Citric acid

Citric acid is an organic compound with a chemical formula HOCCO₂HCH₂CO₂H₂. it is for a colorless weak organic acid. It occurs naturally in citrus fruits. In biochemistry, it is an intermediate in the citric acid cycle, which occurs in the metabolism of any aerobic organisms.

More than two million tons of citric acid are manufactured every year. It is used widely as an acidifier, as a flavoring, together with a chelating agent.

A citrate is a derivative of citric acid; that is, the salts, esters, and the polyatomic anion found in solution. An example of the former, a salt is trisodium citrate; an ester is triethyl citrate. When factor of a salt, the formula of the citrate anion is calculation as HO or HOCOO.

Biochemistry

Citrate is an intermediate in the TCA cycle aka TriCarboxylic Acid cycle, or Krebs cycle, Szent-Györgyi, a central metabolic pathway for animals, plants, and bacteria. Citrate synthase catalyzes the condensation of oxaloacetate with acetyl CoA to draw citrate. Citrate then acts as the substrate for aconitase and is converted into aconitic acid. The cycle ends with regeneration of oxaloacetate. This series of chemical reactions is the mention of two-thirds of the food-derived power in higher organisms. Hans Adolf Krebs received the 1953 Nobel Prize in Physiology or Medicine for the discovery.

Some bacteria notably E. coli can earn and consume citrate internally as part of their TCA cycle, but are unable to use it as food because they lack the enzymes required to import it into the cell. After tens of thousand of evolutions in a minimal glucose medium that also contained citrate during Richard Lenski's Long-Term Evolution Experiment, a variant E. coli evolved with the ability to grow aerobically on citrate. Zachary Blount, a student of Lenski's, and colleagues studied these "Cit^{+" E. coli as a proceeds example for how novel traits evolve. They found evidence that, in this case, the innovation was caused by a rare duplication mutation due to the accumulation of several prior "potentiating" mutations, the identity and effects of which are still under study. The evolution of the Cit+ trait has been considered a notable example of the role of historical contingency in evolution.}

Citrate can be transported out of the mitochondria and into the cytoplasm, then broken down into acetyl-CoA for fatty acid synthesis, and into oxaloacetate. Citrate is a positive modulator of this conversion, and allosterically regulates the enzyme acetyl-CoA carboxylase, which is the regulating enzyme in the conversion of acetyl-CoA into malonyl-CoA the commitment step in fatty acid synthesis. In short, citrate is transported into the cytoplasm, converted into acetyl-CoA, which is then converted into malonyl-CoA by acetyl-CoA carboxylase, which is allosterically modulated by citrate.

High concentrations of cytosolic citrate can inhibit phosphofructokinase, the catalyst of a rate-limiting step of glycolysis. This issue is advantageous: high concentrations of citrate indicate that there is a large provide of biosynthetic precursor molecules, so there is no need for phosphofructokinase to remain to send molecules of its substrate, fructose 6-phosphate, into glycolysis. Citrate acts by augmenting the inhibitory effect of high concentrations of ATP, anotherthat there is no need to carry out glycolysis.

Citrate is a vital component of bone, helping to regulate the size of apatite crystals.