Mitochondria in health and disease by Carolyn D Berdanier

By Carolyn D Berdanier

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The enzyme is inactive in the absence of its allosteric activator, N-acetylglutamate, a compound synthesized from acetyl CoA and glutamate in the liver. As arginine levels increase in the liver, N-acetylglutamate synthetase is activated, which results in an increase in N-acetylglutamate. The urea cycle is initiated in the hepatic mitochondria and finished in the cytosol. The urea is then liberated from arginine via arginase and released into the circulation whereupon it is excreted from the kidneys in the urine.

4 Initial steps in the oxidation of fatty acids by the mitochondrial enzymes. Without carnitine, the oxidation of fatty acids, especially the long chain fatty acids, cannot proceed. Acyl CoA cannot traverse the membrane into the mitochondria by itself; the translocase requires carnitine. Normally, the body synthesizes all the carnitine that it needs for fatty acid oxidation. However, in some instances, endogenous synthesis is inadequate. Premature infants, for example, may require carnitine supplementation and some children with mitochondrial disease may benefit from carnitine supplementation.

The tricarboxylate transporter exchanges malate for citrate. The phosphate transporter exchanges phosphate for a hydroxyl group. The adenine nucleotide transporter exchanges ADP for ATP. The aspartate–glutamate transporter exchanges glutamate for aspartate and, finally, the malate–α-ketoglutarate transporter exchanges malate for α-ketoglutarate. These shuttles are needed because several metabolic intermediates cannot cross the mitochondrial membrane without a carrier and, if no carrier is available, they must be generated within the compartment.

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