Doxycycline and tetracycline are broad-spectrum antibiotics targeting bacterial protein synthesis. They achieve this by binding to the 30S ribosomal subunit of susceptible bacteria.
This binding inhibits the attachment of aminoacyl-tRNA to the mRNA-ribosome complex. Consequently, the bacteria cannot synthesize necessary proteins for growth and survival. This blockage leads to bacteriostatic effects, halting bacterial growth.
The specific mechanism differs slightly. Tetracycline binds more tightly to the 30S subunit than doxycycline. Doxycycline, however, shows better penetration into certain tissues, like the lungs and prostate, offering advantages in treating specific infections.
Resistance mechanisms vary but frequently involve changes in the bacterial ribosome structure, reducing the antibiotic’s binding affinity. Efflux pumps, which actively expel the drug from the bacterial cell, also contribute significantly to resistance.
| Tetracycline | 30S ribosomal subunit | Inhibits aminoacyl-tRNA binding | Ribosomal mutations, efflux pumps |
| Doxycycline | 30S ribosomal subunit | Inhibits aminoacyl-tRNA binding | Ribosomal mutations, efflux pumps |
Understanding these mechanisms allows for informed treatment decisions and strategies to mitigate the development of antibiotic resistance. Clinicians should consider factors like bacterial susceptibility profiles and patient-specific needs when selecting between doxycycline and tetracycline.
