 Everybody, Dr. O'Hare, if you're watching this series on antibiotics, you'll see we're switching gears. So we just went through all the cell wall inhibitors, and now we're going to look at the major classes of antibiotics that inhibit protein synthesis. So what you see here is a ribosome. You've got the 50s large subunit, the 30s small subunit, and there's going to be antibiotics that interfere with different parts, making what would be a 70s ribosome with bacteria. One of the reasons this is a selectively toxic treatment in most cases is that bacteria, prokaryotic cells, have 70s ribosomes, whereas eukaryotic cells have 80s ribosomes. Now hopefully remember that our cells, our mitochondria, do have some 70s ribosomes. So there is always a little bit of a concern there, and I think that might be why some people do have maybe some evidence of impaired mitochondrial function when they take antibiotics, but that's a discussion for another day. So as a group, first of all, this is not true with all of them, but if you're a protein synthesis inhibiting antibiotic, you're much more likely to be broad spectrum, right? If you're a cell wall inhibitor, you're much more likely to impact gram positive bacteria than gram negative bacteria, because gram positive bacteria care about their cell walls more than gram negatives do. They have that outer lipid membrane that gram negatives do. But all bacteria have to make proteins. So these are much more likely to be broad spectrum, not always the case, but they're also more likely to be bacteriostatic, meaning they slow or inhibit growth of microbes rather than killing them. And that's, again, not always true, right? Some of the antibiotics are bacteriostatic at lower doses and bactericidal that kill bacteria at higher doses, or they're bacteriostatic alone, bactericidal in combination. And this is not a pharmacology class, but we'll cover the basics there. So you can see that the top group there, chloramphenicol, the macrolides and lincosamines, they're going to actually bind to the 50s, a large subunit of the ribosome, and they'll prevent the formation of peptide bonds, which means that amino acids can't be added to the chain. That's going to stop protein synthesis. The amino glycosides, which we're going to cover here in this first video, they actually bind to the 30s subunit, but not in a way to stop the production of proteins. It actually impacts the ability of these ribosomes to do the proper proofreading, which means they're going to make faulty proteins that hopefully won't work and hopefully will destroy the cytoplasmic elements or the internal structures of bacteria. And then you have tetracycline, they're going to bind to that 30s subunit as well, but they're actually going to block the production of proteins. So we'll cover them separately. All right, so I'll probably show you this image several times just to remind you of what we're looking at here, the protein synthesis or translation inhibitors. All right, so the first group we're going to talk about here are going to be the amino glycosides, and these are the ones that they do impact the 30s subunit just like tetracycline, but they're the ones that I'll just read it here. They cause mismatches between codons and anticodons, which means the wrong amino acid is going to be put into the chain of proteins, leading to faulty proteins that insert into and disrupt cytoplasmic membrane. So again, hopefully that will destroy the cell. But since they are making faulty cells, these are bacteriocidal. Look down the right hand side there, all the rest say bacteriostatic, and that's usually bacteriostatic. But in this case, these are the ones that are bacteriocidal. All right, let's see streptomycin. I won't let us go in whatever order, but streptomycin, these are all broad spectrum. Streptomycin isn't used a whole lot anymore. It was cheap and used a lot, which means there's now a lot of resistance. You think about every single time you use an antibiotic, there's the risk that you are forcing evolution forward a little bit. And antibiotics basically cause microbes to leap forward when it comes to evolution. But it is still useful. It's effective against mycobacterium, which means that this could still be useful against mycobacterium tuberculosis, causative agent of TB, and mycobacterium lepre. So it does still have some uses, but you don't see it used a whole lot anymore. Let's see, gentomycin, another broad spectrum one. The reason this one is important is it's useful against pseudomonas infections. And pseudomonas infections can be a problem for everyone. We've talked about it as one of these potential coming up nightmare bacteria. But pseudomonas infections are a real big problem for people with cystic fibrosis. So it's used a lot. So gentomycin is used a lot to treat pseudomonas infections in patients with CF, cystic fibrosis. Next, we have neomycin. So neomycin is used topically. So this is going to be the neomycin that's in your triple antibiotic or neosporin. That's the key thing with neomycin there. All right, the problem with some of these antibiotics, so we say strepomycin is not used a lot, but it's useful against mycobacterium. Neomycin is just used topically, really. Gentomycin is used for the cystic fibrosis patients. There's a lot of toxicity concerns with these antibiotics. So nephrotoxic, which means they impact the kidneys. Neurotoxic, nervous system, I think they can impact the ears as well. So these antibiotics, if you're going to use them, you want to make sure that it's worth the risk. And that's why a life-threatening pseudomonas infection with a patient with cystic fibrosis or tuberculosis, which is a huge scourge on our planet, they might be worth some more risk. But for other infections, we've moved on to other types of antibiotics. All right, so these are the, I just wanted to quickly introduce the protein synthesis inhibitors because this happens to be the first video in the series. And then also, these are your amino glycoside antibiotics. I hope this helps. Have a wonderful day. Be blessed.