Spring Break
New theory explains antibiotic mechanism
Issue date: 12/4/08
Antibiotics work to disrupt this usually effective process. If the mRNA sequence is a group of excited children waiting for their presents on Christmas, and the presents were the peptides, then antibiotics would be the Scrooge who went around switching all the name tags on the presents so that child A would get child G's present, and child U would get child C's present, and so on and so forth.
If the mRNA sequence isn't being matched up with the right peptide sequence, then the proteins that are being pumped out are going to be pretty odd.
This manipulation of the ribosomal machinery leads to the production of faulty proteins. When a cell's proteins do not work properly, this introduces stress into the cell - often via the creation of free radicals. Free radicals are atoms with an unstable unpaired electron that react quickly to steal another atom's electron to satisfy themselves.
When free radicals steal other atoms' electrons, however, this creates free radicals that then go on to steal other electrons, and so on. These radical chain reactions, as they are known, can propagate damage throughout the cell.
When too much oxidative stress is built up from free radicals floating around in the cell, the cell will die. Thus, the antibiotic has conquered the bacteria, and the organism playing host to this epic battle avoids a bacterial infection.
This enhanced understanding of how antibiotics work could prove invaluable, especially since the problem of bacterial resistance to antibiotics is looming larger and larger all the time. Kohanski realizes the importance of this looming problem.
"Our work has uncovered new pathways that could aid in the design of combination therapies for [antibiotics]. A compound targeting the pathway we have uncovered could be used in combination with an [antibiotic] to enhance the potency of this drug class. This means that we could use less antibiotic which would reduce drug side effects while still maintaining the ability to fight an infection."
If the mRNA sequence isn't being matched up with the right peptide sequence, then the proteins that are being pumped out are going to be pretty odd.
This manipulation of the ribosomal machinery leads to the production of faulty proteins. When a cell's proteins do not work properly, this introduces stress into the cell - often via the creation of free radicals. Free radicals are atoms with an unstable unpaired electron that react quickly to steal another atom's electron to satisfy themselves.
When free radicals steal other atoms' electrons, however, this creates free radicals that then go on to steal other electrons, and so on. These radical chain reactions, as they are known, can propagate damage throughout the cell.
When too much oxidative stress is built up from free radicals floating around in the cell, the cell will die. Thus, the antibiotic has conquered the bacteria, and the organism playing host to this epic battle avoids a bacterial infection.
This enhanced understanding of how antibiotics work could prove invaluable, especially since the problem of bacterial resistance to antibiotics is looming larger and larger all the time. Kohanski realizes the importance of this looming problem.
"Our work has uncovered new pathways that could aid in the design of combination therapies for [antibiotics]. A compound targeting the pathway we have uncovered could be used in combination with an [antibiotic] to enhance the potency of this drug class. This means that we could use less antibiotic which would reduce drug side effects while still maintaining the ability to fight an infection."
Viewing Comments 1 - 2 of 2
who gmp
posted 1/09/09 @ 11:35 AM EST
Good article
keep writing
can you write some thing like this over antibiotic resitance mechanism.
Tom
posted 1/09/09 @ 5:27 PM EST
Nicely written article. One correction, though.
"Ribosomes are able to match up the mRNA sequence to peptides, the single-unit building blocks of proteins, thus creating a specific chain of peptides. (Continued…)
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