bacitracin brands

Molecular formula: C66H103N17O16S

Bacitracin binds to a divalent metal ion such as Mn(II), Co(II), Ni(II), Cu(II), or Zn(II). These complexes bind C₅₅-isoprenyl pyrophosphate, preventing the hydrolysis of a lipid dolichol pyrophosphate, which finally inhibits cell wall synthesis. Bacitracin metal complexes also bind and oxidatively cleave DNA. Bacitracin interferes with bacterial cell wall synthesis by blocking the function of the lipid carrier molecule that transfers cell wall subunits across the cell membrane. It is active against many gram positive bacteria including staphylococci, streptococci (particularly group A streptococci), corynebacteria, and clostridia. It is also active against Actinomyces, Treponema pallidum and some gram negative species such as Neisseria and Haemophilus influenzae, although most Gram-negative organisms are resistant. . Bacitracin may be bactericidal or bacteriostatic in action, depending on the concentration of the drug attained at the site of infection and the susceptibility of the infecting organism. Bacitracin inhibits bacterial cell wall synthesis by preventing the incorporation of amino acids and nucleotides into the cell wall. The drug probably interferes with the final dephosphorylation step in the phospholipid carrier cycle and in this manner bacitracin prevents the transfer of the mucopeptide to the growing cell wall. Bacitracin also damages the bacterial plasma membrane and is active against protoplasts. Bacitracin is a polypeptide antibiotic active against Gram-positive bacterial strains. Its mechanism of action postulates disturbing the cell wall synthesis by inhibiting dephosphorylation of the lipid carrier. We have discovered that bacitracin induces degradation of nucleic acids, being particularly active against RNA. In the examination of the nucleolytic activity of bacitracin several model RNA and DNA oligomers were used. The oligomers were labeled at their 5' ends with (32)P radioisotope and following treatment with bacitracin the cleavage sites and efficiency were determined. Bacitracin induces degradation of RNA at guanosine residues, preferentially in single-stranded RNA regions. Bacitracin is also able to degrade DNA to some extent but comparable effects to those observed with RNA require its 10-fold higher concentration. The sites of degradation in DNA are very infrequent and preferentially occur near cytidine residues. Free radicals are not involved in the reaction, and which probably proceeds via a hydrolytic mechanism. The phosphate groups at the cleavage sites are present at the 3' ends of RNA products and at the 5' ends of DNA fragments. Importantly, the presence of EDTA does not influence RNA degradation but completely inhibits the degradation of DNA. For DNA degradation divalent metal ions like Mg(2+), Mn(2+) or Zn(2+) are absolutely necessary. The ability of bacitracin to degrade nucleic acids via a hydrolytic mechanism was a surprising observation, and it is of interest whether these properties can contribute to its mechanisms of action during antibiotic treatment.

Source: PubChem (NCBI) · compound 10909430