The Leading Cellular Regeneration Formula Available


Research and Summary Comments
ACR regen Extra Strength

PQQ (pyrroloquinoline quinone), Idebenone, Methylcobalamin, L-Carnitine, L-Glutamine, L-Alanine, L-Isoleucine, L-Leucine, L-Valine, Glycine, L-Aspartic Acid, L-Arginine, L-Ornithine, L-Histidine, L-Lysine, L-Methionine, L-Phenylalanine, L-Threonine, L-Cysteine, L-Glutamic Acid, L-Proline, L-Serine, L-Tryptophan, L-Ascorbic Acid

PQQ (Pyrroloquinoline quinone)

1. Pyrroloquinoline quinone enhances the resistance to oxidative stress and extends lifespan upon DAF-16 and SKN-1 activities in C. elegans.

Pyrroloquinoline quinone (PQQ) is linked to fundamental biological processes such as mitochondrial biogenesis and lipid metabolism. PQQ may also function as an essential micronutrient during animal development. Recent studies have shown the therapeutic potential of PQQ for several age-related diseases due to its antioxidant capacity. However, whether PQQ can promote longevity is unknown. Here, we investigate the effects of PQQ on oxidative stress resistance as well as lifespan modulation in Caenorhabditis elegans.

We find that PQQ enhances resistance to oxidative stress and extends the lifespan of C. elegans at optimal doses. The underlying molecular mechanism involves the increased activities of the primary lifespan extension transcriptional factors DAF-16/FOXO, the conserved oxidative stress-responsive transcription factor SKN-1/Nrf2, and upregulation of daf-16, skn-1 downstream targets including sod-3, hsp16.2, gst-1 and gst-10.

Our findings uncover a novel role of PQQ in longevity, supporting PQQ as a possible dietary supplement for overall health improvement.

• Beyond its known role in mitochondrial biogenesis, PQQ’s antioxidant capacity contribute to its potential benefit as it relates to aging.

2. Dietary pyrroloquinoline quinone (PQQ) alters indicators of inflammation and mitochondrial-related metabolism in human subjects.

Pyrroloquinoline quinone (PQQ) influences energy-related metabolism and neurologic functions in animals. The mechanism of action involves interactions with cell signaling pathways and mitochondrial function. However, little is known about the response to PQQ in humans. Using a crossover study design, 10 subjects (5 females, 5 males) ingested PQQ added to a fruit-flavored drink in two separate studies.

In study 1, PQQ was given in a single dose (0.2 mg PQQ/kg). In study 2, PQQ was administered as a daily dose (0.3 mg PQQ/kg)

Dietary PQQ exposure (Study 1) resulted in apparent changes in antioxidant potential based on malonaldehyde-related TBAR assessments. In Study 2, PQQ supplementation resulted in significant decreases in the levels of plasma C-reactive protein, IL-6 and urinary methylated amines such as trimethylamine N-oxide, and changes in urinary metabolites consistent with enhanced mitochondria-related functions. The data are among the first to link systemic effects of PQQ in animals to corresponding effects in humans.

• Highlighted here is PQQ’s three-pronged benefit package of increasing antioxidant capacity, serving as an anti-inflammatory agent and mitochondrial biogenesis.


3. Idebenone Prevents Oxidative Stress, Cell Death and Senescence of Retinal Pigment Epithelium Cells by Stabilizing BAX/Bcl-2 Ratio.

Age-related macular degeneration (AMD) is one of the leading causes of blindness. Degeneration of the retinal pigment epithelium (RPE) is pathognomonic for the disease, and oxidative stress plays an important role in the pathogenesis of this disease. This study investigates potential antiapoptotic and cytoprotective effects of idebenone on cultured RPE cells (ARPE-19) under conditions of oxidative stress.

Idebenone concentrations from 1 to 20 µM showed no toxic effects on ARPE-19 cells. When cells were treated with H2O2, pretreatment with 5, 7.5, 10, and 20 µM idebenone led to a significant increase in the viability of ARPE-19 cells. In addition, idebenone pretreatment significantly attenuated the induction of SA-β-Gal and intracellular ROS as well as the amount of histone-associated DNA fragments after treatment with H2O2.

• Idebenone shows promise in reducing cell death, proliferation and oxidative stress.

4. NQO1-dependent redox cycling of idebenone: effects on cellular redox potential and energy levels.

Using recombinant NAD(P)H:quinone oxidoreductase (NQO) enzymes, we observed that contrary to CoQ10 short-chain quinones such asidebenone are good substrates for both NQO1 and NQO2. Furthermore, the reduction of short-chain quinones by NQOs enabled an antimycin A-sensitive transfer of electrons from cytosolic NAD(P)H to the mitochondrial respiratory chain in both human hepatoma cells (HepG2) and freshly isolated mouse hepatocytes. Consistent with the substrate selectivity of NQOs, both idebenone and CoQ1, but not CoQ10, partially restored cellular ATP levels under conditions of impaired complex I function. The observed cytosolic-mitochondrial shuttling of idebenone and CoQ1 was also associated with reduced lactate production by cybrid cells from mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) patients.

• This study supports Idebenone as a treatment option for mitochondrial disorders through the restoration of cellular ATP levels when function is impaired.

5. Dramatic improvement in mitochondrial cardiomyopathy following treatment with idebenone.

Idebenone, a synthetic analogue of coenzyme Q10, has been shown to improve cardiac function in patients with Friedreich ataxia and a deficiency of respiratory chain complexes I-III. We describe a woman with severe combined right and left heart failure due to a mitochondrial cardiomyopathy. The patient underwent an endomyocardial biopsy as part of an evaluation for cardiac transplantation. It showed severely decreased respiratory complex activities dependent on CoQ, pointing to CoQ depletion.
Following idebenone treatment there was a dramatic improvement in her clinical status with resolution of the heart failure.

• This study confirms idebenone as a viable treatment option to be considered for patients with mitochondrial cardiomyopathy.

6. Idebenone protects against oxidized low density lipoprotein induced mitochondrial dysfunction in vascular endothelial cells via GSK3β/β-catenin signaling pathways.

The early stages of the atherosclerotic process are initiated by accumulation of oxidized low-density lipoprotein (oxLDL) and damage to the structure or function of the endothelium. Antioxidant supplementation may be a plausible strategy to prevent atherosclerotic disease by quenching excessive reactive oxidative species. In the present study, we demonstrated that idebenone at suitable concentrations significantly prevented oxLDL-induced endothelial dysfunction.

The underlying mechanisms of idebenone included inhibition of oxidative damage, suppression of the down-regulation of Bcl-2 and up-regulation of Bax and cleaved caspase-3 in human umbilical vein endothelial cells (HUVECs) exposed to oxLDL. Moreover, idebenone pretreatment inhibited oxLDL-mediated HUVECs damage by attenuating lipid peroxidation and promoting SOD activity. Finally, pro-incubation with idebenone inhibited mitochondrial dysfunction induced by oxLDL through the mitochondrial-dependent apoptotic pathway and GSK3β/β-catenin signaling pathways.

• Idebenone shows promise in the treatment or prevention of atherosclerosis through the inhibition of oxidative stress and improvement of mitochondrial function.


7. Effects of methyl-B12 on the in vitro immune functions of human T lymphocytes.

Studies were performed using an in vitro assay system to determine whether or not methyl-B12 could affect human T-cell function. Concentrations of methyl-B12 sufficient to enhance cellular proliferation were able to enhance the activity of helper T cells for immunoglobulin synthesis of B cells by pokeweed mitogen. Furthermore, the presence of methyl-B12 significantly potentiated the induction of suppressor cells in Con A-activated cultures.

Methylcobolamin B12 could regulate lymphocyte function via improved human T-Cell activities.

8. Methylcobalamin promotes proliferation and migration and inhibits apoptosis of C2C12 cells via the Erk1/2signaling pathway.

Methylcobalamin (MeCbl) is a vitamin B12 analog that has some positive effects on peripheral nervous disorders. Although some previous studies revealed the effects of MeCbl on neurons, its effect on the muscle, which is the final target of motoneuron axons, remains to be elucidated. This study aimed to determine the effect of MeCbl on the muscle.

We found that MeCbl promoted the proliferation and migration of C2C12 myoblasts in vitro and that these effects are mediated by the Erk1/2 signaling pathway without affecting the activity of the Akt signaling pathway. We also demonstrated that MeCbl inhibits C2C12 cell apoptosis during differentiation.

• Methylcobolamin B12 has beneficial effects on the muscle in vitro. Its administration may provide a novel therapeutic approach for muscle injury or degenerating muscle after denervation.


9. L-carnitine attenuates oxidant injury in HK-2 cells via ROS-mitochondria pathway.

Oxidative stress has been considered as the possible mechanism of renal ischemia/reperfusion injury. L-carnitine is an endogenous mitochondrial membrane compound and could effectively protect ischemia-reperfusion injury in the kidney. To elucidate the nephroprotective effects of L-carnitine, here we assessed the effect of L-carnitine on hydrogen peroxide (H (2) O (2))-mediated oxidative stress in the human proximal tubule epithelial cell line, HK-2 cells.

The results showed that pretreatment with L-carnitine 12h inhibited H (2) O (2)-induced cell viability loss, intracellular reactive oxygen species generation and lipid peroxidation in a concentration-dependent manner. Also, L-carnitine promoted endogenous antioxidant defense components including total antioxidative capacity, glutathione peroxidase, catalase and superoxide dismutase.

• Study results suggest that L -carnitine can provide protection for cells through the inhibition of oxidative damage, mitochondria dysfunction and ultimately inhibition of cell apoptosis.


10. Determination of the anti-inflammatory and cytoprotective effects of l-glutamine and l-alanine, or dipeptide supplementation in rats submitted to resistance exercise.

We evaluated the effects of chronic oral supplementation with l-glutamine and l-alanine in their free form or as the dipeptide l-alanyl-l-glutamine(DIP) on muscle damage, inflammation and cytoprotection, in rats submitted to progressive resistance exercise (RE).

GLN+ALA and DIP groups also exhibited increased level of HSP70 in EDL and PBMC, consistent with the reduction of NF-κB p65 activation and cytokines in EDL. Muscle protection was also indicated by attenuation in plasma levels of CK, LDH, TNF-α and IL-1β, as well as an increase in IL-6, IL-10 and MCP-1.

Our study demonstrates that chronic oral l-glutamine treatment (given with l-alanine or as dipeptide) following progressive RE induces cyto-protective effects mediated by HSP70-associated responses to muscle damage and inflammation.

• These observations produce potential long-term effects of L-alanine in regulating gene expression, secretory function and the integrity of insulin-secreting cells.

11. L-glutamine Improves Skeletal Muscle Cell Differentiation and Prevents Myotube Atrophy after Cytokine (TNF-α) Stress via Reduced p38 MAPK Signal Transduction.

Tumor Necrosis Factor- Alpha (TNF-α) is chronically elevated in conditions where skeletal muscle loss occurs. As L-glutamine can dampen the effects of inflamed environments, we investigated the role of L-glutamine in both differentiating C2C12 myoblasts and existing myotubes in the absence/presence of TNF-α (20 ± L-glutamine (20 mM).

L-glutamine resulted in upregulation of genes associated with growth and survival including; Myogenin, Igf-Ir, Myhc2 & 7, Tnfsfr1b, Adra1d and restored atrophic gene expression of Fox03 back to baseline in TNF-α conditions.

• Glutamine administration could represent an important therapeutic strategy for reducing muscle loss (prevents muscle fiber atrophy) in catabolic diseases and inflamed aging.


12. L-Alanine induces changes in metabolic and signal transduction gene expression in a clonal rat pancreatic beta-cell line and protects from pro-inflammatory cytokine-induced apoptosis.

In the present study, the effects of prolonged exposure (24 h) to the amino acid L-alanine on insulin secretory function, gene expression and pro-inflammatory cytokine-induced apoptosis were studied using clonal BRIN-BD11 cells.

Subsequent functional experiments confirmed that L-alanine provided protection of BRIN-BD11 cells from pro-inflammatory cytokine-induced apoptosis. Protection from apoptosis was mimicked by NMA or DPI suggesting L-alanine enhances intracellular antioxidant generation.

• These observations produce potential long-term effects of L-alanine in regulating gene expression, secretory function and the integrity of insulin-secreting cells.

13. Determination of the anti-inflammatory and cytoprotective effects of l-glutamine and l-alanine, or dipeptide, supplementation in rats submitted to resistance exercise.

We evaluated the effects of chronic oral supplementation with l-glutamine and l-alanine in their free form or as the dipeptide l-alanyl-l-glutamine (DIP) on muscle damage, inflammation and cytoprotection, in rats submitted to progressive resistance exercise (RE). Wistar rats (n 8/group) were submitted to 8-week RE, which consisted of climbing a ladder with progressive loads. In the final 21 d before euthanasia, supplements were delivered in a 4 % solution in drinking water. Glutamine, creatine kinase (CK), lactate dehydrogenase (LDH), TNF-α, specific IL (IL-1β, IL-6 and IL-10) and monocyte chemoattractant protein-1 (MCP-1) levels were evaluated in plasma.

L-glutamine supplements (l-alanine plus l-glutamine (GLN+ALA) and DIP groups) restored glutamine levels in plasma (by 40 and 58 %, respectively) and muscle (by 93 and 105 %, respectively). GLN+ALA and DIP groups also exhibited increased level of HSP70 in EDL and PBMC, consistent with the reduction of NF-κB p65 activation and cytokines in EDL. Muscle protection was also indicated by attenuation in plasma levels of CK, LDH, TNF-α and IL-1β, as well as an increase in IL-6, IL-10 and MCP-1.

• L-glutamine when combined with L-alanine (also in ACR Regen) was shown to have cyto-protective effects, as well reduce muscle damage and inflammation during resistance exercise

Branched Chain Aminos (L-Leucine, L-Isoleucine, L-Valine)

14. In a single-blind, matched group design: branched-chain amino acid supplementation and resistance training maintains lean body mass during a caloric restricted diet.

Athletes and active adults many times have the goal of improving/maintaining fitness while losing weight and this is best achieved by caloric restriction in combination with exercise. However, this poses a risk for lean tissue loss, which can limit performance. Thus, the purpose of this study was to determine the effectiveness of a branched-chain amino acid (BCAA) supplement, in conjunction with heavy resistance training and a carbohydrate caloric-restricted “cut diet” on body composition and muscle fitness.

Seventeen resistance-trained males (21-28 years of age) were randomized to a BCAA group (n = 9) or a carbohydrate (CHO) group (n = 8) who both received their respective supplement during the 8 weeks of a prescribed body building style resistance training protocol. Subjects were prescribed a hypocaloric diet (based upon pre-intervention analysis) that was to be followed during the study.

• Results show that BCAA supplementation in trained individuals performing resistance training while on a hypocaloric diet can maintain lean mass and preserve skeletal muscle performance while losing fat mass.

15. Branched-chain amino acid supplementation and the immune response of long-distance athletes.

Intense long-duration exercise has been associated with immunosuppression, which affects natural killer cells, lymphokine-activated killer cells, and lymphocytes. The mechanisms involved, however, are not fully determined and seem to be multifactorial, including endocrine changes and alteration of plasma glutamine concentration. Therefore, we evaluated the effect of branched-chain amino acid supplementation on the immune response of triathletes and long-distance runners.

• Branched-chain amino acid supplementation recovers the ability of peripheral blood mononuclear cells proliferate in response to mitogens after a long distance intense exercise, as well as plasma glutamine concentration.
• BCAA’s also modify the pattern of cytokine production leading to a diversion of the immune response toward a Th1 type of immune response.


16. Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation.

Aging is associated with oxidative stress, but underlying mechanisms remain poorly understood.

We tested whether glutathione deficiency occurs because of diminished synthesis and contributes to oxidative stress in aging and whether stimulating glutathione synthesis with its precursors cysteine and glycine could alleviate oxidative stress.

Eight elderly and 8 younger subjects received stable-isotope infusions of [2H (2)] glycine, after which red blood cell (RBC) glutathione synthesis and concentrations, plasma oxidative stress, and markers of oxidant damage (eg, F(2)-isoprostanes) were measured. Elderly subjects were restudied after 2 wk of glutathione precursor supplementation.

• Dietary supplementation with the glutathione precursors cysteine and glycine fully restores glutathione synthesis and concentrations and lowers levels of oxidative stress and oxidant damages, suggesting a practical and effective approach to decreasing oxidative stress in aging.

L-Aspartic Acid

17. Aspartic Acid 397 in Subunit B of the Na+-pumping NADH: Quinone Oxidoreductase from Vibrio choleraeForms Part of a Sodium-binding Site, Is Involved in Cation Selectivity, and Affects Cation-binding Site Cooperativity

The Na+-pumping NADH: quinone complex is found in Vibrio cholerae and other marine and pathogenic bacteria. NADH: ubiquinone oxidoreductase oxidizes NADH and reduces ubiquinone, using the free energy released by this reaction to pump sodium ions across the cell membrane.

In a previous report, a conserved aspartic acid residue in the NqrB subunit at position 397, located in the cytosolic face of this protein, was proposed to be involved in the capture of sodium. Here, we studied the role of this residue through the characterization of mutant enzymes in which this aspartic acid was substituted by other residues that change charge and size, such as arginine, serine, lysine, glutamic acid, and cysteine.

Our results indicate that NqrB-Asp-397 forms part of one of the at least two sodium-binding sites and that both size and charge at this position are critical for the function of the enzyme. Moreover, we demonstrate that this residue is involved in cation selectivity, has a critical role in the communication between sodium-binding sites, by promoting cooperativity, and controls the electron transfer step involved in sodium uptake (2Fe-2S → FMNC).

• This study suggests that Aspartic acid is critical to the function of the coenzyme NADH, which is used to produce adenosine triphosphate (ATP). This coenzyme is needed to transport chemical energy throughout the cell, facilitating metabolism.


18. Evidence for an involvement of the ammonia-decreasing action of L-arginine in suppressing picrotoxin-induced convulsions in rats and its additive action with diazepam.

The effects of pre- (30 min before challenge) and post-treatment (5 min after challenge) of L-arginine (840 mg kg (-1)) were tested on picrotoxin-induced increase in ammonia concentrations in brain regions (cerebral cortex, brain stem and cerebellum) and the accompanying convulsive responses in adult male rats. The effect of pre- and post-treatment of L-arginine was tested on the action of diazepam against picrotoxin-induced convulsions. Picrotoxin-induced increase in ammonia concentrations in the brain regions was reverted partially by L-arginine pre-treatment.

However, L-arginine pre-treatment failed to inhibit convulsions independently and concurrently with diazepam. On the other hand, L-arginine post-treatment reverted ammonia to control level in all brain regions. A partial but significant inhibition of convulsions was found in these animals. The effect produced concurrently by L-arginine and diazepam post-treatment was much greater than that produced by these agents independently. These results suggest that brain ammonia has a partial but significant participation in the convulsant action of picrotoxin. L-arginine has produced a partial protection of picrotoxin-induced convulsions by reverting brain ammonia to control level.

• This study validates the ammonia decreasing action of L-Arginine, which offsets the necrosis of tissues and cellular destruction from elevated ammonia levels.


19. L-ornithine supplementation attenuates physical fatigue in healthy volunteers by modulating lipid and amino acid metabolism.

We examined the effects of L-ornithine administration on physical fatigue. In a double-blind, placebo-controlled, 2-way crossover study, 17 healthy volunteers were randomized to L-ornithine (2000 mg/d for 7 days and 6000 mg/d for 1 day as L-ornithine hydrochloride) or placebo for 8 days. The fatigue-inducing physical task consisted of workload trials on a cycle ergometer at fixed workloads for 2 hours on 2 occasions. We found that oral L-ornithine administration promoted lipid metabolism and activated the urea cycle from serum triacylglycerol, ketone bodies, free fatty acids, and blood ammonia level changing. L-ornithine significantly attenuated the subjective feeling of fatigue (measured by visual analog scale at post recovery) compared with post load (P < .01). Takeaway:

• These results suggest that L-ornithine has an anti-fatigue effect by increasing the efficiency of energy consumption and promoting the excretion of ammonia.


20. Carnosine, histidine, and wound healing.

The relationships among carnosine, histidine, and wound healing were examined in rats fed either 100% or 50% of the reported histidine required for growth. Animals fed the adequate amount of histidine grew more rapidly and more efficiently than did animals on the low-histidine diet. When the rats reached the experimental weight range of 165 to 180 gm, they were anesthetized and wounded with back skin incision; a polyvinylchloride sponge was implanted under the skin before closure of the wound. Seven days after wounding, the histidine-sufficient animals had greater regenerative skin-breaking strength, collagen deposition, and tissue concentrations of free histidine and carnosine.

• From this study, there is a connection between Histidine and wound healing.


21. Effects of L-lysine and L-arginine on in vitro replication of feline herpesvirus type-1.

The purpose of this study was to determine the effects of various concentrations of L-lysine and L-arginine on in vitro replication of feline herpesvirus type-1 (FHV-1). Uninfected CRFK cells or CRFK cells infected with FHV-1 were cultured in Dulbecco’s modified Eagle’s medium or in 1 of 7 test media containing various concentrations of lysine and arginine. Viral titer and CRFK growth rate were assessed in each medium.

Media depleted of arginine almost completely inhibited viral replication, whereas 2.5 or 5.0 microg of arginine/ml of media was associated with a significant increase in FHV-1 replication. In media with 2.5 microg of arginine/ml, supplementation with 200 or 300 microg of lysine/ml reduced viral replication by 34.2 and 53.9%, respectively. This effect was not seen in media containing 5.0 microg of arginine/ml. Growth rates of CRFK cells also were suppressed in media containing these concentrations of amino acids, but they were not significantly different from each other.

• This study shows that administration of L-lysine and L-arginine was associated with a significant increase in the replication of healthy, non-infected cells and corresponding decrease in the replication of viral cells.


22. Oxidation of Methionine in Proteins: Roles in Antioxidant Defense and Cellular Regulation

The roles of methionine residues in proteins have not been well defined, but a review of available studies leads to the conclusion that methionine, like cysteine, functions as an antioxidant and as a key component of a system for regulation of cellular metabolism. Methionine is readily oxidized to methionine sulfoxide by many reactive species. The oxidation of surface exposed methionines thus serves to protect other functionally essential residues from oxidative damage. Methionine sulfoxide reductases have the potential to reduce the residue back to methionine, increasing the scavenging efficiency of the system.

• L-methionine benefits include antioxidant defense and regulation of cellular function.


23. Vitiligo therapy with oral and topical phenylalanine with UVA exposure

The administration of phenylalanine (Phe) combined with UVA exposure was found to be effective in treating vitiligo. Twenty-one patients with vitiligo were divided in two groups: eleven patients were treated with oral L-Phe in a dose of 100 mg/kg body weight and with UVA exposure and ten patients were treated with oral L-Phe in a dose of 100 mg/kg body weight and with UVA exposure. In addition, in the second group, a cream containing 10% L-Phe was applied to the vitiliginous areas. The best results occurred in the second group. No side effects were found in either group.

• Vitiligo is thought to be an autoimmune disease. It is a disorder in which white patches of skin appear on different parts of the body. This happens because the cells that make pigment (color) in the skin are destroyed.


24. L-threonine regulates G1/S phase transition of mouse embryonic stem cells via PI3K/Akt, MAPKs, and mTORC pathways.

Although amino acids can function as signaling molecules in the regulation of many cellular processes, mechanisms surrounding L-threonine involvement in embryonic stem cell (ESC) functions have not been explored. Thus, we investigated the effect of L-threonine on regulation of mouse (m)ESC self-renewal and related signaling pathways. In L-threonine-depleted mESC culture media mRNA of self-renewal marker genes, [(3) H] thymidine incorporation, expression of c-Myc, Oct4, and cyclins protein was attenuated. In addition, resupplying L-threonine (500 μM) after depletion restores/maintains the mESC proliferation.

In conclusion, L-threonine stimulated ESC G (1)/S transition through lipid raft/caveolae-dependent PI3K/Akt, MAPKs, mTOR, p70S6K, and 4E-BP1 signaling pathways.

• L-Threonine may have application as a signaling molecule in cellular processes based on this study.


25. Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation.

We tested whether glutathione deficiency occurs because of diminished synthesis and contributes to oxidative stress in aging and whether stimulating glutathione synthesis with its precursors cysteine and glycine could alleviate oxidative stress.

L-Glutamic Acid

26. Glutathione biosynthesis in human erythrocytes

The two enzymes required for de novo glutathione synthesis, glutamyl cysteine synthetase and glutathione synthetase, have been demonstrated in hemolysates of human erythrocytes. Glutamyl cysteine synthetase requires glutamic acid, cysteine, adenosine triphosphate (ATP), and magnesium ions to form γ-glutamyl cysteine. The activity of this enzyme in hemolysates from 25 normal subjects was 0.43±0.04 μmole glutamyl cysteine formed per g hemoglobin per min. Glutathione synthetase requires γ-glutamyl cysteine, glycine, ATP, and magnesium ions to form glutathione.

• This study shows that glutamic acid is required to produce the enzymes needed for glutathione synthesis, supporting its role in immune function.


27. Impaired Insulin/IGF1 Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS Signal

Impaired insulin and IGF-1 signaling (iIIS) in C. elegans daf-2 mutants extends life span more than 2-fold. Constitutively, iIIS increases mitochondrial activity and reduces reactive oxygen species (ROS) levels.

IIIS up regulates mitochondrial L-proline catabolism, and impairment of the latter impairs the life span-extending capacity of iIIS while L-proline supplementation extends C. elegans life span. Taken together, iIIS promotes L-proline metabolism to generate a ROS signal for the adaptive induction of endogenous stress defense to extend life span.

• Proline is critically important to the IGF-1 signaling (iIIS) pathway, which plays a major role in human longevity.


28. Serine-deficiency syndromes

Serine-deficiency disorders comprise a new group of neurometabolic diseases and are caused by defects in the biosynthesis of the amino acid L-serine. In contrast to most neurometabolic disorders, serine-deficiency disorders are potentially treatable.

• L-Serine biosynthesis plays an important role in multiple cellular reactions, particularly in the brain, as L-serine is a precursor of important metabolites such as nucleotides, phospholipids and the neurotransmitters glycine and D-serine.


29. Work-Related Exhaustion and Telomere Length: A Population-Based Study.

Psychological stress is suggested to accelerate the rate of biological aging. We investigated whether work-related exhaustion, an indicator of prolonged work stress, is associated with accelerated biological aging, as indicated by shorter leukocyte telomeres, that is, the DNA-protein complexes that cap chromosomal ends in cells.

We used data from a representative sample of the Finnish working-age population, the Health 2000 Study. Our sample consisted of 2911 men and women aged 30–64. Work-related exhaustion was assessed using the Maslach Burnout Inventory – General Survey. We determined relative leukocyte telomere length using a quantitative real-time polymerase chain reaction (PCR) -based method.

After adjustment for age and sex, individuals with severe exhaustion had leukocyte telomeres on average 0.043 relative units shorter (standard error of the mean 0.016) than those with no exhaustion (p = 0.009). The association between exhaustion and relative telomere length remained significant after additional adjustment for marital and socioeconomic status, smoking, body mass index, and morbidities (adjusted difference 0.044 relative units, standard error of the mean 0.017, p = 0.008).

• This study suggests that stress/anxiety may negatively impact cellular aging related to changes to telomere length over time.

30. 5-Hydroxytryptophan: a clinically-effective serotonin precursor.

As noted in this study, an important byproduct of tryptophan is 5HTP (5-hyrdoxytryptophan), which works in the brain and central nervous system to boost feelings of well-being, connection and safety. It does this by increasing production of one of the body’s main feel-good hormones, serotonin. The resultant calming effect of tryptophan may reduce work related stress and anxiety, which was shown in the above noted study to negatively impact cellular aging.

L-Ascorbic Acid

31. Antioxidant Role of Ascorbic Acid and its Protective Effects on Chronic Diseases

Ascorbic acid (AA), commonly known as vitamin C, plays an important role in the human body. It is necessary for the synthesis of collagen, a protein that has many connective functions in the body. Among the substances and structures that contain collagen are bone, cartilage and the surrounding material, as well as carrier substances and materials of union muscle, skin and other tissues.

The body also requires (AA) for the synthesis of hormones, neurotransmitters and in the metabolism of certain amino acids and vitamins. Participate in the liver for detoxification of toxic substances and blood level for immunity. As an antioxidant reacts with histamine and peroxide for reducing inflammatory symptoms.

In the case of Ascorbic Acid, its antioxidant role is useful since it contributes to the maintenance of the vascular system and the reduction of atherogenesis through regulation in collagen synthesis, production of prostacyclin and nitric oxide. In addition to this antioxidant role, the AA has actions at the molecular level because it acts as a cofactor of enzymes such as dopamine hydroxylase (EC, influencing neurotransmitter concentration, improves lysosomal protein degradation and mediates consumer monosodium glutamate.
Antioxidants play important roles in cellular function and have been implicated in processes associated with aging, including vascular, inflammatory damage and cancer.

• There is evidence to suggest that Ascorbic Acid does play a role in cellular function, in addition to the host of other benefits that come with its supplementation.

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Standard Dose

Take 6 sprays by mouth, twice daily.

Higher Dose

Take 12 sprays by mouth, twice daily.

Optimal Use

• Spray, swish and swallow. You may take other Results RNA formulas immediately.
• Do not eat or drink for 2 minutes following.
• Take as recommended by your physician.



Serving size: 12 Sprays
Servings Per Container (2oz/60mL): Approx. 60
Servings Per Container (4oz/120mL): Approx. 120

Proprietary Blend 250 mg*



PQQ (pyrroloquinoline quinone), Idebenone (CV-2619), Methylcobalamin, L-Carnitine, L-Glutamine, L-Alanine, L-Isoleucine, L-Leucine, L-Valine, Glycine, L-Aspartic Acid, L-Arginine, L-Ornithine, L-Histidine, L-Lysine, L-Methionine, L-Phenylalanine, L-Threonine, L-Cysteine, L-Glutamic Acid, L-Proline, L-Serine, L-Tryptophan, L-Ascorbic Acid, Peppermint Leaf (Mentha x piperita) and Natural Trace Minerals.

* % Daily value not established


For Best Results:

Take ACR Regen Extra Strength with the Ultimate Body Detox System to achieve enhanced immune system support and exceptional total body rejuvenation.


Total Body Healing
ACR Regen promotes rapid, total body regeneration and healing; providing essential nutrients and cellular building blocks to speed the body’s recovery from illness, injury or stress.*

Optimized Cell Signaling
Cellular regeneration and healing can only occur when cell signaling is functional. ACR Regen represents the first of its kind regenerative health formula with specific nutrients to optimize cell signaling and function.

Enhanced Cell Protection
Provides cyto-protective effects, proven to reduce muscle damage and inflammation during periods of high oxidative stress, inhibiting oxidative damage.

Promotes Cell Activation
Activates cells to enter the growth and proliferation cycle, facilitating rapid healing and relief.*

2 oz $29.95
4 oz $49.95

Improved Cellular Regeneration
Living cells are chemo-electromagnetic units. Utilizing ionic and neuronal signaling within a range of growth factor pathways, ACR Regen heightens chemo-electromagnetic cell function; promoting tissue healing and cellular regeneration

Amplification and Synergy
ACR Regen amplifies healing and regenerative effects when combined with intracellular detoxification, immune system and glutathione support as provided by the Ultimate Body Detox and Ultimate Lyme Support Systems.

Advanced Cellular Technology
ACR Regen delivers the power of each ingredient in the most effective manner possible; achieving maximum results without stomach discomfort or side effects. With Advanced Cellular Technology, ACR Regen Extra Strength Intra-oral spray is immediately absorbed, simple to take, and has a pleasant taste with a hint of natural mint. Just spray, swish, and swallow.

Purity and Quality Guaranteed:quality-glutathione-GSH

ACR Regen Extra Strength is produced under strict GMP manufacturing controls in conformance with guidelines for dietary supplements set forth in USP XXVII. For purity and quality, ACR Regen Extra Strength contains no preservatives • no alcohol • no artificial coloring or flavoring. For customer support, please call 1 888 823 3869.

* These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.