The oxidation of propionyl-CoA to form pyruvate is influenced by its necessity in Mycobacterium tuberculosis. Accumulation of propionyl-CoA can lead to toxic effects. In Mycobacterium tuberculosis, it has been suggested that the metabolism of propionyl-CoA is involved in cell wall biogenesis. A lack of such catabolism would therefore increase the susceptibility of the cell to various toxins, particularly to macrophage antimicrobial mechanisms. Another hypothesis regarding the fate of propionyl-CoA, in M. tuberculosisis, is that since propionyl-CoA is produced by beta odd chain fatty acid catabolism, the methylcitrate cycle is activated subsequently to negate any potential toxicity, acting as a buffering mechanism.