The effectiveness of Tetracycline as an antibiotic in eukaryotic cells primarily stems from its selective targeting of prokaryotic ribosomes, which differ significantly from eukaryotic ribosomes. Tetracycline binds specifically to the 30S subunit of bacterial ribosomes, inhibiting the binding of aminoacyl-tRNA to the ribosomal mRNA. Since eukaryotic ribosomes have a different structure (the 40S and 60S subunits), Tetracycline does not effectively bind to them and thus does not interfere with the eukaryotic protein synthesis process.
In summary, Tetracycline is effective as an antibiotic because it specifically targets bacterial ribosomes (70S) without affecting eukaryotic ribosomes (80S), allowing it to inhibit protein synthesis in bacteria while leaving eukaryotic cells unharmed.