Silver sulfadiazine (CF-100) binds to deoxyribonucleic acid (DNA) but not to ribonucleic acid (RNA). DNA degradation is not observed. Nucleic acid and protein synthesis are not inhibited by silver sulfadiazine in cell-free systems. Conformational changes in the DNA are observed as evidenced by altered thermal transition, suggesting that silver sulfadiazine is inhibiting DNA replication.

Silver chelates of uracil and uracil derivatives yield biologically active compounds effective against several strains of bacteria including P. aeruginosa with minimal toxicity to the host in vitro. Toxicity studies conducted in tissue culture revealed comparative toxicity equal to that of the control containing penicillin and streptomycin. In vivo studies indicated no apparent toxicity. These silver uracil derivatives do not react with chlorides, hydroxides or iodides and are extremely toxic to Protozoa such as Paramecium and Euglena in vitro. One of thesecompounds (AgBU) was studied by Cs₂SO₄ density gradient ultracentrifugationwhich revealed no combination with the DNA of B. subtilis.

Abstract. A comparison of repair synthesis after ex posure to ultraviolet light (UV) or the antimicrobial silver sulfadiazine (sublethal dose) was made in Pseudo monas aeruginosa, strain 2 (ATCC 15693), by use of a D,'5N,i:,C density labeling system. During the initial 15 min of incubation after treatment with both agents, both a 'repair' synthesis and a reduced semi-conservative deoxyribonucleic acid (DNA) synthesis occurred. In the sublethal dose range used, the latter was greater than the former. Normal cells showed only a semi-conservative type of replication and, therefore, within the limits of the resolution of the system used (the incorporation of 1,000-5,000 nucleotides per replicating chromosome could be measured), DNA in normal cells did not appear to undergo a repair synthesis involving thymine ex change. The silver sulfadiazine treated cells appear to use a repair mechanism similar to UV irradiated cells. The bacteriostatic-bacteriocidal activity may be related to the rate of drug interaction with Pseudomonas DNA compared to the rate of 'excisionrepair'.Silver sulfadiazine has proved effective in controlling burn wound sepsis caused by Pseudomonas aeruginosa in burned mice and rats and in the treatment of burned patients [1][2][3][4][5][6][7]. Preparation, characterization and biological properties are described elsewhere [8], Unlike other silver anti microbials effective in vitro [9][10][11] silver sulfadiazine is effective in vivo. Of noteworthy significance is the observation that silver sulfadiazine causes no adverse reactions and there is conspicuous regeneration of epithelium and take of skin grafts [12,13]. Furthermore, unlike sulfadiazine and

The reaction catalyzed by the glucose oxidase (EC 1.1.3.4) from Aspergillus niger was markedly inhibited by Ag+, Hg^++, Cu^++, PCMB and mercuric sulfadiazine, while the silver antimicrobials, silver sulfadiazine, and silver uracil had no inhibitory effect. Characteristic difference spectra due to the absorption by the FAD moiety of the enzyme were obtained by the addition of Ag^+, Hg^++, Cu^++, PCMB and mercuric sulfadiazine, while no spectral changes were seen on the addition of silver sulfadiazine and various silver uracil compounds. Using the ‘flow method’ to study overall kinetics, it was determined that mercuric sulfadiazine inhibited the reduction of the FAD moiety, thereby competing with the molecular oxygen used as a hydrogen acceptor.