Nitrogen Monoxide
- Product NameNitrogen Monoxide
- CAS10102-43-9
- MFNO*
- MW30.01
- EINECS233-271-0
- MOL File10102-43-9.mol
Chemical Properties
Melting point | −163.6 °C(lit.) |
Boiling point | −151.7 °C(lit.) |
Density | d-150.2 (liq) 1.27; Relative d (gas) 1.036 (air = 1); Absolute d (gas) 1.227 (air = 1) |
vapor density | 1.05 (vs air) |
refractive index | nD25 1.0002697 |
solubility | At 20 °C and at a pressure of 101 kPa, 1 volume dissolves in about 21 volumes of water. |
form | colorless gas |
color | colorless |
Water Solubility | slightly soluble H2O [HAW93] |
Merck | 13,6611 |
Exposure limits | TLV-TWA 25 ppm (~30 mg/m3) (ACGIH, MSHA, and OSHA). |
Stability | Spontaneously reacts with oxygen in air to yield brown nitrogen dioxide. Reacts violently or explosively with ammonia and many organic materials. |
InChIKey | MWUXSHHQAYIFBG-UHFFFAOYSA-N |
CAS DataBase Reference | 10102-43-9(CAS DataBase Reference) |
EPA Substance Registry System | Nitric oxide (10102-43-9) |
Safety Information
Hazard Codes | O,T |
Risk Statements | 8-23-34-44 |
Safety Statements | 17-23-36/37/39-45 |
RIDADR | UN 1660 2.3 |
OEB | A |
OEL | TWA: 25 ppm (30 mg/m3) |
WGK Germany | 1 |
RTECS | QX0525000 |
DOT Classification | 2.3, Hazard Zone A (Gas poisonous by inhalation) |
HazardClass | 2.3 |
Hazardous Substances Data | 10102-43-9(Hazardous Substances Data) |
Toxicity | LCLo inhalation in dog: 5000ppm/25M |
IDLA | 100 ppm |
MSDS
Provider | Language |
---|---|
SigmaAldrich | English |
Usage And Synthesis
Nitric oxide is an important intermediate in the production of nitric acid. Fluorine, chlorine, and bromine react with nitric oxide to form the corresponding nitrosyl halide. [t is also used in making mixtures for calibration standards for stationary and mobile exhaust emission measurements.
near room temperature (its liquid density at 20°C is 1.45 g/cm3).
Nitrogen monoxide (NO) is commonly called nitric oxide,Nitric oxide is colorless and has a sharp sweet odor;Nitric oxide is nonfl ammable, toxic gases.Nitric oxide is a free radical that quickly reacts in air to produce nitrogen dioxide.It is also an
important biological messenger and transmitter.
Nitric oxide is a colorless gas with a sharp, sweet
odor; brown at high concentration in air. Shipped as a nonliquefied
compressed gas.
Nitric oxide,NO, also known as nitrogen oxide and nitrogen monoxide, is a colorless gas that will react with oxygen at room temperature to form nitrogen dioxide, N202, a reddish-brown gas.It is soluble in water and alcohol and is used primarily to form other compounds.
Colorless gas; paramagnetic; density 1.3402 g/L; slightly heavier than air, air density 1.04 (air=1); liquefies at -151.8°C to a blue liquid; the refractive index of the liquid 1.330 at -90°C; the density of the liquid 1.269 g/mL at -150.2°C; solidifies at -163.6°C to a bluish-white snow-like solid; critical temperature -94°C; critical pressure 65 atm; slightly soluble in water, 4.6 mL gas dissolves in 100 mL water at 20°C while 7.34 mL and 2.37 mL dissolve in the same volume of water at 0 and 60°C, respectively; more soluble in alcohol than water; soluble in carbon disulfide, and in ferrous sulfate solution (reacts).
Nitric oxide was prepared in 1772 by Joseph Priestley
(1733–1804) and described in his volumes Experiments and Observations of Different Kinds
of Air published between 1774 and 1786. Priestley called nitric oxide nitrous air, nitrogen
dioxide nitrous acid vapor, and nitrous oxide phlogisticated nitrous air, but also referred to the
latter as diminished nitrous air. He observed the change of clear nitric oxide to red nitrogen
dioxide. Priestley prepared nitric oxide by reacting nitric acid with a metal such as copper:
3Cu(s) + 8HNO3(aq) → 2NO(g) + 3Cu(NO3)2(aq) + 4H2O(l).
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Industry
Application
Role/benefit
Chemical manufacture
Manufacture of nitric acid
Intermediate
Manufacture of hydroxylamine
Intermediate
Medcine
Treatment of primary pulmonary hypertension
Active ingredient/helps to promote capillary and pulmonary dilation
Treatment of respiratory failure in premature babies
Active ingredient/can relax smooth muscle to widen (dilate) blood vessels
Treatment of impotence or erectile dysfunction
Active ingredient/enhances nitric oxide’s relaxant effects on smooth muscle cells in the corpus cavernosa
Chemical analysis
Detecting surface radicals on polymers
Radicals quenching agent
Analysis for nitric acid or its salts
Analytical agent
Others
Narcotics and preservatives
Effective component
Rayon production
Decolorizer
Propylene and dimethyl ether preservation
Stabilizing agent
Semiconductor manufacturing
Oxidation and chemical vapor deposition gas
Nitric oxide is produced as an intermediateusing the Ostwald method to make nitric acid (see Nitric Acid). Nitrogen compoundsproduced from nitric acid are use to manufacture fertilizers, explosives, and other chemicals.
Nitric oxide is used as an intermediate in themanufacture of nitric acid, in the preparationof metal nitrosyls, in bleaching of rayon,and in incandescent lamps. It is produced byheating air at high temperatures.
Nitric oxide is commercially produced by the catalytic oxidation of ammonia using aplatinum catalyst: 4NH3(g) + 5O2(g) → 4NO(g) + 6H2O(g).
A colorless gas that is insoluble
in water but dissolves in a solution
containing iron(II) ions owing to the formation
of the complex ion (FeNO)2+: the
nitrogen monoxide can be released by
heating. Nitrogen monoxide is prepared by
the action of nitric acid on copper turnings;
the impure product can be purified by
using a solution of iron(II) ions to absorb
the product. Commercially, nitrogen
monoxide is prepared by the catalytic oxidation
of ammonia or by the direct union
of nitrogen and oxygen in an electric arc.
Nitrogen monoxide is the most heat-stable
of the oxides of nitrogen, only decomposing
above 1000°C. At ordinary temperatures it combines immediately with oxygen
to give nitrogen dioxide:2NO(g) + O2(g) → 2NO2(g).
ChEBI: Nitric Oxide is a nitrogen oxide which is a free radical, each molecule of which consists of one nitrogen and one oxygen atom.
Nitric oxide is a small, unstable free radical that acts as a
biological messenger in many physiological responses.
Because it can diffuse freely in all directions from its site
of origin, regulation of the activity of nitric oxide is primarily
through control of its synthesis. Formation of nitric
oxide occurs through oxidation of the amino acid Larginine,
a reaction catalyzed by the enzyme nitric oxide
synthase (NOS), to produce nitric oxide and L-citrulline.
The forms of NOS differ in their cellular location and
expression (constitutive expression versus inducible expression).
Activation of synthesis of the inducible form of NOS results in continued synthesis of nitric oxide for
several hours. Inhibitors of NOS are analogues of arginine,
including L-Nw nitroarginine (L- NNA) and L-Nw
methylarginine (L-NMA), both of which decrease nitric
oxide synthesis.
Physiological sites proposed for nitric oxide action include the immune system, where nitric oxide acts as a cytostatic agent, is tumoricidal, and can inhibit viral replication. In the cardiovascular system, nitric oxide is the biological mediator of vasodilator responses to agents such as acetylcholine and bradykinin, which act as receptors on endothelial cells to activate NOS and stimulate nitric oxide production. Diffusible nitric oxide then activates guanylate cyclase in vascular smooth muscle cells, leading to the production of cyclic guanosine monophosphate (GMP) and vasodilation. In the brain, stimulation of N-methyl-D-aspartate receptors on neurons leads to activation of the brain form of NOS and stimulates production of nitric oxide. The function of brain nitric oxide is thought to involve actions as a retrograde neurotransmitter whereby nitric oxide diffuses back to the presynaptic neuron to activate guanylate cyclase and increase cyclic GMP levels. Through these retrograde actions nitric oxide is thought to play a role in the neural circuitry involved in memory.
Even though nitric oxide is the physiological mediator of a variety of responses, excess nitric oxide is toxic to many cells as a result of its role in the production of peroxynitrite and resultant lipid oxidation. Inhibitors of the NOS enzyme are in clinical trials for the treatment of hypotension associated with septic shock. Administration of low concentrations of nitric oxide through respiratory ventilators has been implemented to treat persistent pulmonary hypertension of the newborn.
Physiological sites proposed for nitric oxide action include the immune system, where nitric oxide acts as a cytostatic agent, is tumoricidal, and can inhibit viral replication. In the cardiovascular system, nitric oxide is the biological mediator of vasodilator responses to agents such as acetylcholine and bradykinin, which act as receptors on endothelial cells to activate NOS and stimulate nitric oxide production. Diffusible nitric oxide then activates guanylate cyclase in vascular smooth muscle cells, leading to the production of cyclic guanosine monophosphate (GMP) and vasodilation. In the brain, stimulation of N-methyl-D-aspartate receptors on neurons leads to activation of the brain form of NOS and stimulates production of nitric oxide. The function of brain nitric oxide is thought to involve actions as a retrograde neurotransmitter whereby nitric oxide diffuses back to the presynaptic neuron to activate guanylate cyclase and increase cyclic GMP levels. Through these retrograde actions nitric oxide is thought to play a role in the neural circuitry involved in memory.
Even though nitric oxide is the physiological mediator of a variety of responses, excess nitric oxide is toxic to many cells as a result of its role in the production of peroxynitrite and resultant lipid oxidation. Inhibitors of the NOS enzyme are in clinical trials for the treatment of hypotension associated with septic shock. Administration of low concentrations of nitric oxide through respiratory ventilators has been implemented to treat persistent pulmonary hypertension of the newborn.
A colorless gas. Noncombustible but accelerates the burning of combustible material. Vapors heavier than air. Very toxic by inhalation and skin absorption. Heating the containers may cause them to rupture violently and rocket.
Nitric oxide was discovered by Van Helmont in 1620. It occurs in the exhaust gases from automobiles along with other oxides of nitrogen, at trace concentrations. It also is found in minute quantities in the upper atmosphere, resulting from the oxidation of nitrogen in the presence of ionizing radiation or by electric discharge. Nitric oxide is the most stable oxide of nitrogen. It is used as an intermediate or as a starting reactant in the production of many nitrogen compounds, including nitrogen dioxide, nitric acid and nitrosyl chloride.
Nitric oxide was discovered by Van Helmont in 1620. It occurs in the exhaust gases from automobiles along with other oxides of nitrogen, at trace concentrations. It also is found in minute quantities in the upper atmosphere, resulting from the oxidation of nitrogen in the presence of ionizing radiation or by electric discharge. Nitric oxide is the most stable oxide of nitrogen. It is used as an intermediate or as a starting reactant in the production of many nitrogen compounds, including nitrogen dioxide, nitric acid and nitrosyl chloride.
Combines very rapidly with oxygen in the air to form nitrogen dioxide. Nitrogen dioxide reacts with water to form nitric acid and NITRIC OXIDE, reacts with alkalis to form nitrates and nitrites [Merck 11th ed. 1989].
NITRIC OXIDE can serve as both an oxidizing agent and as a reducing agent. Sustains the combustion of powdered aluminum [Mellor 5:209-212. 1946-47]. Enflames or explodes when mixed with vapors of carbon disulfide [Mellor 8, Supp. 2:232. 1967]. Reacts vigorously with sodium monoxide above 100°C [Mellor 2, Supp. 2:629. 1961]. Reacts on contact with oxygen at room temperature to form brown gaseous nitrogen dioxide. Reacts with alkalis to form nitrates and nitrites [Merck 11th ed. 1989]. The liquid is very sensitive to detonation in the presence of water.
Supports combustion. Toxic by inhalation,
strong irritant to skin and mucous membranes.
Hypoxia/cyanosis, nitrosyl-hemoglobin formation,
and upper respiratory tract irritant.
Can cause death or permanent injury after a very short exposure to small quantities. Irritant of eyes, nose, throat; can cause unconsciousness. NITRIC OXIDE forms acids in the respiratory system which are irritating and cause congestion in the lungs. Concentrations of 60-150 ppm cause immediate irritation of the nose and throat with coughing and burning in the throat and chest. 6-24 hours after exposure, labored breathing and unconsciousness may result. Concentrations of 100-150 ppm are dangerous for short exposure of 30-60 minutes. Concentrations of 200-700 ppm may be fatal after very short exposure.
Nitric oxide is an irritant to the eyes, nose,and throat. Inhalation of this gas causesmethemoglobinemia. Its actions are somewhat similar to those of carbon monoxide.It binds with hemoglobin (Hb) in bloodto form metheglobin (NOHb), affecting thetransportation of oxygen to body tissues andorgans:Animal experiments indicate nitric oxide tobe much less toxic than nitrogen dioxide.However, because of its spontaneous oxidation to highly toxic nitrogen dioxide, nitricoxide should be viewed as a severe healthhazard.
Noncombustible gas; burns with fuels,
hydrocarbons, or when heated with hydrogen.
Nitric oxide reacts violently with carbon
disulfide vapors, producing green luminous
flame; with fluorine, it produces a pale yel low flame. It explodes when mixed with
ozone, chlorine monoxide, or a nitrogen tri halide. Reactions with many pyrophoric met als produce incandescence. Reaction with
amorphous boron produces brilliant flashes.
Nitric oxide is noncorrosive, and most common
structural materials may be used. However, in
the presence of moisture and oxygen, corrosive
conditions will develop as a result of the formation
of nitric and nitrous acids. Prior to use,
systems to contain nitric oxide must first be
purged with an inert gas. Where air contamination
cannot be eliminated, stainless steel should
be used.
A poison gas. A severe
eye, skin, and mucous membrane irritant. A
systemic irritant by inhalation. Mutation data
reported. Exposure may occur whenever
nitric acid acts upon organic material, such
as wood, sawdust, and refuse; it occurs
when nitric acid is heated, and when organic
nitro compounds are burned, for example,
celluloid, cellulose nitrate (guncotton), and
dynamite. The action of nitric acid upon
metals, as in metal etchng and pickling, also
liberates the fumes. In hgh-temperature
weldmg, as with the oxyacetylene or electric
torch, the nitrogen and oxygen of the air
unite to form oxides of nitrogen.
Automobile exhaust and power plant
emissions are also sources of NOx.
Exposure occurs in many manufacturing nitric and nitrous acids. This is the action
that takes place deep in the respiratory
system. The acids formed are irritating and
can cause congestion in the throat and
bronchi and edema of the lungs. The acids
are neutralized by the alkalies present in the
tissues, with the formation of nitrates and
nitrites. The latter may cause some arterial
ddation, fall in blood pressure, headache,
and dizziness, and there may be some
formation of methemoglobin. However, the
nitrite effect is of secondary importance.
Because of their relatively low solubllity in
water, the nitrogen oxides are initially only
slightly irritating to the mucous membranes
of the upper respiratory tract. Their warning
power is therefore low, and dangerous
amounts of the fumes may be breathed
before the worker notices any real
discomfort. Higher concentrations (60-150
ppm) cause immediate irritation of the nose
and throat, with coughing and burning in
the throat and chest. These symptoms often
clear upon breathing fresh air, and the
worker may feel well for several hours.
Some 6-24 hours after exposure, a sensation
of tightness and burning in the chest
develops, followed by shortness of breath,
sleeplessness, and restlessness. Dyspnea and
air hunger may increase rapidly with
development of cyanosis and loss of
consciousness followed by death. In cases
that recover from the pulmonary edema,
there is usually no permanent disabiltty, but
pneumonia may develop later.
Concentrations of 100-150 ppm are
dangerous for short exposures of 30-60
minutes. Concentrations of 200-700 ppm
may be fatal after even very short exposures.
Continued exposure to low concentrations
of the fumes, insufficient to cause
pulmonary edema, is said to result in chronic
irritation of the respiratory tract, with cough,
headache, loss of appetite, dyspepsia,
corrosion of the teeth, and gradual loss of
strength.
Exposure to NOx is always potentially
serious, and persons so exposed should be hours.
An oxidizer. The liquid is a sensitive
explosive. Explosive reaction with carbon
disulfide (when ignited), methanol (when
ignited), pentacarbonyl iron (at 50℃),
phosphine + oxygen, sodium diphenylketyl,
dichlorine oxide, fluorine, nitrogen
trichloride, ozone, perchloryl fluoride (at
100-300°C), vinyl chloride. Reacts to form
explosive products with dienes (e.g., 1,3-
butadiene, cyclopentadiene, propadiene).
Can react violently with acetic anhydride,
Al, amorphous boron, BaO, BCl3, CsHC2,
calcium, carbon + potassium hydrogen
tartrate, charcoal, Cl0, pyrophoric
chromium, 1,2-dichloroethane,
dichloroethylene, ethylene, fuels,
hydrocarbons, hydrogen + oxygen, NasO,
uns-dimethyl hydrazine, NH3, CHCl3, Fe,
Mg, Mn, CH2Cl2, olefins, phosphorus,
PNH2, PH3, potassium, potassium sulfide,
propylene, rubidum acetylide, Na, S,
tungsten carbide, trichloroethylene, 1,1,1-
trichloroethane, uns-tetrachloroethane,
uranium, uranium dicarbide. Wdl react with
water or steam to produce heat and
corrosive fumes; can react vigorously with
reducing materials.
processes when nitric acid is made or used.
Oxides of nitrogen have been implicated as
a cause of acid rain.
The oxides of nitrogen are somewhat
soluble in water, reacting with it to form
Nitric oxide is used in the manufacture
of nitric acid; it is also used in the bleaching of rayon;
it is a raw material for nitrosyl halide preparation.
Nitric oxide with the attendant formation of
nitrogen dioxide results in a strong respiratory
irritant that may be fatal. Symptoms may be
moderate at first and include tightness in the
chest, headaches, irritation of the eyes, nausea,
and a slow loss of strength. Delayed symptoms
may be severe and cause increased difficulty in
breathing, chemical pneumonitis, and pulmonary
edema. Untreated cases could lead to
eventual death. Exposure to 100 ppm to 150
ppm of nitrogen oxides for 30-60 minutes could
lead to delayed pulmonary edema, and a few
breaths of nitrogen oxides in 200 ppm to 700
ppm concentrations may result in fatal pulmonary
edema after 5-8 hours have passed.
Acute exposure to nitric oxide alone at high levels results in the rapid formation of methemog[ obin. Nitric oxide itself does not have the marked irritant effect of nitrogen dioxide. However, due to the rapid formation of methemoglobin, greater lethality can be associated with high acute levels of exposure to nitric oxide than with nitrogen dioxide exposures. Initial symptoms such as muscular tremors, drowsiness, a brownish-blue hue to the mucous membranes, increased heart and respiratory rate, vertigo, and vomiting can occur at methemoglobin levels of 30 percent to 40 percent. Coma and death can ensue when methemoglobin levels reach 70 percent to 90 percent.
ACGIH recommends the Threshold Limit Value-Time-Weighted Average (TLV-TWA) of 25 ppm (31 mg/m3 ) for nitric oxide. The TLV-TWA is the time-weighted average concentration for a normal 8-hour workday and a 40-hour workweek, to which nearly all workers may be repeatedly exposed, day after day, without adverse effect.
OSHA lists the 8-hour Time-Weighted Average- Permissiable Exposure Limit (TWA-PEL) of 25 ppm (30 mg/m3 ) for nitric oxide. TWAPEL is the exposure limit that shall not be exceeded by the 8-hour TWA in any 8-hour work shift of a 40-hour workweek. At normal ambient temperatures, nitric oxide combines with atmospheric oxygen to form nitrogen dioxide at a rate dependent on the concentration of oxygen and the square of the concentration of nitric oxide.
Acute exposure to nitric oxide alone at high levels results in the rapid formation of methemog[ obin. Nitric oxide itself does not have the marked irritant effect of nitrogen dioxide. However, due to the rapid formation of methemoglobin, greater lethality can be associated with high acute levels of exposure to nitric oxide than with nitrogen dioxide exposures. Initial symptoms such as muscular tremors, drowsiness, a brownish-blue hue to the mucous membranes, increased heart and respiratory rate, vertigo, and vomiting can occur at methemoglobin levels of 30 percent to 40 percent. Coma and death can ensue when methemoglobin levels reach 70 percent to 90 percent.
ACGIH recommends the Threshold Limit Value-Time-Weighted Average (TLV-TWA) of 25 ppm (31 mg/m3 ) for nitric oxide. The TLV-TWA is the time-weighted average concentration for a normal 8-hour workday and a 40-hour workweek, to which nearly all workers may be repeatedly exposed, day after day, without adverse effect.
OSHA lists the 8-hour Time-Weighted Average- Permissiable Exposure Limit (TWA-PEL) of 25 ppm (30 mg/m3 ) for nitric oxide. TWAPEL is the exposure limit that shall not be exceeded by the 8-hour TWA in any 8-hour work shift of a 40-hour workweek. At normal ambient temperatures, nitric oxide combines with atmospheric oxygen to form nitrogen dioxide at a rate dependent on the concentration of oxygen and the square of the concentration of nitric oxide.
Nitric oxide is converted spontaneously in the air to nitrogen
dioxide; hence, some of the latter gas is present whenever nitric
oxide is found in air (at concentrations below 50 ppm). Nitric
oxide is a contributor to photochemical air pollution.
Nitric oxide should only be used in
well-ventilated areas. Valve protection caps and
valve outlet threaded plugs must remain in place
unless the container is secured and the valve
outlet piped to the point of use. Do not drag,
slide, or roll cylinders. Use a suitable hand truck
to move cylinders. Use a pressure reducing
regulator when connecting a cylinder to lower
pressure (1000 psig or 6900 kPa) piping systems.
Do not heat a cylinder of nitric oxide by
any means to increase the discharge rate from
the cylinder. Use a check valve or trap in the
discharge line to prevent hazardous reverse flow
into the cylinder.
UN1660/124 Nitric oxide, compressed, Hazard
Class: 2.3; Labels: 2.3-Poisonous gas, 5.1-Oxidizer,
8-Corrosive material, Inhalation Hazard Zone A. Cylinders
must be transported in a secure upright position, in a wellventilated
truck. Protect cylinder and labels from physical
damage. The owner of the compressed gas cylinder is the
only entity allowed by federal law (49CFR) to transport
and refill them. It is a violation of transportation regulations
to refill compressed gas cylinders without the express
written permission of the owner.
Bubble the gas through 10M NaOH which removes NO2. It can also be freed from NO2 by passage through a column of Ascarite followed by a column of silica gel held at -197oK. The gas is dried with solid NaOH pellets or by passing through silica gel cooled at -78o, followed by fractional distillation from a liquid N2 trap. This purification does not eliminate nitrous oxide. Other gas scrubbers sometimes used include one containing conc H2SO4 and another containing mercury. It is freed from traces of N2 by the freeze and thaw method. [Blanchard Inorg Synth II 126 1946, Schenk in Handbook of Preparative Inorganic Chemistry (Ed. Brauer) Academic Press Vol I pp 485-487 1963.] TOXIC.
A cytotoxic free radical, nitric oxide impairs mitochondrial ATP
synthesis by inhibiting the citrate cycle and other cellular
mechanisms of electron transport.
A strong oxidizer but may also act as a
reducing agent. Explosive reaction with nitrogen
trichloride, ozone, carbon disulfide; pentacarbonyl iron;
chlorine monoxide. Incompatible with halogens, combustibles,
metals, oil, alcohols, chlorinated hydrocarbons (e.g.,
trichloroethylene), reducing agents (such as NH3), oxygen,
fluorine, metals. Reacts with water to form nitric acid.
Rapidly converted in air to nitrogen dioxide. Combines
very rapidly with oxygen in the air to form nitrogen dioxide.
Nitrogen dioxide reacts with water to form nitric acid
and nitric oxide, reacts with alkalis to form nitrates and
nitrites.
Return refillable compressed
gas cylinders to supplier. Incineration with added hydrocarbon
fuel, controlled so as to produce elemental nitrogen,
CO2, and water. Consult with environmental regulatory
agencies for guidance on acceptable disposal practices.
Generators of waste containing this contaminant (≥100 kg/
mo) must conform with EPA regulations governing storage,
transportation, treatment, and waste disposal.
1.https://en.wikipedia.org/wiki/Nitric_oxide
2.https://www.drugs.com/mtm/nitric-oxide-inhalation-gas.html
3.https://www.britannica.com/science/nitric-oxide
4.http://pediatrics.aappublications.org/content/106/2/344
5.http://www.mensfitness.com/nutrition/supplements/supplement-guide-nitric-oxide
6.https://www.chemicalbook.com/productchemicalpropertiescb5433122.htm
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