2,4-Dinitrophenol

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2,4-Dinitrophenol
2,4-Dinitrophenol.svg
2,4-Dinitrophenol 3D.png
2,4-Dinitrophenol.jpg
Sample of pure compound
Names
Preferred IUPAC name
2,4-Dinitrophenol
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.000.080
KEGG
UNII
UN number 0076Dry or wetted with less than 15% water. Class 1.1D explosives
1320Wetted with not less than 15% water. DT Solid desensitized explosives, toxic
1599Toxic solution
Properties
C6H4N2O5
Molar mass 184.107 g·mol−1
Density 1.683 g/cm3
Melting point 108 °C (226 °F; 381 K)
Boiling point 113 °C (235 °F; 386 K)
Acidity (pKa) 4.114
-73.1·10−6 cm3/mol
Hazards
Safety data sheet International Chemical Safety Card 0464
GHS pictograms The exploding-bomb pictogram in the Globally Harmonized System of Classification and Labelling of Chemicals (GHS) The skull-and-crossbones pictogram in the Globally Harmonized System of Classification and Labelling of Chemicals (GHS) The health hazard pictogram in the Globally Harmonized System of Classification and Labelling of Chemicals (GHS) The environment pictogram in the Globally Harmonized System of Classification and Labelling of Chemicals (GHS)
GHS signal word DANGER
H201, H300, H311, H331, H372, H400
P261, P273, P280, P301+310, P311
NFPA 704
Flammability code 3: Liquids and solids that can be ignited under almost all ambient temperature conditions. Flash point between 23 and 38 °C (73 and 100 °F). E.g., gasolineHealth code 3: Short exposure could cause serious temporary or residual injury. E.g., chlorine gasReactivity code 3: Capable of detonation or explosive decomposition but requires a strong initiating source, must be heated under confinement before initiation, reacts explosively with water, or will detonate if severely shocked. E.g., fluorineSpecial hazards (white): no codeNFPA 704 four-colored diamond
3
3
3
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Infobox references

2,4-Dinitrophenol (2,4-DNP or simply DNP) is an organic compound with the formula HOC6H3(NO2)2. It is a yellow, crystalline solid that has a sweet, musty odor. It sublimes, is volatile with steam, and is soluble in most organic solvents as well as aqueous alkaline solutions.[1] It is a precursor to other chemicals and is biochemically active, inhibiting energy (adenosine triphosphate, ATP) production in cells with mitochondria. Its use in high doses as a dieting aid has been identified with severe side-effects, including a number of deaths.[2]

Synthesis[edit]

DNP is produced by hydrolysis of 1-chloro-2,4-dinitrobenzene.[3] Another route of DNP synthesis is by nitration of phenol with nitric acid.[4][5]

Uses[edit]

Commercial DNP is used as an antiseptic and as a non-selective bioaccumulating pesticide.[6] It is a chemical intermediate in the production of sulfur dyes,[3] wood preservatives[6] and picric acid.[7] DNP has also been used to make photographic developers and explosives (see shellite).[8] DNP is classified as an explosive in UK[9] and USA.[10] From December 2018 DNP is classified as "illegal poisonous substance" in Russia.[11][12]

DNP is particularly used as a herbicide alongside with other closely related dinitrophenol herbicides like 2,4-dinitro-o-cresol (DNOC), dinoseb and dinoterb.[13]

Chemical hazards[edit]

Dust explosion possible if in powder or granular form, mixed with air. May explosively decompose on shock, friction or concussion. May explode on heating.[14] DNP forms explosive salts with strong bases and ammonia, and emits toxic fumes of nitrogen dioxide when heated to decomposition.[15] DNP explosive strength is 81% of TNT according to Trauzl lead block test.[16] DNP was the cause of explosion in 1916 Rainham Chemical Factory, 7 dead and 69 injured.[17][18]

Biochemical aspects[edit]

In living cells, DNP acts as a proton ionophore, an agent that can shuttle protons (hydrogen cations) across biological membranes. It dissipates the proton gradient across mitochondria and chloroplast membranes, collapsing the proton motive force that the cell uses to produce most of its ATP chemical energy. Instead of producing ATP, the energy of the proton gradient is lost as heat.[2]

DNP is often used in biochemistry research to help explore the bioenergetics of chemiosmotic and other membrane transport processes.

Health effects[edit]

DNP is considered to have high acute toxicity.[6] Acute oral exposure to DNP has resulted in increased basal metabolic rate, nausea, vomiting, sweating, dizziness, headache, and loss of weight.[6] Chronic oral exposure to DNP can lead to the formation of cataracts and skin lesions and has caused effects on the bone marrow, central nervous system, and cardiovascular system.[6][19] Contact with skin or inhalation can cause DNP poisoning. In 2009, an incident occurred in a Chinese chemical factory and 20 persons suffered acute DNP poisoning.[20]

Dieting aid[edit]

DNP was used extensively in diet pills from 1933 to 1938 after Cutting and Tainter at Stanford University made their first report on the drug's ability to greatly increase metabolic rate.[21][22] After only its first year on the market Tainter estimated that at least 100,000 people had been treated with DNP in the United States, in addition to many others abroad.[23] DNP acts as a protonophore, allowing protons to leak across the inner mitochondrial membrane and thus bypass ATP synthase. This makes ATP energy production less efficient. In effect, part of the energy that is normally produced from cellular respiration is wasted as heat. The inefficiency is proportional to the dose of DNP that is taken. As the dose increases and energy production is made more inefficient, metabolic rate increases (and more fat is burned) in order to compensate for the inefficiency and to meet energy demands. DNP is probably the best known agent for uncoupling oxidative phosphorylation. The "phosphorylation" of adenosine diphosphate (ADP) by ATP synthase gets disconnected or "uncoupled" from oxidation.

The factor that limits ever-increasing doses of DNP is not a lack of ATP energy production, but rather an excessive rise in body temperature due to the heat produced during uncoupling. Accordingly, DNP overdose will cause fatal hyperthermia, with body temperature rising to as high as 43.1 °C (109.6 °F)[24] shortly before death. In light of this, when it was used clinically, the dose was slowly titrated according to personal tolerance, which varies greatly.[25]

Case reports have shown that an acute administration of 10–20 mg per kilogram of body weight in humans can be lethal.[26][27][28][29][30] The lowest published fatal ingested dose is 4.3 mg/kg.[8][31] One dose, as few as two tablets have proved fatal.[28][32] "In studies of intermediate-duration oral exposure to 2,4-DNP, cases of death from agranulocytosis (described in the discussion of Hematological Effects) have been attributed to 2,4-DNP. These cases occurred during the usual dosing regimens for weight loss, employing increasing doses in one case from 2.9 to 4.3 mg/kg/day of 2,4-DNP for 6 weeks (Dameshek and Gargill 1934); a dose of 1.03 mg/kg/day 2,4-DNP for 46 days in another case (Goldman and Haber 1936); and in another, from 0.62 to 3.8 mg/kg/day 2,4-DNP as sodium 2,4-DNP for 41 days (Silver 1934). In all cases, the patients were under medical supervision."[33]

Concerns about dangerous side-effects and rapidly developing cataracts[34] resulted in DNP being discontinued in the United States by the end of 1938.[35] DNP, however, continues to be used by some bodybuilders and athletes to rapidly lose body fat. Fatal overdoses include cases of accidental exposure,[36] suicide,[26][37][38] and excessive intentional exposure (overdose).[37][39][40] The substance's use as a dieting aid has also led to a number of accidental fatalities,[41][42][43][44][45][46] including 25 confirmed DNP-related deaths in UK since 2007.[47] Annual Reports of the American Association of Poison Control Centers identifies 15 DNP poisoning fatalities between 2013 and 2017 in US.[48] Swedish Poisons Information Centre has reported three fatal DNP cases between June 2012 and May 2013. “Forensic analysis of DNP is not routinely performed so the true number of DNP deaths may be higher.”[49] DNP may not be detected in post mortem blood samples.[32]

Although DNP is widely considered too dangerous for clinical use, its mechanism of action remains under investigation as a potential approach for treating obesity.[50] Currently, research is being conducted on uncoupling proteins naturally found in humans.[51]

The United Kingdom's Food Standards Agency identifies DNP as "an industrial chemical known to have serious short-term and long-term effects, which can be extremely dangerous to human health." and advises "consumers not to take any product containing DNP at any level. This chemical is not suitable for human consumption."[52]

Pharmacokinetics[edit]

Information about pharmacokinetics of DNP in humans is limited and conflicting. The EPA states that "Data on the elimination kinetics of the dinitrophenols or their metabolic products in humans were not found."[53] The ATSDR's Toxicological Profile for Dinitrophenols also states that "No studies were located regarding distribution in humans after oral exposure to 2,4-DNP. Limited information is available regarding distribution in animals after oral exposure to 2,4-DNP." However, they do state that "Elimination from the body appears to be rapid, except possibly in cases of compromised liver function."[54] This coincides with a review in the NEJM on the biological actions of dinitrophenol, which stated that "Judging from the metabolic response, DNP appears to be eliminated entirely in three or four days; in the presence of liver or kidney damage it is possible that the drug will be retained over a longer period."[55] Oddly, more recent papers give an array of possible half-lives, ranging from 3 hours,[56] to 5–14 days.[26] Other recent papers maintain that the half-life in humans is unknown.[37]

Although further investigation is needed, one case report notes that dinitrophenol-induced hyperthermia has been successfully resolved with dantrolene administration.[57] However, the latest fatal case in UK reports dantrolene use in acute DNP poisoning may be ineffective.[28]

"Dinitrophenol uncouples oxidative phosphorylation, causes release of calcium from mitochondrial stores and prevents calcium re-uptake. This leads to free intracellular calcium and causes muscle contraction and hyperthermia. Dantrolene inhibits calcium release from the sarcoplasmic reticulum which reduces intracellular calcium. The resulting muscle relaxation allows heat dissipation. There is little risk to dantrolene administration. Since dantrolene may be effective in reducing hyperthermia caused by agents that inhibit oxidative phosphorylation, early administration may improve outcome."[58]

Just a few successful DNP overdose treatment cases has been published in the medical literature.[59][29][60] Currently is no antidote available and "death may occur in spite of the best possible medical treatment."[61][62]

Potential DNP/DNOC antidote MIGU-2 research was published in Ukrainian Journal of Emergency Medicine.[63] Study published in India “demonstrates the efficacy of purified compound TCCP from T. cordifolia in neutralizing DNP induced oxidative stress in blood components.”[64]

Commerce[edit]

In 2003, a vendor of DNP was sentenced to prison for mail fraud, with the FDA's OCI investigators having gathered evidence that the vendor's encapsulation of DNP was neither accurate nor sanitary.[65] In 2018, a seller in United Kingdom was convicted of manslaughter for selling DNP as "fatburner" for human consumption.[66][67] In 2019, a company selling DNP in UK was found "guilty of placing an unsafe food product on to the market" and fined £100000. Director of the company was given suspended prison sentence.[68]

Environmental effects[edit]

DNP is considered an important environmental contaminant by the United States Environmental Protection Agency. It has been found in 61 of 1400 priority sites that need clean-up of industrial waste. It can enter the air from automobile exhaust, burning of certain industrial substances, and from reaction of nitrogen in air with other atmospheric chemicals. The major site of degradation is the soil, where microorganisms metabolize it.

However, the effects of DNP on anaerobic micro-organisms are still largely undetermined. Some studies suggest that there is anaerobic toxicity due to a reduced methane production.

References[edit]

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Further reading[edit]

External links[edit]