The biochemical effects of chloramphenicol

Chloramphenicol antibiotics can act on the 50S subunit of bacterial ribonucleosomes and block protein synthesis. They are bacteriostatic broad-spectrum antibiotics.
The 70S ribosome of bacterial cells is the main cellular component for protein synthesis and consists of two subunits, 50S and 30S. Chloramphenicol blocks the action of transpeptidylase by reversibly binding to the 50S subunit, interfering with the binding of the aminoacyl-tRNA terminal with amino acids to the 50S subunit, thus blocking the formation of new peptide chains and inhibiting protein synthesis. . Since chloramphenicol can also bind to the 70S of human mitochondria, it can also inhibit the protein synthesis of human mitochondria and cause toxicity to the human body. Because the binding of chloramphenicol to 70S ribosomes is reversible, it is considered a bacteriostatic antibiotic. However, it can also have a bactericidal effect on certain bacteria at high drug concentrations, and it can even kill influenza bacteria at lower concentrations. Produce bactericidal effect.
Chloramphenicol has inhibitory effects on both Gram-positive and Gram-negative bacteria, and has a stronger effect on the latter. Among them, it is more effective against typhoid bacteria, influenza bacteria, parainfluenza bacteria and pertussis bacteria than other antibiotics. It is also effective against rickettsial infections such as typhus, but it is not as effective against gram-positive cocci as penicillin and tetracycline. The antibacterial mechanism of action is to bind to the 50S subunit of the ribosome and inhibit peptide acyltransferase, thereby inhibiting protein synthesis.
Various bacteria can become resistant to chloramphenicol, among which Escherichia coli, Shigella dysenteriae, Proteus, etc. are more common, while Typhoid bacilli and Staphylococcus aureus are less common. Bacteria develop resistance to chloramphenicol relatively slowly, possibly through gradual mutation of genes, but it can disappear automatically. Bacteria can also acquire drug resistance through the transfer of R factors. Bacteria that acquire R factors can produce chloramphenicol acetyltransferase to inactivate chloramphenicol.