Xenobiotic Metabolism: Glutathione Conjugation

What is the primary role of acetyl CoA in the acetylation process?

Which of the following statements about methylation is accurate?

What defines an individual as a 'slow' acetylator?

In the representation of the acetylation reaction, what do X and CoA represent?

What is the result of glutathione conjugation in xenobiotic metabolism?

Xenobiotic Metabolism: Glutathione Conjugation

Xenobiotics (toxic compounds) react with glutathione (GSH) to form glutathione conjugates.
The toxic compound (R) is converted to a non-toxic form (R-S-G).
Glutathione conjugates are metabolised before excretion
The glutamyl and glycinyl groups are removed from the glutathione molecule
An acetyl group is added to the remaining cysteine amino acid
The resulting compound (mercapturic acid) is then excreted in the urine

Acetylation

Acetylation involves the conjugation of hydroxylated xenobiotics with an acetyl group.
Acetyl CoA is the active donor of the acetyl group.
The reaction is catalyzed by acetyl transferase enzymes in the liver and various other tissues.
Individuals can be classified as slow or fast acetylators based on the variations in acetyltransferase enzymes.
Variations in acetyltransferase enzymes can affect how quickly drugs are cleared from the blood (e.g., isoniazid for tuberculosis treatment).

Methylation

Some xenobiotics are excreted as methylated conjugates.
S-adenosylmethionine (SAM) is the active methyl donor.
The reaction is catalyzed by methyl transferase enzymes.

Explore the intricate process of xenobiotic metabolism focusing on glutathione conjugation. Learn how toxic compounds interact with glutathione to form non-toxic derivatives and how acetylation influences drug metabolism. This quiz highlights the key enzymatic reactions and individual variability in drug clearance.