Question

1. Why are aminoglycosides more selectively toxic to bacteria than human cells? (Be sure to be complete and specific in your answer to make it clear why these drugs are more toxic to bacterial cells than to human cells.)

2. Penicillins and cephalosporins are beta-lactam antibiotics. Plasmids coding for beta-lactamase enzymes make the bacterium resistant to these antibiotics. What do beta-lactamases do?

3. The malarial organism possesses the remnants of a chloroplast, called an apicoplast. How does tetracycline inhibit growth of the malarial organism? Be sure to make it clear why it is more toxic to cells of the pathogen than human cells in your answer. "Because it has an apicoplast" is not a sufficient answer!

Answer 1

1. Aminoglycosides can recognise the 30S RNA subunit and subsequently bind with it. After binding it can can regulate the bacterial protein synthesis. And thus the bacterial growth is checked. But human cells are eukaryotic cell and don't contain the 30S subunit as the small subunit of ribosome. So, the toxic effects of aminoglycosides are generally lower in human than the bacteria.

2. The beta-lactamase enzymes can hydrolyse the beta-lactam ring of the antibiotics. So, the antibiotics can't work properly to check the bacterial growth. The bacteria become resistant to the antibiotics.

3. Apicoplast have separate protein synthesis mechanism. The tetracycline binds with the 30S ribosomes of apicoplast and mislead the protein synthesis in various way. Finally mal-functional proteins are produced from apicoplast. For the reason the number of apicoplast is not increased. So, the tetracycline becomes more toxic to bacteria than the human as human cells don't carry the 30S ribosome subunit.