Home » Biology, Darwinism, Evolution, Science » Antibiotic resistance through nitric oxide-producing enzymes

Antibiotic resistance through nitric oxide-producing enzymes

So how did these nitric oxide-producing enzymes arise? By Darwinian processes?

…Nudler’s team found that many antibiotics kill bacteria through the production of harmful charged particles known as reactive oxygen species, otherwise called oxidative stress.

“Antibiotics cause bacteria to produce a lot of reactive oxygen species. Those damage DNA, and bacteria cannot survive. They eventually die,” Nudler said in a telephone interview.

“We found nitric oxide can protect bacteria against oxidative stress.”

He said bacteria produce nitric oxide to resist antibiotics. The defense mechanism appears to apply broadly to many different types of antibiotics, he said.

Nudler said many companies are testing various nitric oxide-lowering compounds called nitric oxide synthase inhibitors for use as anti-inflammatory drugs.

He thinks a compound in this class could be made to reduce the amount of nitric oxide bacteria can produce, reducing their ability to resist antibiotics. That would mean researchers would not need to discover new antibiotics.

SOURCE

  • Delicious
  • Facebook
  • Reddit
  • StumbleUpon
  • Twitter
  • RSS Feed

45 Responses to Antibiotic resistance through nitric oxide-producing enzymes

  1. I fail to see that there is enough information to determine whether organisms developed NO2 production via natural means or not. If ID theory is correct, we need to determine that NO2 production is an irreduceably complex process to determine whether it is likely the product of design, or the product of darwinian evolution. Is there other essential uses for NO2 floating around that easily coopt to fight antibiotics.

  2. bFast: “f ID theory is correct, we need to determine that NO2 production is an irreduceably complex process to determine whether it is likely the product of design…”

    I think this is a good question. Is this an opportunity to apply ID design detection tools and methods to determine if a design inference can be made? How would one go about doing this? Is there an algorithm, template process, formula etc to use? Or is there just a declaration that it must have been designed because a) we don’t know it occurred with evolution b) and it “looks” designed

  3. Denitrification.

  4. So how did these nitric oxide-producing enzymes arise? By Darwinian processes?

    In 1998, you wrote:

    Intelligent Design properly formulated is a theory of information. Within such a theory, information becomes a reliable indicator of intelligent causation as well as a proper object for scientific investigation. Intelligent Design thereby becomes a theory for detecting and measuring information, explaining its origin, and tracing its flow. Intelligent Design is therefore not the study of intelligent causes per se, but of informational pathways induced by intelligent causes.

    and

    It is the empirical detectability of intelligent causes that renders Intelligent Design a fully scientific theory, and distinguishes it from the design arguments of philosophers, or what has traditionally been called “natural theology.” The world contains events, objects, and structures which exhaust the explanatory resources of undirected natural causes, and which can be adequately explained only by recourse to intelligent causes. Scientists are now in a position to demonstrate this rigorously.[My emphases]

    If that was the position in 1998 then we can assume that, eleven years later, the tools available to Intelligent Design researchers must be even more refined and discriminating. It would seem, therefore, that the question of the origin of “these nitric oxide-producing enzymes” offers a splendid opportunity to put these tools to the test.

  5. Well first of all, biochemistry contains many examples of mechanisms designed to reduce oxidative stress. This is something that happens routinely in the cell and a cellular designer would have to consider ways to deal with free radicals. I think we can assume that these enzymes are designed. An interesting test would be to see if antibiotic resistant bacteria are producing these enzymes at higher levels than normal. Then the ID hypothesis would be that this is not a designed difference, and so can be traced to one or possibly two mutations. Probably those mutations would not be in the enzyme itself, but rather in the code for its expression. We can hypothesize that a repressor gene for the enzyme was broken by a random mutation, leading to a higher expression of nitric oxide synthases.

  6. Sorry about the one-word comment. When I submitted it, that it was an answer to the question “Is there other essential uses for NO2 floating around that easily coopt to fight antibiotics” seemed obvious. But I neglected to take into account the moderation delay.

    In any case, “denitrification” is a recommended google term for readers of this thread.

  7. Mr Mishap,

    I think we can assume that these enzymes are designed.

    What are the implications of this assumption? What avenue of research should be pursued as a result, and what should not be pursued?

  8. Nakashima,

    It terms of combating drug resistant bacteria, if one could design an antibiotic that required mutations on the part of the bacteria that are beyond the edge of evolution, then you would a very effective antibiotic.

  9. Nakashima,

    It terms of combating drug resistant bacteria, if one could design an antibiotic that required mutations on the part of the bacteria that are beyond the edge of evolution, then you would a very effective antibiotic.

  10. Mr Jehu,

    I think that is the current thinking behind using combinations (cocktails) of drugs for infections, including HIV. But it is based on a pretty well agreed upon edge of evolution – likely change in a population over a few generations. Microevolution, if you will. I’m asking more about the implication of assuming that design was responsible for the structure of the enzymes. For purposes of the discussion, I’d be interested in talking about the implications of the assumption, more than the design.

  11. Nakashima,

    I believe I spelled out exactly what avenue of research I was suggesting. What don’t you understand about my suggestion?

    Let me spell out my assumption for you. It’s an ID hypothesis based on the idea that the enzymes involved are:

    1) Part of a system engineered to deal with oxidative stress.

    2) As highly specified as any other enzyme.

    3) As highly complex as any other enzyme.

    For instance, I heard an argument awhile back about some enzyme that was discovered which could digest nylon. Since nylon is a man-made chemical, if there is an enzyme that can digest it it would have to have evolved via natural processes assuming there was no intelligence agency involved. Some quick research revealed that this enzyme digested nylon at 2% the efficiency of other similar enzymes. Therefore the specificity of the enzyme was much lower, and therefore the design hypothesis was not warranted.

    There was also a case of a polypeptide in cold water fish that acts as an anti-freeze. Turns out though that the proteins involved are very short, and therefore not very complex.

    If these nitric oxide synthases are both complex and specified in the way that most enzymes are, and we can do tons of biochemical tests to determine whether this is the case, then the ID hypothesis is that they are designed, and designed to do exactly what they are now doing.

    My further hypothesis is that if these bacteria are resistant to anti-biotics because of increased nitric oxide synthase, then we will find that the adjustment was a very simple mutation probably in the gene expression system for the enzyme. It’s possible that this is not the case, but even if it’s not, I’m not done.

    As these researchers suggest, a possible avenue for research would be to find direct inhibitors for these enzymes. This is a common approach for making new drugs. Find a man-made chemical that inhibits the enzyme by a variety of different mechanisms, such as blocking the active site.

    A possible ID hypothesis would be that there is probably already a designed control mechanism for nitric oxide synthase. We should look for it, learn how to rig the system towards less production of nitric oxide synthase and then try to get these pathogens to stop producing it. In other words, instead of working to inhibit the enzyme directly, we should try going over its head to the boss, its gene expression system.

    We should find that repressor gene, produce the protein coded for in large quantities and include it with any anti-biotic cocktail. This would have to be after we confirmed it has no ill affects towards normal cells of course. Then we would be effectively reducing nitric oxide synthases in the pathogen and thus reducing it’s ability to deal with the anti-biotics.

  12. Nakashima,

    “I think that is the current thinking behind using combinations (cocktails) of drugs for infections, including HIV. But it is based on a pretty well agreed upon edge of evolution – likely change in a population over a few generations. Microevolution, if you will.”

    Excuse me, but do you know how quickly bacteria reproduce? We are not talking about a “few generations” here.

  13. I was just thinking another possibility would be to try and find an inhibitor for the signaling mechanism for the gene expression system. The gene expression system is probably controlled by the levels of either oxygen radicals or nitric oxide in the cell, perhaps both. If we could interrupt the signaling mechanism which detects one or both of those signals in a way that induces the cell to stop producing nitric oxide synthases, we could accomplish the same thing.

    Basically, we’d be tricking the cell into acting as if there’s fewer free radicals in the cell and/or too much nitric oxide.

  14. jTaylor, there absolutely is a method of determining whether something like this is irreduceably complex. We simply answer a few questions:

    Question 1, What are the steps that are taken to make and deliver the NO2?

    Question 2, What is the list of steps that is fully reduced — each step is required to produce the end result, NO2.

    Question 3, Can one divide this list of steps into two (not three or more) sublists which are part of lists that do something else for the organism. Consider that creating NO2 require steps b,g,j,k and l. Consider that there are two other functions, one of which is a,b,c,d,e,f and g, and the other is j,k,l and m. Using these two other functions, you are only one event away from getting to NO2 production, neo-Darwinism can probably do this. If 3 or more lists must be gleaned to produce the NO2, then neo-Darwinism is not reasonably able to do it.

    The formula is simple. Irreduceable complexity theory produces reasonable research. Irreduceable complexity theory produces predictions. Irreduceable complexity is imminantly testable. This is science, plain and simple.

  15. tragic mishap: “Some quick research revealed that this enzyme digested nylon at 2% the efficiency of other similar enzymes. Therefore the specificity of the enzyme was much lower, and therefore the design hypothesis was not warranted.”

    I thought poor functionality (like the Panda’s Thumb) was not an argument against design? I’m getting confused.

  16. ellazimm,

    First of all, I did not infer design there, but that doesn’t mean design didn’t happen. It could be a case of a false negative, which as explained by Dembski is unavoidable in the design inference. A real problem would be a false positive.

    Secondly, this was more a parable than a real analysis. My hypothesis would be that since this enzyme was not designed, the change from the wild type must be the result of one or at most two mutations, going off Behe’s arguments in Edge of Evolution. That’s a testable prediction. If that prediction was wrong, then according to my test this enzyme was designed. That would be a clear case of a false positive, invalidating my test.

    So in answer to your question, poor functionality is a result of random mutations from the intended design. Darwinists argue that poor functionality, anywhere they see it, is evidence against design. What we are actually saying is that the original design must not have been poorly functional, but rather exquisitely functional. Therefore a design theorist would hypothesize that any poor function in nature is the result either of mutations away from the original design or there is something we don’t yet know about the system that is causing us to erroneously assume poor functionality. This too is a testable prediction and could generate a large amount of fruitful research in every case where Darwinists shrilly claim poor function, like the panda’s thumb.

    NOTE: Causing information loss (destroying a function) is easy and much more than one or two mutations could be evident. Very generally, the one or two mutations limit is for new functions caused by a change in protein structure. Behe goes a bit further and puts a limit of six mutations as the high threshold for new protein-protein binding sites.

  17. “My hypothesis would be that since this enzyme was not designed, the change from the wild type must be the result of one or at most two mutations, going off Behe’s arguments in Edge of Evolution.”

    The problem with this hypothesis (nicely stated though it is) is that Behe is wrong.

  18. Arthur Hunt,

    You continue to post about T-urf13 even though it has been pointed out to you that it is a result of artificial selection and therefor does not go against Behe who only argues against NATURAL selection.

    IOW Hunt is being dishonest and he thinks his dishonesty is meaningful discourse.

    Thank you for continuing to prove that your only methodology for debate is lying and deception.

  19. I read both your articles on TREE a long time ago Mr. Hunt. Joseph is correct. The T-urf13 protein resulted in a devastating loss of fitness for the plant by causing it to be vulnerable to a toxin from a certain fungus. Also, the intelligently designed goal of the project was to create a plant that was male sterile, hardly something natural selection would select for. In fact, natural selection would select against both these mutations.

    Also, as Joseph says, these plants were artificially selected for by human beings with a purpose in mind. So we know that it wasn’t natural selection because humans did the selecting. The influence of intelligence cannot be denied here, as intelligence preserved and preferentially propogated all the intermediate steps whereas natural selection would never have done so.

  20. Another thing to consider pertaining to T-URF 13 and Behe’s “Edge of evolution”:

    Dr Behe was talking about new bunding sites evolving.

    Did the T-URF 13 binding sites evolve or were they always present?

  21. the intelligently designed goal of the project was to create a plant that was male sterile, hardly something natural selection would select for. In fact, natural selection would select against both these mutations.

    That’s why cytoplasmic male sterility is a trait that is seen in the wild.

    Fact is, plant breeders weren’t intelligently designing anything; they were just looking for things that natural mechanisms provide through normal genetic processes.

    Also, as Joseph says, these plants were artificially selected for by human beings with a purpose in mind. So we know that it wasn’t natural selection because humans did the selecting. The influence of intelligence cannot be denied here, as intelligence preserved and preferentially propogated all the intermediate steps whereas natural selection would never have done so.

    I read this comment and think that tragic mishap and joseph are clsiming that plant breeders in the 50′s and 60′s deliberately and painstakingly designed T-URF13. Our two IDists here are insisting that scientists in that era: 1. knew that a protein like T-URF13 could incite male sterility; 2. knew exactly how to design, from scratch, this protein; 3. knew how to assemble a gene encoding the protein; and 4. knew how to introduce the gene into the maize mitochondrial genome to yield exactly what is seen in the cmsT mitochondria.

    Frankly, tragic mishap and joseph have wandered way past the line of respectable credibility in their suggestion. They should read Meyer’s latest book so that they can get an inkling of the history of molecular biology and understand how preposterous their claims are.

    The fact is, T-URF13 arose strictly via random and natural (NOT intelligent) processes. The maize mitochondrial genome was shuffled without any specific protein-coding purpose, and a protein that far exceeds the limits Behe has placed on random processes was the product.

    You continue to post about T-urf13 even though it has been pointed out to you that it is a result of artificial selection and therefor does not go against Behe who only argues against NATURAL selection.

    Um, Behe’s entire argument was built around the evolutionary response of a parasite that has been exposed to a selective agent of decidedly human origin. In this regard, there is no difference between the origins of chloroquine resistance in Plasmodium and the origins of T-URF13.

  22. Arthur Hunt:

    I read this comment and think that tragic mishap and joseph are clsiming that plant breeders in the 50’s and 60’s deliberately and painstakingly designed T-URF13

    That thought never crossed my mind.

    IOW Art has erected yet another strawman.

    The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize.

    IOW because of artificial selection this type of thing had the opportunity.

    Without AS thgere wouldn’t have been that opportunity.

    Dr Behe’s entire argument is against blind watchmaker type processes.

    Had maize arisen solely via those types of processes you would have a point.

    Also it appears that URF13-T came with the ability to form a pore in the membrane.

    IOW URF13-T didn’t form and then evolve those binding sites.

    That proves Arthur is wrong and has misrepresented Dr Behe’s arguments once again.

    That’s why cytoplasmic male sterility is a trait that is seen in the wild.

    We aren’t talking about mere CMS. We are talking about this one particular protein.

    Try to stay focused.

  23. The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize.

    And the evidence for this is …. ?

    And how is this statement not a flat-out assertion that “artificial selection” was in fact an explicit designing, from the ground up, of the protein?

  24. Mr. Hunt,

    It’s definitely an interesting case. I was fascinated by it. Never did I suggest that scientists designed the protein. All I said was that intelligence was involved in making it, and there is no evidence that anything like this could have been done without intelligence. All this example proves is that intelligent design is more powerful than RM + NS when it’s not even trying. It’s really a very interesting, fringe case that validates ID predictions about intelligence being necessary for this kind of structure. Just because some of these mutations piggy-backed intelligently selected mutations does not make it random.

    You could convince me that this was a fully random process by answering the following question:

    How did all the intermediate steps spread throughout the population leading to subsequent fortuitous mutations? Presumably the mutations occurred originally in a single individual plant. That would have to be the case if they were truly random. The next step would be spreading throughout the population even though they do not confer an advantage visible to natural selection. So how did those mutations spread? I’m talking specifically now about the mutations leading to the Turf-13 protein.

  25. Also, Mr. Hunt, just because cytoplasmic male sterility exists in the wild doesn’t mean that natural selection favored it in any way or that it was formed by Darwinian processes. You are assuming what you are trying to prove.

  26. A couple of things re: Cytoplasmic male sterility.

    1. CMS maize may be susceptible to fungus, but as to whether its ‘devastating’ to fitness, as our ID friends maintain, one has to wonder if the susceptibility is density-dependent. Under densely-packed agricultural conditions, the disdvanatge may be high, but not as much of a problem in the wild.

    2.Does the susceptibility of CMS maize to fungus outweigh the known selective advantage of higher yield? It has long been known that CMS plants often have higher yields than their hermaphroditic counterparts.

    3. CMS also offers the known selective advantage of outcrossing. Does this outweigh the susceptibility to fungus?

    Until our ID friends consider and explore these known selective advantages for CMS, and then compare them to the one selective disadvantage in a natural setting, their objections really don’t hold much water.

  27. Art writes:

    Um, Behe’s entire argument was built around the evolutionary response of a parasite that has been exposed to a selective agent of decidedly human origin. In this regard, there is no difference between the origins of chloroquine resistance in Plasmodium and the origins of T-URF13.

    It seems our ID friends want to have it both ways.

  28. Dave Wisker:

    1. CMS maize may be susceptible to fungus, but as to whether its ‘devastating’ to fitness, as our ID friends maintain, one has to wonder if the susceptibility is density-dependent.

    “Devastating to fitness”?

    Also if one reads the papers on this one finds out that they STOPPED using the seeds because of the susceptability to fungal toxins.

    T-URF 13 protein, second sentence.

    3. CMS also offers the known selective advantage of outcrossing.

    Except that outcrossing isn’t possible if all males are sterile.

    Until the evolutionists can demonstrate that maize can arise without agency involvement, that the protein in question would also arise in that scenario, they don’t have a case.

    Also until the demonstrate the binding sites/ properties in question “evolved”, as opposed to being present from the origin of the protein, they don’t have anything.

    Art sez:

    Um, Behe’s entire argument was built around the evolutionary response of a parasite that has been exposed to a selective agent of decidedly human origin.

    It’s called an “arms race”.

    In this regard, there is no difference between the origins of chloroquine resistance in Plasmodium and the origins of T-URF13.

    Just because you can say it doesn’t make it so.

    Again Art uses “debate by declaration” and “debate via straman”.

    And he talks about credibility.

  29. The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize.

  30. Joseph, Can maize, or the maize genome, tell the difference between differential reproduction rates caused by human activity and rates caused by a change in climate?

  31. BillB:

    Joseph, Can maize, or the maize genome, tell the difference between differential reproduction rates caused by human activity and rates caused by a change in climate?

    Do you have a point?

    Neither maize, nor the maize genome, would exist without artificial selection.

    No corn, no corn-dogs. No popcorn.

    No children of the corn…

  32. 1. Turf-13 arose naturally in maize. That is, it was neither engineered nor planned by humans.

    2. That CMS maize plants weren’t used in agricultrural settings settings says absolutely nothing abouit how CMS plants fare in the wild.

    3. Joseph writes “Except that outcrossing isn’t possible if all males are sterile.” This is about as empty a statement as one can get. Perusal of literature on the evolutionary dynamics of CMS in the wild shows that CMS is maintained polymorphically– females with selective advanatge rise in frequency until they reach an equilibrium with hermaproditic plants (there are no ‘male’ plants in these situations. This equilibrium is reached via standard population genetic processes.

  33. Dave Wisker:

    1. Turf-13 arose naturally in maize.

    Maize arose artificially.

    The protein in question wouldn’t have arisen if we didn’t artificially screw around with the plant.

    As far as anyone knows it arose as a direct consequence of our meddling.

    3. Joseph writes “Except that outcrossing isn’t possible if all males are sterile.”

    That is a true statement.

    You do understand biology, don’t you?

    Perusal of literature on the evolutionary dynamics of CMS in the wild

    We aren’t talking about things in the wild.

    Why do you keep changing the topic?

  34. I make a point:

    The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize.

    Instead of actually addressing that point what do our evolutionist guests do?

    Ignore it and prattle on about more irrelevancies.

    All this to hide the fact that Art is wrong because new binding sites did not evolve.

    The protein in question came with all the binding sites Art sez refutes Behe.

    Except that Art doesn’t know what he is talking about because new binding sites didn’t evolve on this protein.

    What it has it came with.

  35. The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize.

    Art:

    And the evidence for this is …. ?

    It’s pretty simple actually- no maize no maize protein URF 13-T.

    And how is this statement not a flat-out assertion that “artificial selection” was in fact an explicit designing, from the ground up, of the protein?

    You should explain how it is such an assertion.

    I know I never thought nor implied such a thing.

    But anyway you also said:

    The maize mitochondrial genome was shuffled without any specific protein-coding purpose, and a protein that far exceeds the limits Behe has placed on random processes was the product.

    That is not Dr Behe’s argument.

    When the protein in question “evolves” an new binding site- that is other than the binding sites it had from the beginning, then you will have something.

  36. Dave,

    Until our ID friends consider and explore these known selective advantages for CMS, and then compare them to the one selective disadvantage in a natural setting, their objections really don’t hold much water.

    Do you have a grant in mind? One in which I could be explicit about the purpose of the experiment? Because I have a perfect test in mind.

    1. Take a CMS and non-CMS batch of seeds mixed 50/50, and plant them randomly in a field.

    2. Leave them be for several seasons, taking samples of every generation. The plants would be allowed to breed naturally.

    3. See which version wins out.

  37. tragic,

    Do you have a grant in mind?

    Not particularly, but then I don’t work with plants or agriculture. Art Hunt might know of some for which you could apply.

    I’d work a bit more on your experimental design first, however. Just one example of the top of my head: how would you set up your controls for density effects when assessing fungus resistance?

  38. The test is not for fungus, it’s to see if CMS would be positively selected for by nature. The plants would be exactly the same except one would be CMS and the other not. There would be no need to include a gene for the Turf-13 protein.

    Anyway, let me know about that grant, and in twenty years after I have tenure I’ll see if it’s worth my time. Wouldn’t want to expose my real beliefs to the thought police before I’m safely home.

  39. tragic mishap, is your expectation that the CMS plants would not persist in the mixed population you describe?

  40. So apparently you don’t seem to care if the results might be affected by your experimental methodology rather than reflect what you are actually trying to examine.

    Good luck on that grant then.

  41. Tragic, Hmm. So you eliminate plants with the Turf-13 gene from your experiment, and instead look at another CMS genotype.

    If the CMS plants rise in frequency vs the hermaphroditic plants in your field over time, how would you know the results weren’t just due to chance?

  42. Okay. So it’s believable that CMS would not only persist but perhaps be maintained at a ratio higher than 50/50 to non-CMS.

    The fact remains that this is not natural selection. The fact remains that even if no fungal toxin were present, T-urf13 provides no positively selectable trait and would likely not persist, low density of the toxin notwithstanding.

    In fact, I’d be willing to bet the binding to the fungal toxin is non-specific to the toxin. In other words I bet there’s other chemicals that could open the channel.

    Also, my earlier hypothesis:

    My hypothesis would be that since this enzyme was not designed, the change from the wild type must be the result of one or at most two mutations, going off Behe’s arguments in Edge of Evolution.

    This should be qualified to mean that no more than one or two mutations can be traversed without each one being visible in some way to natural selection. Behe’s hypothesis is about how far you can go before you get a selectable trait, not how far you can go period.

  43. The fact remains that this is not natural selection. The fact remains that even if no fungal toxin were present, T-urf13 provides no positively selectable trait and would likely not persist, low density of the toxin notwithstanding.

    ??? The fungal toxin isn’t really relevant, except for refuting a later statement of tragic mishap’s. The primary trait associated with T-URF13 is cms, a characteristic that is not uncommon in nature, and a trait whose general origins (not just in maize, but in plants in general) is often traceable to the occurrence, via natural and random mechanisms analogous to those that gave rise to T-URF13, of novel proteins that have no “parents”. Basically, these are numerous cases of multifunctional proteins, each of which likely has many more “CCC’s” than Behe could ever stomach, evolving via natural and random mechanisms in circumstances that Behe predicts absolutely preclude such events.

    In fact, I’d be willing to bet the binding to the fungal toxin is non-specific to the toxin. In other words I bet there’s other chemicals that could open the channel.

    The binding of toxin to protein is rather specific. But that of course does not preclude the existence of chemical mimics. That would not be very surprising.

    This should be qualified to mean that no more than one or two mutations can be traversed without each one being visible in some way to natural selection. Behe’s hypothesis is about how far you can go before you get a selectable trait, not how far you can go period.

    This makes no sense to me. I think you are just putting words in Behe’s mouth, to try and rescue from the fatal insult that is the example we are discussing.

    Regardless, the “CCC” represented by the toxin-binding site almost certainly involves many more than two amino acids, and it evolved without any selection at all.

  44. Just a thought on the original topic.

    Somebody should do a study on the effect of using nitric oxide with antibiotics versus straight anti-biotics. If nitric oxide synthase is down regulated by higher conentrations of its product, nitric oxide, then higher levels of nitric oxide would reduce expression of nitric oxide synthase. If this study is correct then that would give a big assist to the antibiotics. You could do this in the lab fairly easily, but even a human clinical trial should not be that hard. We already have an FDA approved drug that delivers a healthy dose of nitric oxide – Viagra.

  45. Course if the down regulation is broken via mutation, this wouldn’t work. In fact it would be pretty easy to mutate so that it did break. An ID solution would be to find something that attacks a critical function that the bacteria can’t break and remain viable.

Leave a Reply