7 topics with concise reviews: definitions, key facts, and class questions.
The liver is the body's primary biochemical laboratory. In this section, we examine how endogenous metabolites (e.g., amino acid putrefaction products in the gut) and exogenous xenobiotics are converted into safe, water-soluble compounds for elimination from the body.
The material covers all key detoxification pathways. We will break down conjugation reactions (glucuronidation and sulfation), the protective role of glutathione, as well as applied medical topics: drug biotransformation, ethanol metabolism, and the mechanisms of chemical carcinogenesis.
In colloquia and exams, professors most frequently expect a clear understanding of the two phases of detoxification (oxidation and conjugation), the structure and function of cytochrome P450, and the biochemistry of hangovers—the toxic effects of acetaldehyde. This foundational knowledge will serve as your basis for studying pharmacology and clinical toxicology.
What substance is UDP-glucuronic acid formed from?
The precursor substance is UDP-glucose, which is oxidized in the presence of the enzyme UDP-glucose dehydrogenase.
What is the difference between the GSH and GSSG forms of glutathione?
GSH is the reduced, functionally active form of the molecule with a free thiol (SH) group of cysteine. GSSG is the oxidized form, in which two glutathione molecules are tightly linked together by a disulfide bridge.
Which amino acids are the precursors of the main intestinal toxins?
Phenol and p-cresol are formed during the breakdown of tyrosine. Indole and skatole are products of bacterial degradation of tryptophan.
Why is the dose of a drug often required to be increased with prolonged use?
Due to enzyme induction. Drugs stimulate the synthesis of enzymes of the monooxygenase system and conjugation reactions, which accelerates the metabolism and elimination of the drug from the body.
Why can hypoglycemia develop with alcohol consumption?
Alcohol oxidation is accompanied by a massive accumulation of the reduced coenzyme NADH. Its excess inhibits gluconeogenesis (the synthesis of glucose from non-carbohydrate precursors), leading to a drop in blood sugar levels.
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