selective removal of damaged mitochondria. Equally important is the moderate activation of p53 and FOXO3a, which restores the balance between repair and apoptosis, and the enhancement of collagen and growth factor synthesis (TGF-beta, VEGF)—a reaction to mild membrane irritation and a local Ca²⁺ signal. Thanks to these mechanisms, cold plasma, specifically PlasmaHealth Gas Ionization Technology, acts systemically, stimulating regeneration, increasing cellular energy, and renewing the tissue matrix.
At the tissue level, these processes manifest as clinical signs of the anti-aging effect. At the tissue level, especially in the dermis, plasma metabolites cause a number of positive changes. We observe improved microcirculation and oxygenation through NO-mediated vasodilation. There is an increase in fibroblast proliferation and stimulation of type I and III collagen synthesis. Chronic inflammation is significantly reduced through the lowering of NF-kappa B and cytokine levels (NF-κB and cytokines  IL-6, TNF-α.). These effects lead to the acceleration of micro-injury healing and renewal of the extracellular matrix, which, in turn, increases skin elasticity and turgor due to the remodeling of the collagen-elastin network. Furthermore, in combination with cosmetic or pharmacological protocols, plasma stimulation increases the sensitivity of cells to bioactive substances, promoting the deeper absorption of peptides, vitamins, and antioxidants.
  The most important aspect ensuring safety is controlled dosing. The biological effect of plasma exposure is strictly dose-dependent. Excessive exposure or high energy leads to cytotoxicity, whereas moderate stimulation causes “beneficial stress” (eustress), which trains the cell. Critical parameters include the gas mixture composition (He, Ar, O₂, N₂), power and frequency of impulses, distance to the tissue surface, and duration of exposure. Only short dosing ensures the hormetic “window of benefit”, where plasma functions as a regenerator, not a destructor. When working with PlasmaHealth technologies, the recommended exposure time is 10–15 minutes per 10 sq. cm. area.
Finally, the systemic effect via intercellular signaling should be emphasized. Studies show that after plasma exposure, cells release exosomes, enriched with antioxidant proteins, microRNAs, and growth factors. These nanoparticles act on neighboring cells, transmitting a signal of restoration—a phenomenon that can be viewed as a “regeneration cascade”. Consequently, even local plasma intervention can induce a systemic rejuvenation reaction through tissue communication networks.
  The Formula for the Action of Plasma Metabolites and the Potential for Longevity. First, let’s define the fundamental logic of plasma intervention. In biological systems, longevity is not merely the absence of destruction but the ability to maintain homeostasis in changing conditions. Every cell, tissue, and organ operates within the framework of a constant exchange of energy, signals, and substances. When this interaction is disrupted—defective organelles, protein fragments, and excess ROS accumulate—the system transitions into a state of chronic stress and accelerated aging. Cold Atmospheric Plasma (CAP) is a unique tool capable of controllably intervening in this cycle, acting not destructively but biomodulatingly: it creates a short, dosed stress that stimulates self-clearing, adaptation, and cell renewal.
This biomodulating effect is carried out at three key levels of plasma regulation. At the molecular level, RONS modify sulfur-containing protein residues (Cys, Met), which activates the Nrf2, AMPK, MAPK signaling cascades. Cell redox-reprogramming occurs: strengthening of antioxidant systems, DNA repair, synthesis of heat shock proteins. At the organelle level, the activation of autophagy and mitophagy leads to the clearing of energetic systems. Mitochondria are rejuvenated, restoring Δψm and OXPHOS efficiency; lysosomes increase V-ATPase and enzyme activity. The basal level of ROS and inflammation is reduced. Finally, at the tissue level, through the release of exosomes and regeneration cytokines (VEGF, TGF-beta, EGF), a restoration signal is formed. Intercellular communication, microcirculation, and oxygenation are improved. The regenerative response spreads cascadedly, even beyond the zone of exposure.
Therefore, plasma can be viewed as “soft evolutionary selection”. In this model, Cold Plasma in the form of Gas Ionization Technology acts as a distinctive selective biofilter: it supports viable cells capable of adaptation and eliminates those that have lost metabolic control. This process imitates natural evolutionary logic at the cellular level—the “survival of the functionally fittest”. Such selectivity ensures tissue renewal without compromising structural integrity, which is the foundation of long-term rejuvenation.
In addition to the chemical signal, the electromagnetic field plays an important role in the coordination of effects. Plasma creates a dynamic electromagnetic environment in which fluctuations in cellular membrane potentials stimulate: the opening of calcium channels, activation of PLC/IP₃/Ca²⁺ signaling pathways, and remodeling of the cytoskeleton and intercellular contacts. This effect synergizes with the action of RONS, creating multi-level bioelectrical communication that coordinates regeneration at the tissue level.
  The Action of Cold Plasma is Subject to the Phenomenon of Hormesis. The action of Cold Plasma in the form of Gas Ionization Technology is governed by the principle of hormesis—where a small dose of a stressor causes a compensatory enhancement of protective systems. The cell, reacting to a short redox impulse, activates: antioxidant enzymes, DNA repair pathways, and energetic balance systems (AMPK, PGC-1 alpha). Thus, cold plasma functions not as a stimulus for damage but as a training irritant that “teaches” cells to remain functionally young.
All this brings us to the Integrative Concept of Longevity from PlasmaHealth. Ultimately, a unified model of plasma longevity can be formulated: Controlled plasma exposure – short-term redox stress – activation of clearance systems – renewal of mitochondria and lysosomes – optimization of metabolism – restoration of cellular homeostasis – increase in tissue resilience – prolongation of youth. This cycle describes the natural pathway of self-regeneration, in which plasma does not “cure” in the classical sense but restores the cell’s capacity for self-organization.
  Final Conclusion. Gas Ionization Technology is a physiological tool for restoring cellular homeostasis. It acts as an intelligent stressor, activating natural mechanisms of clearance, mitophagy, antioxidant defense, and regeneration. However, it is worth noting that not every device implementing gas ionization technology possesses the optimal combination of electromagnetic characteristics and air ionization efficiency. The result is influenced by: the type and composition of the gas undergoing ionization (which determines the profile of ionization metabolites — RONS); the frequency, amplitude, and strength of electric impulses, which set the energetics of the process; and the stability of electromagnetic field generation. The specific bioactive RONS species formed and the biological effect achieved—from mild regeneration to cytotoxic exposure—depend on these parameters.

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