Antibióticos: o que são? de onde vêm? como agem? #InstanteBiotec 40

Antibióticos: o que são? de onde vêm? como agem? #InstanteBiotec 40


Antibiotics are substances that in
low concentrations inhibit the growth and can lead to death of bacteria. Today they may seem ordinary, but
antibiotics are so powerful that they are considered the most important discovery
for the treatment of infections. They can be naturally produced by
other microorganisms such as bacteria and fungi, in order to prevent the growth of
other competing bacteria, or they can be a similar product produced entirely
or partly by chemical synthesis. Targets of antibiotics are the physiology
and the biochemistry of bacteria. And there are five main targets: the bacterial cell wall, the cell membrane, protein synthesis, DNA and RNA synthesis
RNA, and folic acid metabolism. By interfering in any of these processes,
antibiotic is threatening the survival of cell. But no need to worry, these bacterial targets
are different or non-existent in eukaryotic cells, such as in human beings, which means that antibiotics are relatively non-toxic drugs to
we. β-lactam antibiotics such as penicillins,
cephalosporins and carbapenems block the synthesis of the bacterial cell wall. This structure is absent in animal cells,
but it is essential for the survival of bacteria The bacterial ribosome is the target of tetracycline,
aminoglycosides, macrolides and other antibiotics. This ribosome is different enough
from the eukaryotic ribosome preventing cross-inhibition to occur. In the case of folic acid metabolism,
it is present in bacteria but not in humans, whose intake is through the diet. Thus, the antibiotic, such as benzenesulfonamide,
that acts in the synthesis of folic acid in bacteria does not have a target on our cells. Antibiotic resistance, on the other hand, is something
to worry about. It is the ability of microorganisms to
withstand the effects of an antibiotic or antimicrobial. The inadequate use of antibiotics, either by
exacerbated and indiscriminate use in humans, precisely because it does not affect us directly
during treatment, or the use in animal diets, promote selective pressure for resistant strains. Mutations and genetic material sharing
followed by selection drive the growth and appearance of strains
resistant to many antibiotics. So the story complicates for us,
since we have no weapons to fight infection. Bacterial resistance to antibiotics
manifested primarily through four mechanisms: the modification of the target; efflux;
immunity; and destruction catalyzed by enzymes. The target modification can occur by
mutation of own targets, such as topoisomerases that help unwind the DNA strand during replication. They are the target of fluoroquinolone antibiotics. The antibiotic makes the enzyme to
cut DNA more than necessary. With the mutation in topoisomerase, it becomes
less susceptible to bonding with the antibiotic, preventing it to change its function in
DNA replication. The target modification can also occur
by the production of enzymes that modify antibiotic targets, such as methyltransferase. The bacterial 23S ribosomal RNA
is methylated by this enzyme at or near the place where the antibiotic would bind,
so he can not bind and interfere in protein synthesis. Efflux occurs through a large family of
protein pumps that expel, among other molecules, antibiotics from the inside of the cell. On immunity, antibiotics or their
targets are bound by several proteins preventing antibiotic-target binding. Another mechanism of antibiotic resistance
are enzymes that recognize antibiotics and modify them in order to eliminate functional features
that allow them to interact with their targets. The β-lactamases, for example, cleave the
β-lactam ring which is characteristic of antibiotics and essential for their action. You must have heard of the antibiotic
Vancomycin. It acts by preventing bacteria from forming
cell wall by binding to peptides that are required for wall construction,
particularly those ending with two copies of the amino acid D-alanine (D-Ala). But some pathogenic bacteria through
horizontal gene transfer, acquired from non-pathogenic vancomycin producing organisms
the resistance mechanisms to this molecule. This resistance is a version of target modification, where the resistant bacteria has a new biosynthetic machinery that alters
the cell wall structure. They replace one of these D-ala present
in the peptide of its cell wall with one D-lactate (D-lac), reducing the vancomycin ability
to bind to its target. Today, this resistance has spread making
that dangerous vancomycin-resistant Enterococci (VRE) and Staphyllococcus aureus (VRSA) infections become more common. To solve the problem, American researchers,
in 2011, synthesized a new version of vancomycin which binds to peptides with either
D-Ala and D-Ala, or D-Ala and D-Lac. Other research groups have made changes
in the antibiotic structure to prevent the construction of the bacterial cell wall
and to cause its permeability, leading to cell death. Recently, the researchers who created
the new version of the antibiotic in joined these three changes in one vancomycin. The new antibiotic is at least 25,000 times
more potent against organisms such as VRE and VRSA. Vancomycin-resistant bacteria were
tested with this new version of the antibiotic and even after 50 days adding the antibiotic
they were not able to generate resistance, suggesting that the novel compound can be
more lasting than current antibiotics. This new compound is not yet ready
for human testing. The researchers want to reduce the number
steps necessary for its production and to reduce costs. Then they will test the antibiotics in animals
and only then in humans. This new version of Vancomycin may even
be more lasting and more powerful, but we cannot continue to use antibiotics
irresponsibly and exaggeratedly. For the emergence of resistance is only one
a matter of time. If you liked this video, give a thumbs-up
and also share it in your networks. See you next time!

24 Replies to “Antibióticos: o que são? de onde vêm? como agem? #InstanteBiotec 40”

  1. Muito bom, pena que no meu Estado biotecnologia seja tao desvalorizado, mesmo nós estando dianta da maior floresta equatorial do mundo.

  2. E você, está fazendo a sua parte na luta contra a resistência? Nada de tratar gripe com antibiótico, ein.

  3. Acabei de conhecer o canal por meio de outro canal de biotecnologia e estou amando! Vídeos bem feitos e com as devidas referências para consulta. Estão de parabéns! Já tentaram contato com o pessoal do Blablalogia e do ScienceVlogs? Seu canal tem um formato que acho que se enquadraria muito bem lá.

  4. Pretendo cursar biotecnologia em 2018, o que me leva a sempre procurar meios de comunicação que me informem mais sobre esse assunto. O seu canal impressiona tanto pelos temas como pela qualidade.
    CONTINUA FAZENDO ISSO PF

  5. Explicação perfeita. Eu apenas usaria, além da vancomicina, exemplos mais atuais e alarmantes como a resistência aos carbapenêmicos e à colistina (polimixina E). Parabéns pelos vídeos e pelo excelente trabalho em prol da biotec com esse canal!

  6. Eu fiz um tratamento de 3 dias com Azitromicina 1mg por dia mesmo depois do terceiro dia ainda sinto ardência voltei no medico e ele disse que é normal que mesmo eu tendo terminado o tratamento o antibiótico vai continuar agindo por alguns dias é verdade isso? ou corro risco de para mesmo e depois não resolver o problema é a bacteria ficar mais forte

  7. Oi meu filho tem 4 anos e tomou um antibiótico astro por 6 dias para infecção de garganta depois que acabou o remédio ele continua com umas bolinhas brancas na garganta eu quero saber se o antibiótico vai continuar agindo no corpo dele e por quantos dias ele faz efeito?!!!!!

  8. Minha filha tem 1 ano e 3 meses e esta com inflamaçao no ouvido ..foi médicada com antibiótico,gostaria de saber quanto tempo demora para fazer efeito ?…obg

  9. Tomando antibiótico surgiu minha herpes labial … existe alguma ligação entre eu estar usando antibiótico e herpes labial se manifestar?

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