My colic acid

The answer is a. (Hardman, p 1157. Katzung, p 804J Isoniazid inhibits mycobacterial cell-wall synthesis by inhibiting my colic acid synthesis by a mechanism that is not fully understood. 

Fractionation of mycobacteria resulted in the identification of two cellular immunostimulatory components, namely TDM and MDPs. Both are normally found in association with the mycobacterial cell wall. TDM is composed of a molecule of trehalose (a disaccharide consisting of two molecules of a-D-glucose linked via an a 1-1 glycosidic bond), linked to two molecules of my-colic acid (a long-chain aliphatic hydrocarbon-based acid) found almost exclusively in association with mycobacteria. TDM, although retaining its adjuvanticity, is relatively non-toxic. 

Mechanism of Action An isonicotinic acid hydrazide (INH) derivative that inhibits my-colic acid synthesis and causes disruption of the bacterial cell wall and loss of acid-fast properties in susceptible mycobacteria. Active only during bacterial cell division. Therapeutic Effect Bactericidal against activelygrowingintracelleluar and extracellular susceptible mycobacteria. 

These are further modified by esterification with my-colic acids.133 Information on some other cell wall components is given in Chapter 20. 

Colorless wax. Yields trehalose and my colic acid upon alkaline hydrolysis. 

Isoniazid is bacteriostatic for resting bacilli but bactericidal for dividing microorganisms. Isoniazid is a prodrug that is converted by mycobacterial catalase-peroxidase into an active metabolite. It inhibits biosynthesis of my colic acids—long, branched lipids that are attached to a unique polysaccharide in the mycobacterial cell wall. Mycolic acids are unique to mycobacteria. The target of the isoniazid derivative is enoyl-ACP reductase of fatty acid synthase II, which converts unsaturated to saturated fatty acids in mycolic acid biosynthesis. 

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