Antibiotic resistance through nitric oxide-producing enzymes

_{William Dembski

September 12, 2009

Biology, Darwinism, Evolution, Science}

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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.

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Comments

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.ellazimm_{September 14, 2009
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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.bFast_{September 13, 2009
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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.tragic mishap_{September 13, 2009
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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.tragic mishap_{September 13, 2009
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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.tragic mishap_{September 13, 2009
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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.Nakashima_{September 13, 2009
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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.Jehu_{September 13, 2009
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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?Nakashima_{September 13, 2009
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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.Arthur Hunt_{September 13, 2009
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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.tragic mishap_{September 13, 2009
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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.Seversky_{September 12, 2009
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Denitrification.Arthur Hunt_{September 12, 2009
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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" designedJTaylor_{September 12, 2009
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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.bFast_{September 12, 2009
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