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The Citric Acid Cycle
Published in Jean-Louis Burgot, Thermodynamics in Bioenergetics, 2019
It is a redox reaction. NAD+ oxidizes the pyruvate ion whereas it is reduced itself in NADH. More precisely, it is an oxidative decarboxylation reaction which evolves under the enzymatic action of the pyruvate dehydrogenase. The pyruvate dehydrogenase is a complex of three enzyme components (We shall not describe further the mechanism of action mechanism of this enzymatic complex) formed by three kinds of enzymes.
In-situ transesterification of single-cell oil for biodiesel production: a review
Published in Preparative Biochemistry & Biotechnology, 2023
Tasneem Gufrana, Hasibul Islam, Shivani Khare, Ankita Pandey, Radha P.
De novo lipid production can occur in oleaginous microbes in nitrogen-limited environments with abundant carbon supply. Figure 1 depicts the de novo lipid mechanism pathway. Under nitrogen deficiency, the microbial cells ingest the carbon source by converting it to storage lipids, which are then deposited in the cytosol as lipid droplets.[78–82] Lipid production takes place in two stages when carbon is present in excess. First, there is cell division, followed by growth and exhaustion of all nutrients except carbon, and the second phase is followed by the transformation of excess carbon into lipid reserves. Hence, cells can no longer expand and multiply as they do not have enough nitrogen.[76] Microbial cells undergo the glycolysis pathway in the cytoplasm, where glucose gets converted to pyruvate and releases ATP in the form of energy. Pyruvate is transported to mitochondria, and it further undergoes oxidative decarboxylation to generate acetyl CoA, which then enters the Tricarboxylic acid (TCA) cycle or Kreb’s cycle. The microbes produce huge amounts of citric acid and iso-citric acid (intermediates of the TCA cycle), which cannot be further catabolized by the TCA cycle. Moreover, as nitrogen is exhausted, cells require NH4+ ions for cell maintenance. This is achieved by cleavage of available adenosine monophosphate (AMP) to inosine5’monophosphate (IMP) and NH3.[83] The decrease in the AMP level affects the function of the NAD+-isocitrate dehydrogenase. Consequently, isocitrate is not metabolized, which results in a build-up of isocitrate and citric acid in mitochondria.[34,84] Finally, the ATP-citrate lyase (ACL), a key enzyme in lipid accumulation, cleaves citric acid to produce acetyl-CoA and oxaloacetate. Hence, citric acid must be readily available in the cell’s cytoplasm, where fatty acid synthesis occurs. As a result, citric acid, and specifically acetyl-CoA, becomes a substrate for fatty acid production.[83]