OPAHYDE

Mechanism of action

Alizarine is believed to interact with various biological pathways, including those involved in the regulation of cellular functions. Its mechanism may involve the modulation of oxidative stress and the influence on signaling pathways, contributing to its potential antioxidant properties. The alizarin biosynthesis pathway is significant in understanding its biological role and pharmacological effects.

Pharmacodynamics

Alizarine exhibits properties that may influence cellular processes, including apoptosis and anti-inflammatory effects. However, specific pharmacodynamic parameters for alizarine in human subjects are not well-documented, and the clinical significance of these actions remains to be fully elucidated.

Pharmacokinetics

The pharmacokinetics of alizarine, including absorption, distribution, metabolism, and excretion, have not been thoroughly studied in humans. Data from animal studies suggest that alizarine may be metabolized in the liver and excreted primarily through the renal system, but specific human pharmacokinetic profiles are lacking.

Pregnancy

Not established. Safety in pregnancy has not been evaluated.

Breast-feeding

Not established. Safety in breastfeeding has not been evaluated.

Storage

Store in a cool, dry place, protected from light.

Formulations

• {'name': 'Alizarine', 'type': 'powder', 'strength': None}

Mechanism of action

Benzotriazole functions primarily through its ability to inhibit the corrosion of metals by forming a protective layer on the surface of the metal. It acts as a chelating agent that can bind to metal ions, preventing their reactivity. This mechanism helps in stabilizing certain compounds and preventing degradation.

Pharmacodynamics

The pharmacodynamic properties of benzotriazole are not well-characterized in clinical literature. Its primary function relates to its chemical stability and its role as a protective agent in various formulations rather than direct therapeutic effects on biological systems.

Pharmacokinetics

Data regarding the pharmacokinetics of benzotriazole in humans is limited. However, it is known that compounds similar to benzotriazole may undergo metabolism via hydroxylation and conjugation, with elimination primarily occurring through renal pathways. The exact absorption, distribution, metabolism, and excretion characteristics of benzotriazole in humans require further study.

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Use during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether benzotriazole is excreted in human milk. Caution should be exercised when administering to a nursing woman.

Storage

Store in a cool, dry place, away from moisture and light. Keep container tightly closed.

Indications

• Molecular imaging
• Fluorescence microscopy
• Staining of biological tissues
• Cellular imaging

Mechanism of action

Cyanine dyes, including cyanine, function as fluorescent markers. They absorb light at specific wavelengths and re-emit it at longer wavelengths. This property allows them to be used in various imaging techniques, where they bind to specific biomolecules or structures within cells, enabling visualization under a fluorescence microscope.

Pharmacodynamics

The pharmacodynamics of cyanine relate to its role as a fluorescent dye rather than a pharmacological agent with therapeutic effects. The binding of cyanine to biomolecules can alter the fluorescence properties, facilitating the detection and quantification of target molecules in biological samples. The dye's effectiveness is influenced by factors such as pH, solvent polarity, and the presence of other chemical entities.

Pharmacokinetics

The pharmacokinetics of cyanine dyes are not typically studied in the context of traditional drug absorption, distribution, metabolism, and excretion since they are mainly used for research purposes. However, when applied in biological systems, the distribution of cyanine may depend on its binding affinity to cellular components and its solubility in various media.

Pregnancy

There is insufficient data on the use of cyanine in pregnancy. Caution is advised.

Breast-feeding

Cyanine is not recommended during breastfeeding due to limited information on its safety.

Storage

Store in a cool, dry place, away from direct light. Keep out of reach of children.

Indications

• Vascular health
• Oxidative stress-related conditions
• Anti-aging applications
• Inflammatory disorders

Dosage

Children: Refer to the BNF for Children for pediatric dosing information regarding hydrogen-rich water.

Adults: Refer to the BNF for specific dosages and administration guidelines for hydrogen-rich water.

Mechanism of action

Molecular hydrogen exerts its effects primarily through its antioxidant properties, which involve the activation of the Nrf2 pathway. This pathway regulates the expression of various antioxidant enzymes, thereby reducing oxidative stress and inflammation. In endothelial cells, H2 has been shown to prevent TCDD-induced senescence and promote cellular longevity by maintaining cellular homeostasis and modulating redox status.

Pharmacodynamics

The pharmacodynamics of dihydrogen are characterized by its ability to scavenge free radicals and reduce oxidative stress. It also influences cellular signaling pathways related to inflammation and aging. Specifically, H2 aids in maintaining the balance of NAD+/NADH, which is crucial for cellular metabolism and energy production. The modulation of the Nrf2 pathway leads to enhanced production of endogenous antioxidants, contributing to its protective effects on vascular endothelial cells.

Pharmacokinetics

Dihydrogen is rapidly absorbed and distributed in the body. When administered as hydrogen-rich water, it is absorbed through the gastrointestinal tract. Its concentration decreases over time, becoming nearly undetectable after 12 hours in aqueous solutions. The pharmacokinetic profile indicates that the effects of hydrogen may persist even after the gas has been eliminated, likely due to the activation of protective cellular mechanisms.

Pregnancy

There is insufficient data on the use of dihydrogen during pregnancy. Consult a healthcare provider for guidance.

Breast-feeding

Limited information is available regarding the safety of dihydrogen during breastfeeding. Consult a healthcare provider before use.

Storage

Store in a cool, dry place away from direct sunlight. Keep container tightly closed.

Formulations

• Hydrogen-rich water

Dosage

Children: Refer to specific clinical guidelines or protocols for dosing information.

Adults: Refer to specific clinical guidelines or protocols for dosing information.

Mechanism of action

Diphosphate acts primarily as an energy donor in biochemical reactions. It is hydrolyzed to inorganic phosphate and adenosine triphosphate (ATP), providing energy for cellular processes. This reaction is critical in pathways such as fatty acid oxidation, amino acid metabolism, and tRNA charging, facilitating the synthesis of proteins and other essential biomolecules.

Pharmacodynamics

Diphosphate functions as an essential cofactor in numerous enzymatic reactions, influencing metabolic pathways that regulate energy production and utilization. By participating in the cleavage of high-energy bonds, it impacts the metabolic rates of various substrates and the overall energy homeostasis within the cell. Its role in biosynthesis pathways underscores its importance in cellular growth and maintenance.

Pharmacokinetics

Diphosphate is rapidly utilized in cellular metabolism and does not have a defined pharmacokinetic profile like traditional drugs, as it is a naturally occurring substance in biological systems. Its bioavailability and distribution are closely linked to its role in metabolic pathways. The body primarily regulates diphosphate levels through cellular demand and enzymatic activity rather than through absorption and excretion mechanisms.

Pregnancy

There is limited data available on the use of diphosphate during pregnancy. Consult healthcare providers for advice.

Breast-feeding

Limited data on the excretion of diphosphate in breast milk. Caution is advised when using this substance while breastfeeding.

Storage

Store in a cool, dry place away from light. Ensure the container is tightly closed to prevent contamination.

Indications

• Hypokalemia
• Potassium deficiency
• Certain types of arrhythmias related to low potassium levels
• Management of diuretic-induced hypokalemia

Dosage

Children: Refer to BNF for Children for specific dosing recommendations.

Adults: Refer to appropriate clinical guidelines or BNF for specific dosing information.

Mechanism of action

Dipotassium dissociates in solution to release potassium ions (K+). These ions are crucial for the normal functioning of cells, particularly in maintaining the resting membrane potential and facilitating action potentials in excitable tissues such as muscle and nerve cells. Adequate potassium levels help regulate heart rhythm and muscle contraction.

Pharmacodynamics

Potassium plays a vital role in several physiological processes. It is involved in the regulation of intracellular fluid volume, acid-base balance, and muscle function. It also influences the conduction of electrical impulses in the heart, thereby having implications for cardiac function. The balance of potassium in the body is tightly regulated, with hormones such as aldosterone playing a critical role in its homeostasis.

Pharmacokinetics

After oral administration, dipotassium is absorbed in the gastrointestinal tract, with peak plasma concentrations typically occurring within 1 to 2 hours. The distribution of potassium is primarily intracellular, with a significant amount stored in muscle cells. The kidneys are responsible for regulating potassium excretion, and renal function can significantly affect potassium levels in the body. Potassium has a half-life of about 1 hour, but its physiological effects may last longer depending on the specific context of use.

Contra-indications

• Hyperkalemia
• Severe renal impairment
• Addison's disease
• Acute dehydration

Adverse effects

• Hyperkalemia
• Gastrointestinal disturbances such as nausea and diarrhea
• Muscle weakness
• Cardiac arrhythmias
• Metabolic acidosis

Interactions

• Potassium-sparing diuretics may increase the risk of hyperkalemia
• ACE inhibitors and angiotensin receptor blockers may also increase potassium levels
• Non-steroidal anti-inflammatory drugs (NSAIDs) may reduce renal function and increase potassium levels

Precautions

• Monitor serum potassium levels regularly
• Use with caution in patients with renal impairment
• Assess the patient's dietary intake of potassium
• Consider potential drug interactions that may increase potassium levels

Pregnancy

Dipotassium should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult a healthcare provider.

Breast-feeding

Dipotassium is excreted in breast milk. Caution should be exercised when administering to a nursing mother.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Dipotassium phosphate
• Dipotassium citrate

Indications

• Lead poisoning
• Zinc toxicity
• Cadmium poisoning
• Iron overload disorders

Dosage

Adults: Refer to the BNF for specific dosing recommendations for adults, as it may vary based on the condition being treated and the severity of metal poisoning.

Mechanism of action

The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate forms with any metal that can displace calcium from the molecule, which includes lead, zinc, cadmium, and iron. The excretion of zinc is significantly increased, while the effect on calcium excretion is minimal. The chelation process helps to reduce the toxicity of heavy metals in the body by promoting their urinary excretion.

Pharmacodynamics

Edetate calcium acts as a heavy metal chelating agent, forming stable, water-soluble complexes with metal ions that can be excreted in urine. One gram of edetate calcium can theoretically bind up to 620 mg of lead, though actual urinary excretion rates are lower, with approximately 5 mg of lead excreted per gram of EDTA in lead-poisoned patients. It is relatively ineffective against mercury, gold, or arsenic poisoning but can mobilize and eliminate zinc, cadmium, copper, iron, and manganese.

Pharmacokinetics

After intravenous administration, edetate calcium disodium is rapidly distributed in the blood and has a half-life that can vary based on the patient's condition and the presence of heavy metals. The drug is primarily excreted unchanged in the urine. Calcium levels may be transiently lowered during infusion, but significant mobilization of body calcium stores is usually not observed unless very slow infusions are administered. The effects on metal ion excretion are dose-dependent and vary according to the specific metal involved.

Contra-indications

• Hypersensitivity to edetate calcium disodium or any component of the formulation
• Pre-existing renal impairment
• Calcium deficiency states

Adverse effects

• Hypocalcemia
• Renal impairment
• Gastrointestinal disturbances such as nausea and vomiting
• Headache
• Hypotension
• Electrolyte imbalances

Interactions

• Increased risk of toxicity when used with nephrotoxic agents
• May interfere with the absorption of certain minerals and vitamins
• Should not be mixed with other intravenous drugs due to potential chemical interactions

Precautions

• Monitor renal function during treatment
• Use caution in patients with cardiovascular disease due to potential hypotensive effects
• Evaluate calcium levels periodically in patients receiving prolonged therapy
• Use with caution in patients with a history of seizures

Pregnancy

Limited data available on the use of edetate calcium disodium in pregnant women. Use only if clearly needed.

Breast-feeding

It is not known whether edetate calcium disodium is excreted in human milk. Caution is advised.

Storage

Store at room temperature, away from light and moisture. Keep out of reach of children.

Formulations

• Edetate calcium disodium injection

Indications

• Wound healing
• Skin ulceration
• Burns
• Psoriasis
• Dermatitis

Dosage

Children: Refer to the BNF for Children for appropriate dosing information based on the child's age and condition.

Adults: Refer to the BNF for specific formulations and dosing guidelines, as dosages may vary based on the condition being treated and the formulation used.

Mechanism of action

While there is no well-controlled data to formally substantiate the method of action, ongoing studies suggest that allantoin may induce a histological wound healing profile in animal models, leading to improved reestablishment of normal skin. This includes increased vasodilation, inflammatory cell presence, angiogenesis, fibroblast proliferation, and collagen deposition in treated wounds compared to untreated ones.

Pharmacodynamics

There is limited controlled data regarding the pharmacodynamic properties of allantoin. However, studies indicate that allantoin may possess moisturizing and keratolytic effects, increasing the extracellular matrix's water content and enhancing the desquamation of dead skin cells. These activities can promote cell proliferation and facilitate wound healing.

Pharmacokinetics

Specific pharmacokinetic data for allantoin in humans is limited. However, it is known to be applied topically, which suggests local absorption at the site of application. Systemic absorption is considered minimal due to its low molecular weight and hydrophilicity.

Pregnancy

There is limited data on the safety of allantoin in pregnancy. It is advisable to consult a healthcare professional before use.

Breast-feeding

Allantoin is generally considered safe during breastfeeding, but caution is recommended. Consult a healthcare professional before use.

Storage

Store at room temperature, away from direct sunlight and moisture. Keep out of reach of children.

Formulations

• Topical cream
• Gel
• Ointment

Indications

• Oxidative stress-related conditions
• Inflammatory conditions
• Potential anti-aging applications
• Vascular health enhancement

Dosage

Children: Refer to specific product formulations and guidelines, as dosing can vary based on the concentration of hydrogen in the product used.

Adults: Refer to specific product formulations and guidelines, as dosing can vary based on the concentration of hydrogen in the product used.

Mechanism of action

Molecular hydrogen acts primarily as an antioxidant and anti-inflammatory agent. It is believed to exert its beneficial effects through the activation of the Nrf2 pathway, which enhances the expression of antioxidant enzymes and protects cells from oxidative stress. Hydrogen-rich environments have been shown to mitigate the harmful effects of various toxins on human umbilical vein endothelial cells, thereby promoting vascular health and longevity.

Pharmacodynamics

Hydrogen's pharmacodynamic properties are linked to its role as a potent antioxidant, which reduces reactive oxygen species (ROS) and modulates inflammation. It has been documented to counteract cellular senescence in endothelial cells, thereby maintaining vascular integrity and promoting overall health. The long-lasting effects of hydrogen exposure can be observed even after its concentration in the medium has decreased, suggesting a sustained activation of protective cellular pathways.

Pharmacokinetics

Hydrogen is a gaseous molecule that diffuses rapidly across biological membranes. Its absorption and distribution in the body are influenced by the method of administration, with hydrogen-rich water being a common delivery form. Once in the bloodstream, hydrogen is quickly utilized by tissues, and its concentration diminishes rapidly, with a half-life that can vary based on conditions. The elimination of hydrogen primarily occurs via exhalation, making it a non-toxic molecule with a favorable safety profile.

Pregnancy

Hydrogen is generally considered safe during pregnancy, but it is advisable to consult a healthcare provider for specific recommendations.

Breast-feeding

Hydrogen is considered safe during breastfeeding, but as with any substance, it is recommended to discuss with a healthcare provider.

Storage

Hydrogen should be stored in a cool, dry place away from direct sunlight and heat sources, in appropriate gas cylinders designed for compressed gases.

Formulations

• Hydrogen gas (H2)
• Hydrogen-rich water

Mechanism of action

Hydrogenphosphate acts as a substrate for various enzymatic reactions where phosphate groups are transferred or incorporated into organic molecules. It is involved in metabolic pathways such as nicotine biosynthesis and NAD/NADH cycling, facilitating biochemical reactions that are vital for cellular function.

Pharmacodynamics

Hydrogenphosphate is crucial for maintaining cellular homeostasis. It regulates acid-base balance and is involved in energy metabolism. The phosphate groups it provides are integral to the structure and function of ATP, which is the primary energy currency of the cell. Additionally, hydrogenphosphate influences signal transduction pathways through phosphorylation and dephosphorylation processes.

Pharmacokinetics

Hydrogenphosphate is readily absorbed in the gastrointestinal tract and distributed throughout the body. Its elimination primarily occurs through renal excretion, where it is filtered and reabsorbed by the kidneys. The balance of hydrogenphosphate levels is tightly regulated by various physiological mechanisms to ensure proper metabolic function.

Pregnancy

There is limited information regarding the safety of hydrogenphosphate in pregnancy. Consult relevant guidelines and consider potential risks versus benefits.

Breast-feeding

Data on the excretion of hydrogenphosphate in human milk are not available. Caution is advised.

Storage

Store in a cool, dry place away from direct sunlight. Ensure containers are tightly closed.

Indications

• Disinfection of medical instruments
• Sterilization of endoscopes
• General surface disinfection in healthcare settings

Dosage

Children: Refer to specific product guidelines for concentration and exposure time.

Adults: Refer to specific product guidelines for concentration and exposure time.

Mechanism of action

Orthophthalaldehyde acts as a potent biocide by forming cross-links with amino groups in proteins, leading to the denaturation and inactivation of microbial cells. This process disrupts vital cellular functions, ultimately resulting in cell death. The compound's effectiveness is attributed to its ability to penetrate microbial cell walls and interact with cellular components.

Pharmacodynamics

Orthophthalaldehyde exhibits broad-spectrum antimicrobial activity, making it effective against a wide variety of pathogens. The compound is particularly noted for its rapid action, with significant microbial inactivation occurring within a short exposure time. Its efficacy is influenced by factors such as concentration, temperature, and contact time.

Pharmacokinetics

The pharmacokinetic profile of orthophthalaldehyde is not well-characterized, as it is primarily used in external applications for disinfection rather than systemic administration. Its stability and potency as a disinfectant are maintained under various conditions, but specific absorption, distribution, metabolism, and excretion data are limited.

Pregnancy

There is limited information regarding the safety of orthophthalaldehyde in pregnancy. It is advisable to avoid use unless clearly needed and the benefits outweigh the risks.

Breast-feeding

There is no available data on the excretion of orthophthalaldehyde in human milk. Caution should be exercised when administering to breastfeeding women.

Storage

Store in a cool, dry place away from light. Ensure containers are tightly closed when not in use.

Mechanism of action

Substantial evidence indicates that molecular hydrogen (H2) has beneficial vascular effects because of its antioxidant and/or anti-inflammatory effects. Thus, hydrogen-rich water may prove to be an effective anti-aging drink. This study examined the effects of H2 on endothelial senescence and clarified the mechanisms involved. Hydrogen-rich medium was produced by a high-purity hydrogen gas generator. Human umbilical vein endothelial cells (HUVECs) were incubated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for various time periods in normal or hydrogen-rich medium. The baseline H2concentration in hydrogen-rich medium was 0.55 +/- 0.07 mmol/L. This concentration gradually decreased, and H2 was almost undetectable in medium after 12 hr. At 24 hr after TCDD exposure, HUVECs treated with TCDD exhibited increased 8OHdG and acetyl-p53 expression, decreased nicotinamide adenine dinucleotide (NAD(+))/NADH ratio, impaired Sirt1 activity, and enhanced senescence-associated beta-galactosidase. However, HUVECs incubated in hydrogen-rich medium did not exhibit these TCDD-induced changes accompanying Nrf2 activation, which was observed even after H2 was undetectable in the medium. Chrysin, an inhibitor of Nrf2, abolished the protective effects of H2 on HUVECs. H2 has long-lasting antioxidant and anti-aging effects on vascular endothelial cells through the Nrf2 pathway, even after transient exposure to H2. Hydrogen-rich water may thus be a functional drink that increases longevity. /Hydrogen-rich water/ Amyloid beta (Abeta) peptides are identified /as a/ cause of neurodegenerative diseases such as Alzheimer's disease (AD). Previous evidence suggests Abeta-induced neurotoxicity is linked to the stimulation of reactive oxygen species (ROS) production. The accumulation of Abeta-induced ROS leads to increased mitochondrial dysfunction and triggers apoptotic cell death. This suggests antioxidant therapies may be beneficial for preventing ROS-related diseases such as AD. Recently, hydrogen-rich water (HRW) has been proven effective in treating oxidative stress-induced disorders because of its ROS-scavenging abilities. However, the precise molecular mechanisms whereby HRW prevents neuronal death are still unclear. In the present study, we evaluated the putative pathways by which HRW protects against Abeta-induced cytotoxicity /in SK-N-MC cells/. Our results indicated that HRW directly counteracts oxidative damage by neutralizing excessive ROS, leading to the alleviation of Abeta-induced cell death. In addition, HRW also stimulated AMP-activated protein kinase (AMPK) in a sirtuin 1 (Sirt1)-dependent pathway, which upregulates forkhead box protein O3a (FoxO3a) downstream antioxidant response and diminishes Abeta-induced mitochondrial potential loss and oxidative stress. Taken together, our findings suggest that HRW may have potential therapeutic value to inhibit Abeta-induced neurotoxicity. /Hydrogen-rich water/ The NLRP3 inflammasome, an intracellular multi-protein complex controlling the maturation of cytokine interleukin-1beta, plays an important role in lipopolysaccharide (LPS)-induced inflammatory cascades. Recently, the production of mitochondrial reactive oxygen species (mtROS) in macrophages stimulated with LPS has been suggested to act as a trigger during the process of NLRP3 inflammasome activation that can be blocked by some mitochondria-targeted antioxidants. Known as a ROS scavenger, molecular hydrogen (H2) has been shown to possess therapeutic benefit on LPS-induced inflammatory damage in many animal experiments. Due to the unique molecular structure, H2 can easily target the mitochondria, suggesting that H2 is a potential antagonist of mtROS-dependent NLRP3 inflammasome activation. Here we have showed that, in mouse macrophages, H2 exhibited substantial inhibitory activity against LPS-initiated NLRP3 inflammasome activation by scavenging mtROS. Moreover, the elimination of mtROS by H2 resultantly inhibited mtROS-mediated NLRP3 deubi

Mechanism of action

The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate will form with any metal that has the ability to displace calcium from the molecule, a feature shared by lead, zinc, cadmium, manganese, iron and mercury. The amounts of manganese and iron metabolized are not significant. Copper is not mobilized and mercury is unavailable for chelation because it is too tightly bound to body ligands or it is stored in inaccessible body compartments. The excretion of calcium by the body is not increased following intravenous administration of edetate calcium disodium, but the excretion of zinc is considerably increased. Effects on rat liver glucocorticoid receptor in vitro was studied. At 4 °C, 10 mmole EDTA had a stablizing effect on unbound hepatic glucocorticoid receptors. Apparently, endogenous metal ions are involved in the processes of glucocorticoid-receptor complex stabilization and transformation. Edetate disodium injection forms chelates with the cations of calcium and many divalent and trivalent metals. Because of its affinity for calcium, edetate disodium will produce a lowering of the serum calcium level during intravenous infusion. Slow infusion over a protracted period may cause mobilization of extracirculatory calcium stores. Edetate disodium exerts a negative inotropic effect upon the heart. Edetate disodium likewise forms chelates with other polyvalent metals and produces increases in urinary excretion of magnesium, zinc and other trace elements. It does not form a chelate with potassium but may reduce the serum level and increase urinary loss of potassium.

Pharmacodynamics

Edetate calcium is a heavy metal chelating agent. The calcium in edetate calcium can be displaced by divalent or trivalent metals to form a stable water soluble complex that can be excreted in the urine. In theory, 1 g of edetate calcium can theoretically bind 620 mg of lead, but in reality only about 5 mg per gram is actually excreted into the urine in lead poisoned patients. In addition to chelating lead, edetate calcium also chelates and eliminates zinc from the body. Edetate calcium also binds cadmium, copper, iron and manganese, but to a much lesser extent than either lead or zinc. Edetate calcium is relatively ineffective for use in treating mercury, gold or arsenic poisoning.

Mechanism of action

There is no well controlled data that can formally substantiate the method of action. However, ongoing studies suggest that there may exist a histological wound healing profile induced by allantoin in rats that leads to the amelioration and fastening of the reestablishment of normal skin. This facilitation of wound healing is supported by observations that wounds inflicted to rat subjects to which topical allantoin preparations were applied histologically demonstrated increased vasodilation, presence of inflammatory exudates, number of inflammatory cells, angiogenesis, fibroblast proliferation, and increased collagen deposition when compared to rat subjects with wounds that did not receive any allantoin administration.

Pharmacodynamics

There is no well controlled and appropriate data that can formally substantiate the pharmacodynamic properties of allantoin. Nevertheless, ongoing studies suggest that allantoin possesses moisturizing and keratolytic effects, as well as abilities to increase the water content of the extracellular matrix and enhance the desquamation of upper layers of dead skin cells, all of which are activities that can promote cell proliferation and facilitate wound healing.

Mechanism of action

Substantial evidence indicates that molecular hydrogen (H2) has beneficial vascular effects because of its antioxidant and/or anti-inflammatory effects. Thus, hydrogen-rich water may prove to be an effective anti-aging drink. This study examined the effects of H2 on endothelial senescence and clarified the mechanisms involved. Hydrogen-rich medium was produced by a high-purity hydrogen gas generator. Human umbilical vein endothelial cells (HUVECs) were incubated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for various time periods in normal or hydrogen-rich medium. The baseline H2concentration in hydrogen-rich medium was 0.55 +/- 0.07 mmol/L. This concentration gradually decreased, and H2 was almost undetectable in medium after 12 hr. At 24 hr after TCDD exposure, HUVECs treated with TCDD exhibited increased 8OHdG and acetyl-p53 expression, decreased nicotinamide adenine dinucleotide (NAD(+))/NADH ratio, impaired Sirt1 activity, and enhanced senescence-associated beta-galactosidase. However, HUVECs incubated in hydrogen-rich medium did not exhibit these TCDD-induced changes accompanying Nrf2 activation, which was observed even after H2 was undetectable in the medium. Chrysin, an inhibitor of Nrf2, abolished the protective effects of H2 on HUVECs. H2 has long-lasting antioxidant and anti-aging effects on vascular endothelial cells through the Nrf2 pathway, even after transient exposure to H2. Hydrogen-rich water may thus be a functional drink that increases longevity. /Hydrogen-rich water/ Amyloid beta (Abeta) peptides are identified /as a/ cause of neurodegenerative diseases such as Alzheimer's disease (AD). Previous evidence suggests Abeta-induced neurotoxicity is linked to the stimulation of reactive oxygen species (ROS) production. The accumulation of Abeta-induced ROS leads to increased mitochondrial dysfunction and triggers apoptotic cell death. This suggests antioxidant therapies may be beneficial for preventing ROS-related diseases such as AD. Recently, hydrogen-rich water (HRW) has been proven effective in treating oxidative stress-induced disorders because of its ROS-scavenging abilities. However, the precise molecular mechanisms whereby HRW prevents neuronal death are still unclear. In the present study, we evaluated the putative pathways by which HRW protects against Abeta-induced cytotoxicity /in SK-N-MC cells/. Our results indicated that HRW directly counteracts oxidative damage by neutralizing excessive ROS, leading to the alleviation of Abeta-induced cell death. In addition, HRW also stimulated AMP-activated protein kinase (AMPK) in a sirtuin 1 (Sirt1)-dependent pathway, which upregulates forkhead box protein O3a (FoxO3a) downstream antioxidant response and diminishes Abeta-induced mitochondrial potential loss and oxidative stress. Taken together, our findings suggest that HRW may have potential therapeutic value to inhibit Abeta-induced neurotoxicity. /Hydrogen-rich water/ The NLRP3 inflammasome, an intracellular multi-protein complex controlling the maturation of cytokine interleukin-1beta, plays an important role in lipopolysaccharide (LPS)-induced inflammatory cascades. Recently, the production of mitochondrial reactive oxygen species (mtROS) in macrophages stimulated with LPS has been suggested to act as a trigger during the process of NLRP3 inflammasome activation that can be blocked by some mitochondria-targeted antioxidants. Known as a ROS scavenger, molecular hydrogen (H2) has been shown to possess therapeutic benefit on LPS-induced inflammatory damage in many animal experiments. Due to the unique molecular structure, H2 can easily target the mitochondria, suggesting that H2 is a potential antagonist of mtROS-dependent NLRP3 inflammasome activation. Here we have showed that, in mouse macrophages, H2 exhibited substantial inhibitory activity against LPS-initiated NLRP3 inflammasome activation by scavenging mtROS. Moreover, the elimination of mtROS by H2 resultantly inhibited mtROS-mediated NLRP3 deubi