2,4-Dinitrophenol

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Template:Chembox E number
2,4-Dinitrophenol
IUPAC name 2,4-dinitrophenol
Other names Solfo Black
Identifiers
3D model (JSmol)
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Properties
C6H4N2O5
Molar mass 184.106
Density 1.683 g/cm³
Melting point
Boiling point
Hazards
R/S statement R: 10, 23, 24, 25, 33
S: 1, 2, 28, 37, 45
Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)

Infobox disclaimer and references

2,4-Dinitrophenol (DNP), C6H4N2O5, is a cellular metabolic poison. It uncouples oxidative phosphorylation by carrying protons across the mitochondrial membrane, leading to a rapid consumption of energy without generation of ATP.

Dinitrophenols as a class of compounds, of which there are six members, do not occur naturally but are all manufactured compounds.

Chemical properties

2,4-Dinitrophenol is a yellow, crystalline solid that has a sweet, musty odor. It sublimes when carefully heated and is volatile with steam. It is soluble in water (sparingly) (its crystalline sodium salts are also soluble in water), cold water (sparingly), ethyl acetate, acetone, chloroform, pyridine, carbon tetrachloride, toluene, alcohol, benzene, and aqueous alkaline solutions (Merck, 1989). It forms explosive salts with alkalies and ammonia, and emits toxic fumes of nitrogen oxides when heated to decomposition (Sax, 1989). It is incompatible with heavy metals and their compounds.

Industrial uses

Commercial DNP is primarily used for scientific research and in manufacturing. It has been used at times to make dyes, other organic chemicals, and wood preservatives. It has also been used to make photographic developer, explosives, and pesticides.

Pharmacological action

In living cells, DNP acts as a proton ionophore, an agent that can shuttle protons (hydrogen ions) across biological membranes. It defeats 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. Cells counteract the lowered yields of ATP by oxidizing more stored reserves such as carbohydrates and fat.

DNP is often used in biochemistry research to help explore the regulation of bioenergetics in different organisms.

Environmental toxicity

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 there is anaerobic toxicity due to a reduced methane production.

Use as dieting aid

DNP was used extensively in the 1930s in diet pills after Cutting and Tainter at Stanford University made their first report on the drug's ability to greatly increase metabolic rate. DNP acts as a protonophore in the mitochondrial membrane, uncoupling oxidative phosphorylation and making ATP energy production less efficient. In effect, part of the energy that is normally produced from cellular respiration is wasted as heat. This inefficiency is proportional to the dose of DNP that is taken. Thus, as the dose increases and energy production is made less efficient, the metabolic rate is increased (and more fat is burned) in order to compensate for the inefficiency and meet energy demands. Interestingly, 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 a fatal fever. Concerns about dangerous side-effects and rapidly developing cataracts resulted in DNP being discontinued in the United States by the end of 1938. DNP, however, continues to be used by some bodybuilders and athletes to rapidly lose body fat. Fatal overdoses are rare, but are still reported on occasion.[1][2] In 2007, a German woman died after ingesting DNP.[3][4]

While DNP itself is considered by many to be too risky for human use, its mechanism of action remains under investigation as a potential approach for treating obesity.[5] Currently, research is being conducted on uncoupling proteins naturally found in humans.

References

  1. McFee RB, Caraccio TR, McGuigan MA, Reynolds SA, Bellanger P (2004). "Dying to be thin: a dinitrophenol related fatality". Veterinary and human toxicology. 46 (5): 251–4. PMID 15487646.
  2. Miranda EJ, McIntyre IM, Parker DR, Gary RD, Logan BK (2006). "Two deaths attributed to the use of 2,4-dinitrophenol". Journal of analytical toxicology. 30 (3): 219–22. PMID 16803658.
  3. newspaper Die Welt september 18, 2007
  4. newspaper Focus spetember 18, 2007
  5. Harper JA, Dickinson K, Brand MD (2001). "Mitochondrial uncoupling as a target for drug development for the treatment of obesity". Obesity reviews : an official journal of the International Association for the Study of Obesity. 2 (4): 255–65. PMID 12119996.

Further reading

External links

de:Dinitrophenol it:2,4-dinitrofenolo



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