The Step of b Oxidation

After saturated fatty acid enter into mitochondrial matrix (help by Carnitine acyl transferase II that linking fatty acidto mitochondrial CoASH) it begin for beta oxidation procces. There are four steps in b oxidation :

  1. oxidation  of a carbon-carbon single bond by FADH to form a crbon-carbon double bond;
  2. addition of H2O to the double bond, with formation of a hydroxyl group on one carbon;
  3. oxidation of the hydroxyl group by NAD + to produce a keto group;
  4. carbon-carbon bond cleavage, realesing acetyl CoA.

b-Oxidation of saturated fatty acids. One round of b-oxidation consists of four enzyme-catalyzed reactions. Each round generates one molecule each of QH2, NADH, acetyl CoA,and a fatty acyl CoA molecule two carbon atoms shorter than the molecule that entered the round. (ETF is the electron-transferring flavoprotein, a water-soluble protein coenzyme.)

The b-oxidation pathway. (a) In each pass through this four-step sequence, one acetyl residue (shaded in pink) is removed in the form of acetyl-CoA from the carboxyl end of the fatty acyl chain—in this example palmitate (C16), which enters as palmitoyl-CoA. (b) Six more passes through the pathway yield seven more molecules of acetyl-CoA, the seventh arising from the last two carbon atoms of the 16-carbon chain. Eight molecules of acetyl-CoA are formed in all.

The net reaction for the process of b oxidation of a saturated fatty acid, palmitoyl CoA (the CoA ester of palmitic acid), is as follows :

Palmitoyl SCoA + 7 FAD + NAD+ + 7 CoASH + 7 H2O → 8 acetyl SCoA + 7 FADH2 + 7 NADH + 7 H+

The complete degradation of palmitoyl CoA requires seven turns of b oxidation and each round requires the entry of an FADH, NAD+, H2O and CoASH.

Reaction faot fatty acid activation, transport, and the b-oxidation spiral

Reaction Number



Reaction Typea


Fatty acid + CoASH + ATP D Acyl SCoA + AMP + PPi Acyl-SCoA syntheatase



PPi + H2O D 2 Pi Pyrophosphatase



Carnitine + acyl SCoA D acyl carnitine + CoASH (intermembrane space) Carnitine acyltransferase I



Acyl carnitine + CoASH D acyl SCoA + carnitine(mitochondria) Carnitine acyltransferase II



Acyl SCoA + E-FAD D trans-r2-enoyl SCoA + E-FADH2b Acyl-SCoA dehydrogenase



trans-r2-enoyl SCoA + H2O D L-3-Hydroxyacyl SCoA Enoyl-SCoA hydrase



L-3-Hydroxyacyl SCoA + NAD+ D 3-ketoacyl SCoA + NADH + H+ Hydroxyacyl-SCoA dehydrogenase



3-ketoacyl SCoA + CoASH D acetyl SCoA + acyl SCoAc b-ketothiolase


aReaction type : 1.oxidation-reduction; 2. group transfer; 3. Hydrolysis; 4. nonhydrolytic (addition-elimination); 5. Isomerization-rearrangement; 6. Bond formation coupled to ATP cleavagebE-FAD and E-FADH2 refer to the cofactor flavin adenine dinuctiotide covalently linked to the enzyme

cAcyl SCoA product is shortened by a C2 unit

Significance of b Oxidation

Beta product yields products that are of great metabolic importance. The net reaction for the combined activation and b oxidation of palmitic acid is the following :

Palmitic acid+ ATP + 7 FAD + NAD+ + 8 CoASH + 8 H2O → 8 acetyl SCoA + AMP + 2 Pi + 7 FADH2 + 7 NADH + 7 H+

The acetyl CoA is ready for further oxidation by citric acid cycle. The reduced of b oxidation, NADH and FADH2, are recycled by the transport electron chain and ATP is generated by oxidatiove-phosporylation. The Complate oxidation of palmitate to CO2 and H2O yield 129 ATP.

Stages of fatty acid oxidation. Stage 1: A long-chain fatty acid is oxidized to yield acetyl residues in the form of acetyl- CoA. This process is called b oxidation. Stage 2: The acetyl groups are oxidized to CO2 via the citric acid cycle. Stage 3: Electrons derived from the oxidations of stages 1 and 2 pass to O2 via the mitochon- drial respiratory chain, providing the energy for ATP synthesis by oxidative phosphorylation.

Energy yield from the complete oxidation of palmitate

Metabolic Stage



Substrate-level Phosphorylation

CoA activation




b oxidation(seven cycle)

7 (mitochondria)



Citric acid cycle(eight cycle)

24 (mitochondria)







31 NADH X 3 ATP = 93 ATP
15 FADH2 X 2 ATP =30 ATP
     Grand total 129 ATP

β Oxidation of Fatty Acids with Odd Numbers of Carbons


These are catabolized by normal P oxidation. The final cleavage step, yields an acetyl CoA and a C3 unit, propionyl CoA. Propionyl CoA does not enter the citric acid cycle as acetyl CoA does but must be transformed to succinyl CoA. Three reactions are required for this conversion:

(1) carboxylation to D-methylmalonyl CoA,

(2) isomerization to L,-methylmalonyl CoA, and

(3) rearrangement to succinyl CoA.

The enzyme, methylmalonyl CoA mutase is of special interest be­cause its cofactor is the unusual molecule coenzyme B12 (deoxyadenosylcobalamin). This Coenzyme, which is derived from vitamin B12, is associated with enzymes cat­alyzing carbon skeleton rearrangements and with enzymes involved in purine and thymidine synthesis. Ribonucleotide reductase, an en­zyme found in many prokaryotic species, uses a vitamin B12 cofactor.

Neither plants nor animals are able to synthesize vitamin B12;it can be synthesized only by a few species of bacteria. Carnivorous animals obtain sufficient amounts of B12 from meat in their diet; however, herbivorous animals depend on intestinal bacteria for synthesis of B12. Only very small amounts (about 3 µg/day) are required by adult humans so nutri­tional deficiency is rare.

Symptoms of deficiency are observed in individuals with pernicious anemia and occasionally in strict vegetarians. It was discovered in 1926 that pernicious anemia could be prevented by eating large quantities of liver. The ac­tive compound in liver was identified in 1948 and called vitamin B12 or cobalamin.

The final cleavage step in the P oxidation of an odd-numbered fatty acid and the transformation of the product, propionyl CoA, to succinyl CoA for entry into the citric acid cycle. The propionyl CoA undergoes carboxylation to a C4 metabolite, D-methylmalonyl CoA. After two rearrangement steps, succinyl CoA emerges.

Pernicious anemia is caused not by a deficiency of B12,but by impaired absorption of the vitamin in the intestines. Large quantities of B12 obtained in the diet (or by in­jection) permit an affected individual to absorb sufficient amounts. Symptoms of pernicious anemia are sometimes observed in vegetarians, but are slow in develop­ing because the normal adult liver stores enough vitamin B12 for 3 to 5 years.


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