explain the effects of reversible inhibitors, both competitive and non-competitive, on enzyme activity

Enzyme Activity – Factors and Reversible Inhibition

Learning Objectives (Cambridge AS & A‑Level Biology 9700)

  • AO1: Describe the factors that affect enzyme activity and explain how reversible (competitive and non‑competitive) inhibitors influence the rate of reaction.
  • AO2: Analyse experimental data (e.g. Michaelis–Menten and Lineweaver‑Burk plots) to determine the kinetic effect of different inhibitors and other factors.
  • AO3: Plan, carry out and evaluate a practical investigation that investigates the effect of inhibitors (and, where appropriate, temperature, pH or concentrations) on enzyme activity.

1. Factors that Influence Enzyme Activity (AO1)

Enzymes are biological catalysts; their activity can be altered by a range of internal and external factors. The syllabus expects you to be able to name and explain the effect of each factor.

FactorTypical Effect on Reaction RateReason
TemperatureRate ↑ up to an optimum, then ↓ sharplyHigher temperature increases kinetic energy → more collisions; above optimum denaturation destroys active‑site geometry.
pHRate ↑ to an optimum, then ↓pH alters ionisation of active‑site residues; extreme pH causes denaturation.
Enzyme concentrationRate ↑ (linear) when substrate is in excessMore enzyme molecules mean more active sites available.
Substrate concentrationRate ↑ rapidly then plateaus (Vmax)At high [S] all enzyme molecules are saturated (ES complex formation reaches maximum).
Reversible inhibitors (competitive, non‑competitive, uncompetitive)Change apparent Km and/or Vmax without destroying the enzymeInhibitor binds non‑covalently; effect depends on binding site and whether it can bind to ES.
Irreversible inhibitorsPermanent loss of activity (Vmax ↓, Km unchanged)Covalent modification of active‑site residues prevents substrate binding.
Allosteric regulation (activators or inhibitors)Can increase or decrease Vmax; often changes KmBinding at a site distinct from the active site induces conformational change.
Cofactors / co‑enzymesMay be required for activity; absence → ↓ rateProvide essential groups (e.g., metal ions, vitamins) for catalysis.

2. Reversible Inhibitors – Competitive and Non‑competitive (AO1)

2.1 General Features

  • Bind to the enzyme by non‑covalent forces (hydrogen bonds, ionic interactions, Van‑der‑Waals).
  • The binding is reversible – the inhibitor can dissociate, restoring activity.
  • They alter the kinetic parameters Km (affinity) and/or Vmax (maximum rate) in characteristic ways.

2.2 Competitive Inhibition

  • The inhibitor has a structure similar to the substrate and competes for the active site.
  • It can bind only to the free enzyme (E); it cannot bind to the enzyme–substrate complex (ES).
  • Increasing substrate concentration can out‑compete the inhibitor, restoring the original rate.
  • Kinetic effect: Vmax is unchanged; apparent Km increases.

Modified Michaelis–Menten equation

\$v=\frac{V{\max}[S]}{Km\left(1+\frac{[I]}{K_i}\right)+[S]}\$

where [I] = inhibitor concentration and Ki = inhibition constant.

2.3 Non‑competitive Inhibition

  • The inhibitor binds to an allosteric site that is distinct from the active site.
  • It can bind to both free enzyme (E) and the ES complex, forming EI and ESI.
  • Increasing substrate concentration cannot overcome the inhibition because the active site remains accessible but the enzyme’s catalytic efficiency is reduced.
  • Kinetic effect: Vmax decreases; apparent Km is unchanged.

Modified Michaelis–Menten equation

\$v=\frac{V{\max}\left(1+\frac{[I]}{Ki}\right)^{-1}[S]}{K_m+[S]}\$

2.4 Comparison at a Glance

FeatureCompetitive InhibitionNon‑competitive Inhibition
Binding siteActive site (substrate‑like)Allosteric site (different)
Enzyme form boundOnly free enzyme (E)Both free enzyme (E) and ES complex
Effect on VmaxNo changeDecreases
Effect on apparent KmIncreasesNo change
Can be overcome by more substrate?YesNo
Typical exampleMethotrexate vs dihydrofolate reductase (substrate analogue)Lead (Pb²⁺) inhibiting δ‑aminolevulinic acid dehydratase (allosteric binding)

2.5 Real‑World Relevance (Biological, Social & Economic Context)

  • Drug design: Many pharmaceuticals are competitive inhibitors (e.g., statins inhibit HMG‑CoA reductase) or non‑competitive inhibitors (e.g., allosteric modulators of neurotransmitter receptors).
  • Pesticide resistance: Mutations that reduce inhibitor binding (e.g., altered acetylcholinesterase) illustrate the importance of understanding kinetic inhibition.
  • Toxicology: Heavy‑metal poisoning often involves non‑competitive inhibition of key metabolic enzymes.

3. Assumptions of the Michaelis–Menten Model (AO2)

  • Steady‑state: The concentration of the ES complex remains constant during the initial phase of the reaction.
  • Substrate excess: [S] ≫ [E]; substrate concentration does not change appreciably during the short measurement period.
  • Single substrate, single active site: The model applies to simple one‑substrate reactions.
  • Negligible reverse reaction and product inhibition: Measurements are taken before significant product accumulates.

4. Practical Investigation – Effects of Inhibitors (and optionally temperature/pH) (AO2 & AO3)

4.1 Planning Template

SectionContent to Include
AimTo determine how a competitive and a non‑competitive inhibitor affect the kinetic parameters (Km and Vmax) of catalase‑catalysed decomposition of hydrogen peroxide.
HypothesisAzide (competitive) will increase the apparent Km but not change Vmax; lead ions (non‑competitive) will lower Vmax with no change in Km.
Variables

  • Independent: Inhibitor type and concentration; substrate concentration ([H₂O₂]).
  • Dependent: Initial rate of O₂ evolution (ΔV/Δt) or decrease in absorbance at 240 nm.
  • Controlled: Temperature (e.g., 25 °C water bath), pH (phosphate buffer, pH 7.0), enzyme amount (fixed mass of catalase), volume of reaction mixture.

MaterialsCatalase solution (e.g., from potato), H₂O₂ (various concentrations), sodium azide solution, Pb(NO₃)₂ solution, phosphate buffer (pH 7.0), colourimetric reagent (e.g., KI/TiOSO₄), spectrophotometer or gas‑collection apparatus, water bath, pipettes, test tubes.
Method (outline)

  1. Prepare a series of H₂O₂ solutions (0.5, 1.0, 2.0, 4.0 mM) in buffer.
  2. For each substrate concentration set up three reactions: control, + azide (1 mM), + Pb²⁺ (0.5 mM).
  3. Add a fixed volume of catalase to start the reaction; immediately record the change in absorbance at 240 nm every 10 s for 1 min (or collect O₂ gas for 30 s).
  4. Repeat each assay at least three times to ensure reliability.

SafetyHandle H₂O₂ (oxidiser) with gloves; azide is toxic – work in a fume hood; lead salts are hazardous – wear lab coat and dispose of waste according to regulations.
RepeatabilityPerform each measurement in triplicate; randomise the order of substrate concentrations to minimise systematic error.

4.2 Data Analysis Checklist (AO2)

  1. Convert absorbance change to concentration change using Beer‑Lambert law (or calculate gas volume to moles of O₂).
  2. Calculate the initial rate (v) for each [S] (slope of the first linear segment).
  3. Plot a Michaelis–Menten curve (v vs [S]) for each condition.
  4. Construct a Lineweaver‑Burk plot (1/v vs 1/[S]) and determine:

    • y‑intercept = 1/Vmax
    • x‑intercept = –1/Km

  5. Compare the slopes and intercepts:

    • Competitive: lines intersect on the y‑axis (same 1/Vmax, larger slope → higher apparent Km).
    • Non‑competitive: lines intersect on the x‑axis (same –1/Km, higher y‑intercept → lower Vmax).

  6. Calculate % error between observed and literature values of Km and Vmax.

4.3 Evaluation Prompts (AO3)

  • How might oxygen bubbles affect the spectrophotometric measurement? Suggest a method to minimise this (e.g., use a gas‑tight cuvette).
  • Discuss the reliability of the colourimetric assay at high H₂O₂ concentrations (possible substrate inhibition).
  • Identify sources of random error (pipetting, temperature fluctuations) and systematic error (incorrect inhibitor concentration).
  • Propose an improvement: e.g., use a stopped‑flow apparatus for more precise initial‑rate determination.
  • Explain how the experiment could be extended to investigate temperature or pH effects while keeping inhibitor concentration constant.

5. Summary (AO1)

  1. Enzyme activity is modulated by temperature, pH, enzyme/substrate concentrations, cofactors, and inhibitors.
  2. Reversible inhibitors bind non‑covalently:

    • Competitive: bind active site → increase apparent Km, Vmax unchanged; effect can be overcome by excess substrate.
    • Non‑competitive: bind allosteric site → decrease Vmax, Km unchanged; substrate cannot overcome inhibition.

  3. Understanding these kinetic signatures enables prediction of drug action, toxicity, and metabolic regulation.

Key Points to Remember (AO1)

  • An increase in Km reflects reduced affinity of enzyme for substrate.
  • A decrease in Vmax indicates that fewer active enzyme molecules are available for catalysis.
  • Only competitive inhibition can be mitigated by raising substrate concentration; non‑competitive inhibition cannot.
  • When analysing data, the pattern of line intersections on a Lineweaver‑Burk plot tells you instantly which type of reversible inhibition is present.