Phospholipids of ethambutol-susceptible and resistant strains ofMycobacterium smegmatis

Sareen, M. L.; Khuller, G. K.

doi:10.1007/bf02712147

Cited by 9 publications

(7 citation statements)

References 21 publications

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“…Subcellular fractions were isolated and purified by differential centrifugation by the method of Kearney and Goldman (9 was a significant (P < 0.001) decrease in the content of PIMs, phosphatidylethanolamine, and cardiolipin. The decrease in TPL content of the EMB-resistant mutant was in accordance with our previous observations with EMB-resistant Mycobacterium smegmatis (16). Since quantitative changes were observed in the TPL content of the EMBresistant strain, precursor incorporation studies were carried out to determine the rate of phospholipid synthesis.…”

Section: Methodssupporting

confidence: 89%

Cell wall and membrane changes associated with ethambutol resistance in Mycobacterium tuberculosis H37Ra

Sareen

Khuller

1990

Antimicrob Agents Chemother

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Biochemical variations accompanying the acquisition of ethambutol (EMB) resistance in a single-step mutant of Mycobacterium tuberculosis H37Ra were analyzed. Comparative analysis of phospholipids revealed a reduced content in the EMB-resistant strain, particularly in the cell membrane fraction. Significant alterations were observed in the individual phospholipid content and phospholipid fatty acyl group composition of whole cells and subcellular fractions. Quantitative changes were seen in the chemical constituents of the cell walls of resistant cultures in comparison with those of EMB-susceptible cultures of M. tuberculosis. Alterations in the binding of 1-anilinonaphthalene-8-sulfonate to whole cells of an EMB-resistant strain indicated structural changes on the ceHl surface. Structural changes in the cell wall may play an important role in the resistance of M. tuberculosis H37Ra to EMB.

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Section: Methodssupporting

confidence: 89%

Cell wall and membrane changes associated with ethambutol resistance in Mycobacterium tuberculosis H37Ra

Sareen

Khuller

1990

Antimicrob Agents Chemother

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“…The mycobacterial cell wall is a highly hydrophobic structure with a mycoylarabinogalactan-peptidoglycan skeleton (27,105,106,322,389,390,461,530). The peptidoglycan is covalently linked to the polysaccharide copolymer (arabinogalactan) made up of arabinose and galactose esterified to mycolic acids.…”

Section: Intrinsic Bacterial Resistance Mechanismsmentioning

confidence: 99%

“…Treatment of this organism with m-fluoro-DL-phenylalanine (m-FL-phe), which inhibits mycocide C synthesis, produces significant alterations in the outer cell wall layers (106). Ethambutol, an inhibitor of arabinogalactan (391,501) and phospholipid (461,462) synthesis, also disorganizes these layers. In addition, ethambutol induces the formation of ghosts without the dissolution of peptidoglycan (391).…”

Section: Intrinsic Bacterial Resistance Mechanismsmentioning

confidence: 99%

Antiseptics and Disinfectants: Activity, Action, and Resistance

McDonnell¹,

1999

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SUMMARY Antiseptics and disinfectants are extensively used in hospitals and other health care settings for a variety of topical and hard-surface applications. A wide variety of active chemical agents (biocides) are found in these products, many of which have been used for hundreds of years, including alcohols, phenols, iodine, and chlorine. Most of these active agents demonstrate broad-spectrum antimicrobial activity; however, little is known about the mode of action of these agents in comparison to antibiotics. This review considers what is known about the mode of action and spectrum of activity of antiseptics and disinfectants. The widespread use of these products has prompted some speculation on the development of microbial resistance, in particular whether antibiotic resistance is induced by antiseptics or disinfectants. Known mechanisms of microbial resistance (both intrinsic and acquired) to biocides are reviewed, with emphasis on the clinical implications of these reports.

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“…TBSA is a major fatty acid among M. smegmatis phospholipids ( 21 , 22 ); in particular, PIMs exclusively carry TBSA at the sn -1 position of glycerol ( 23 ). If Cfa is involved in TBSA synthesis, the lack of cfa will result in changes in fatty acid composition, which may not be detected by low-resolution HPTLC analysis of bulk lipids.…”

Section: Resultsmentioning

confidence: 99%