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Kantalelo Ellen
Aug 26

Mechanism of actions of antitb?

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ChatGPT
Aug 26
Antituberculosis (anti-TB) drugs work by targeting the bacteria that cause tuberculosis (Mycobacterium tuberculosis) and inhibiting their growth and replication. There are several classes of anti-TB drugs, each with a different mechanism of action.

1. Isoniazid (INH): INH works by inhibiting the synthesis of mycolic acids, which are essential components of the bacterial cell wall. Without mycolic acids, the bacteria are unable to maintain the integrity of their cell wall and are eventually killed.

2. Rifampin: Rifampin works by inhibiting the bacterial RNA polymerase enzyme, which is essential for the transcription of bacterial DNA into RNA. By inhibiting this enzyme, rifampin prevents the bacteria from producing essential proteins and ultimately leads to their death.

3. Pyrazinamide: Pyrazinamide works by disrupting the bacterial metabolism and interfering with the synthesis of fatty acids, which are essential for the growth and survival of the bacteria. This disrupts the energy production and metabolism of the bacteria, leading to their death.

4. Ethambutol: Ethambutol works by inhibiting the synthesis of arabinogalactan, another essential component of the bacterial cell wall. Without arabinogalactan, the bacteria are unable to maintain the integrity of their cell wall and are eventually killed.

5. Streptomycin and other aminoglycosides: These drugs work by binding to the bacterial ribosome and interfering with protein synthesis. By disrupting protein synthesis, these drugs prevent the bacteria from producing essential proteins and ultimately lead to their death.

Overall, the combination of these drugs targets different aspects of bacterial growth and replication, making it more difficult for the bacteria to develop resistance. This is why a combination of multiple anti-TB drugs is typically used to treat tuberculosis.
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G
Google Gemini AI
Aug 26
RIFAMPICIN

- Inhibits DNA-dependent RNA polymerase (RdRp) of bacteria.
- Prevents transcription and RNA synthesis.
- Binds to the beta subunit of RdRp.

ISONIAZID (INH)

- Inhibits mycolic acid synthesis, a component of the bacterial cell wall.
- Inhibits the synthesis of the enzyme inhA, which is involved in mycolic acid synthesis.
- Can also disrupt the formation of the FADH2-NAD+ complex, which is involved in oxidative phosphorylation.

PYRAZINAMIDE (PZA)

- Inhibits the synthesis of nicotinamide adenine dinucleotide (NAD), a coenzyme required for many metabolic processes.
- Inhibits the enzyme glutamine synthetase, which is involved in the production of NAD.
- Can also inhibit the proton pump, which is involved in maintaining the pH gradient across the bacterial cell membrane.

ETHAMBUTOL (EMB)

- Inhibits the synthesis of arabinogalactan, a component of the bacterial cell wall.
- Inhibits the enzyme arabinosyltransferase, which is involved in the synthesis of arabinogalactan.
- Can also disrupt the formation of the mycolic acid-arabinogalactan complex, which is essential for the integrity of the bacterial cell wall.

STREPTOMYCIN

- Inhibits protein synthesis by binding to the 16S rRNA of the bacterial ribosome.
- Prevents the binding of aminoacyl-tRNA to the ribosome, disrupting the process of translation.

AMINOGLYCOSIDES (e.g., KANAMYCIN, AMIKACIN)

- Bind to the 16S rRNA of the bacterial ribosome.
- Disrupt the process of translation by causing miscoding and preventing translocation of the ribosome along the mRNA.
- Can also cause cell membrane damage.

QUINOLONES (e.g., MOXIFLOXACIN)

- Inhibit DNA gyrase and topoisomerase IV, which are enzymes involved in DNA replication and transcription.
- Prevent the unwinding and supercoiling of DNA, leading to inhibition of DNA synthesis.
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