@article{oai:niigata-u.repo.nii.ac.jp:00014896, author = {岸本, 美樹 and 金子, 純也 and 三浦, 智史 and 安達, 聡介}, issue = {5}, journal = {新潟医学会雑誌, 新潟医学会雑誌}, month = {May}, note = {Rifampicin, pyrazinamide, streptomycin, and ethambutol, in addition to isoniazid, are frequently used for treatment of Mycobaeterium tuberculosis infections. Rifampicin exhibits its anti-bacterial action throuth binding to RNA polymerase β subunit, and resistance to the drug is caused by a mutation of the β subunit-encoding gene rpoB. Streptomycin inhibits the initiation as well as elongation steps of protein sinthesis through binding to 30S ribosomal subunit (S12 protein and 16S rRNA regions), which also provide an important mutation site for drug resistance. Ethambutol is a strong inhibitor of cell wall synthesis. In ethambutol-treated bacterial cells, arabinan, a component of arabinogalactan, is not generated. Resistance is mainly caused be a mutation of the key enzyme gene embB. Finally, pyrazinamide is considered to be converted to its toxic form (pyrazinoic acid) by the bacterial pyrazinamidase possibly within the phagosome of alveolar macrophage. A lower level of pyrazinamidase is a cause of resistance to the agent.}, pages = {193--198}, title = {抗結核薬リファンピシン, ストレプトマイシン, エタンブトール, ピラジナミドの作用と耐性メカニズム}, volume = {115}, year = {2001} }