Liver Functions

The liver performs hundreds of distinct biochemical functions, but three of them are central to the OCR specification: detoxification, deamination of excess amino acids, and the ornithine cycle that converts toxic ammonia to urea. These illustrate perfectly how a single organ can integrate nutrient processing, waste disposal and biosynthesis. This lesson covers these key functions in the depth expected for A-Level, with named enzymes, substrates and products, matching OCR A-Level Biology A specification module 5.1.2(d).

Key Definitions:

• Detoxification — the chemical modification of toxic substances so they can be safely excreted or used.
• Deamination — the removal of the amino group (−NH₂) from an amino acid.
• Ornithine cycle — the sequence of reactions in hepatocytes that combines ammonia with CO₂ to form urea.
• Dehydrogenase — an enzyme that catalyses the removal of hydrogen from a substrate, usually passing it to NAD⁺.

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An Overview of Liver Functions

Before focusing on the three OCR functions, it helps to appreciate the breadth of the liver's work:

Function	Example
Nutrient processing	Converts glucose to glycogen for storage (glycogenesis); releases glucose when needed (glycogenolysis); makes glucose from non-carbohydrate sources (gluconeogenesis).
Lipid metabolism	Synthesises cholesterol, bile salts and lipoproteins; β-oxidation of fatty acids.
Protein synthesis	Produces plasma proteins (albumin, clotting factors, transport proteins).
Detoxification	Modifies alcohol, drugs, hormones and toxins for excretion.
Deamination	Removes amino groups from surplus amino acids and converts them to urea.
Storage	Stores iron, vitamins A, D, B₁₂, and glycogen.
Bile production	Produces bile containing bile salts and bile pigments.
Immune function	Kupffer cells phagocytose bacteria and old red blood cells.

OCR focuses on detoxification, deamination and the ornithine cycle — but awareness of this wider context helps you understand why exam questions often integrate liver function with other topics.

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Detoxification

Detoxification is the chemical transformation of potentially harmful substances into less harmful (or more easily excreted) compounds. These include:

• Alcohol (ethanol) from drinks.
• Drugs such as paracetamol, antibiotics and anaesthetics.
• Hormones that have already had their effect and must be inactivated (e.g., oestrogen, cortisol, insulin).
• Toxins produced by gut bacteria or absorbed from food (e.g., ammonia, food colourings).

Most detoxification reactions occur in the smooth endoplasmic reticulum (SER) of hepatocytes, where specific enzymes catalyse:

• Oxidation (adding oxygen or removing hydrogen).
• Reduction (adding hydrogen).
• Hydrolysis (breaking bonds with water).
• Conjugation (attaching a water-soluble molecule such as glucuronic acid to aid excretion).

The Breakdown of Alcohol

Alcohol (ethanol) is the classic detoxification example and the one OCR most commonly asks about.

flowchart LR
    A[Ethanol<br/>CH3CH2OH] -->|alcohol dehydrogenase<br/>NAD+ → NADH| B[Ethanal<br/>CH3CHO]
    B -->|aldehyde dehydrogenase<br/>NAD+ → NADH| C[Ethanoate<br/>CH3COO-]
    C -->|+ CoA, ATP| D[Acetyl CoA]
    D --> E[Krebs cycle<br/>or fatty acid synthesis]

1. Ethanol → ethanal. Catalysed by alcohol dehydrogenase (ADH) in the cytoplasm of hepatocytes. Hydrogen is removed from the ethanol molecule and transferred to NAD⁺, forming NADH + H⁺. The product, ethanal (acetaldehyde), is itself toxic — responsible for many of the symptoms of a hangover.
2. Ethanal → ethanoate. Catalysed by aldehyde dehydrogenase (ALDH) in mitochondria. Again, hydrogen is removed and transferred to NAD⁺. The product is ethanoate (acetate).
3. Ethanoate → acetyl CoA. Ethanoate is combined with coenzyme A to form acetyl CoA, which can enter the Krebs cycle to release energy, or be used to synthesise fatty acids for storage.

Consequences of Heavy Drinking

Chronic alcohol consumption has predictable consequences based on this pathway:

• Each step produces NADH. A high NADH:NAD⁺ ratio inhibits fatty acid oxidation and promotes fatty acid synthesis. The result is fatty liver (steatosis).
• Fatty acids accumulate in hepatocytes, causing inflammation (alcoholic hepatitis).
• Long-term damage triggers stellate cells to deposit collagen — scar tissue replaces functional hepatocytes (cirrhosis), which is irreversible.
• Ethanal is toxic and mutagenic, contributing to hepatic injury.

OCR questions often ask you to explain why alcohol causes fatty liver. The answer lies in the disturbed NAD⁺/NADH balance, not merely in "ingesting fat".

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Deamination

Mammals cannot store excess amino acids. Protein eaten in excess of the body's needs must therefore be disposed of. The liver performs this through deamination: the removal of the amino group (−NH₂) from each excess amino acid.

The Reaction

In simplified form:

$\text{amino acid} + \text{O}_2 \rightarrow \text{keto acid} + \text{NH}_3$amino acid+O2​→keto acid+NH3​

• The amino group is removed as ammonia (NH₃). Ammonia is extremely toxic, so it is immediately fed into the ornithine cycle (see below) for conversion to urea.
• The remaining carbon skeleton is a keto acid, which enters central metabolism. It can be used for respiration (converted to pyruvate or Krebs cycle intermediates), for gluconeogenesis, or for the synthesis of fatty acids.