@article{oai:niigata-u.repo.nii.ac.jp:00015055,
 author = {三浦, 智史},
 issue = {1},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Jan},
 note = {Isoniazid, a synthetic antimicrobial agent, was found to be effective against tuberculosis in 1952 and still remains a valuable drug for the prophlaxis and treatment of Mycobacterium tuberculosis infections. Isoniazid shows its harmful effect on M. tuberculosis through activation by KatG (catalase-peroxidase). The primary target of the activated structure is InhA (NADH-dependent, 2-trans enoyl-acyl carrier protein reductase), whose inactivation results in loss of the precursor to mycolic acid (a major component of the cell wall skeleton) and accumulation of hexacosanoic acid (C26:0), Isoniazid resistance was thus conferred by mutations in the kat G gene as well as inhA gene. Involvement of additional genes such as ahpC (encoding alkyl hydroperoxidase), kasA/B (encoding B-ketoacyl ACP synthase), or ndh (encoding NADH dehydrogenase) have also been proposed. It is considered that the mutations in the katG, inhA, and ahpC genes cover up to 80% of isoniazid resistance of clinical isolates of M. tuberculosis.},
 pages = {13--18},
 title = {結核菌の化学予防剤イソニアジドへの耐性},
 volume = {115},
 year = {2001}
}