144 1. lODOACETATE AND lODOACETAMIDE 



" Radioactivity in counts/min/g dry wt. 



below^ 0.5 mM will not produce much direct effect on fatty acid oxi- 

 dation. 



The oxidation of glycerol by bacteria is inhibited potently by iodoacetate 

 — 63% by 0.1 mM and 86% by 0.5 mM (Mickelson and Shideman, 1947) — 

 v^^hich is not surprising since the pathway postulated is 



Glycerol -> a-glycerol-P -> 3-P-glyceraldehyde -> P-glycerate 



and involves glycerol kinase (which is sensitive, as seen in Table 1-23) and 

 3-PGDH. Inasmuch as the inhibition of the oxidation of a-glycerol-P is 

 just as strong, it is likely that the major site is 3-PGDH. It is surprising 

 that G.J.E. Hunter (1953) found only 34 68% inhibition of glycerol oxi- 

 dation by 10 mM iodoacetate in various mycobacteria. The oxidation of 

 lysolecithin by avian Mycobacterium tuberculosis is reduced 19% by 0.1 mM, 

 46% by 1 mM, and 92% by 10 mM iodoacetate, but the pathway involved 

 is not known (Hoshino, 1959). Oxidation of steroids is resistant to iodoace- 

 tate (Levy and Talalay, 1959). 



Biosynthesis of Lipids 



Determinations of tissue lipid changes with time as affected by iodoace- 

 tate reflect disturbances in the balance between lipid synthesis and catab- 

 olism. The lipid content of pea stems is initially 8.95% (dry weight), after 

 incubation with auxin is 6.18%, and with auxin and iodoacetate (at a con- 

 centration inhibiting growth 50%) is 7.44% (Christiansen and Thimann, 

 1950 b). Is iodoacetate in some way accelerating synthesis of lipid or is it 

 reducing the utilization of lipid? In this instance lipid is being converted to 

 carbohydrate and iodoacetate inhibits this. It is unlikely that the iodoace- 

 tate stimulates lipid synthesis in any case, and all the evidence points to a 

 rather strong depression. Lipid formation in yeast, for example, is inhibited 

 24% by 0.01 mM iodoacetate (Hoffmann-Ostenhof and Kriz, 1949 b). 



