 Hey everybody, Dr. O. This video we're going to cover is the last video I'm going to do in a series of protein synthesis inhibiting antibiotics. So we're going to talk about chloramphenicol, which chloramphenicol does inhibit protein synthesis at the 50s ribosome. So it's been around a long time, so it's got, it was used historically a lot more than now, and we'll talk about why. So it was discovered from another streptomyces, streptomyces Venezuela in 1947. In 1949, it actually was the first broad-spectrum antibiotic that was approved by the FDA, and that's because the only actual antibiotic that had been approved before was penicillin, which was only effective against gram-positive. Now, just as a quick reminder, that doesn't count the sulfa drugs because they're not true antibiotics because they're synthesized in the laboratory. Now, so is chloramphenicol now, so chloramphenicol was a natural antibiotic, it was found in nature, but it was also easily synthesized in the laboratory. So this was the first synthetically mass-produced antibacterial, where you took a natural antibiotic and synthesized it in the lab. So chloramphenicol's been around a long time, a ton of it was produced, it could penetrate our body tissues well, it was super effective against, you know, a broad-spectrum might effective against a lot of bacteria, which means that it got used a lot, which was leading to some resistance issues, but it was used to treat like you name it, right? Typhoid fever conjunctivitis, I mean, pretty much anything, it was being used to treat. The problem and the reason you don't see it in use anywhere near as much now is that there's some pretty serious side effects. There was something called a gray baby syndrome that would kill babies, especially if they were premature babies. The drug would build up, just the enzymes needed to get rid of the drug and the liver's ability to get rid of the drug and kidney's ability to get rid of the drug just seemed to be lacking in babies. So if chloramphenicol would build up in their system, it would basically shut off electron transport, so it would cause all sorts of problems, but it doesn't matter if you know that. But it does have an impact on bone marrow, so it can actually decrease blood cell production in several ways. Some you can actually develop aplastic anemia and never come back from it, but others it's a temporary loss of blood cell production that does go away when you get off the drug. But the reason I want to talk about that is that the reason they believe that happens, at least in this type of loss of blood cells, is this drug is impacting the mitochondria of stem cells that are making new blood cells. And the reason that's important is you do have to remember that our mitochondria have 70S ribosomes. So these drugs that inhibit the 70S ribosomes of bacteria, there are potential side effects in human cells, right? So it's not completely selectively toxic, meaning that it doesn't like with peptidoglycan cell wall inhibitors, we don't have peptidoglycan cell wall, so there's no concern there really. Whereas with these drugs, there is the concern that they're impacting mitochondrial function. I talked about this in the mitochondria video, but I noticed working with athletes that it did appear to impact them in ways it doesn't impact the rest of us. And I think part of that is me sitting here, I'm not taxing my mitochondria. They can keep up with me pretty easy. But I noticed with high level athletes that a lot of these antibiotics did impact their performance. And I do have to wonder how much of it is the impact on these mitochondria. So I'm definitely not saying completely, but it's just worth noting. All right, so that is chloramphenicol. It had a lot of uses in the past. And because of these side effects, just not much anymore. But I hope this helps. Have a wonderful day. Be blessed.