Energy, Thermodynamics, and Enzymes

Vocabulary flashcards covering the laws of thermodynamics, bioenergetics, Gibbs free energy, ATP coupling, enzyme kinetics, and cyclooxygenase inhibitors.

Gibbs Free Energy ($G$)

A thermodynamic quantity representing the amount of energy in a system potentially available to do work, described by the equation $\Delta G = \Delta H - T\Delta S$.

Enthalpy ($H$)

The total energy or heat content of a chemical or biological system.

Entropy ($S$)

A measure of randomness or disorder in a system; in any closed system, entropy constantly increases.

First Law of Thermodynamics

The principle stating that energy cannot be created or destroyed; it can only be transferred or transformed from one form to another.

Second Law of Thermodynamics

The principle stating that every energy conversion releases some energy as heat, increasing the total entropy of a closed system.

Exergonic Reaction

A spontaneous chemical reaction with $\Delta G < 0$ that releases free energy without requiring additional energy input.

Endergonic Reaction

A non-spontaneous chemical reaction with $\Delta G > 0$ that requires an input of free energy to proceed.

Chemical Equilibrium

A state where the forward reaction rate equals the reverse reaction rate ($\Delta G = 0$), producing no net change and leaving no potential to do work.

Anabolism

Cellular metabolic pathways that build new complex biological macromolecules from simpler ones, which are endergonic and require energy input.

Catabolism

Metabolic pathways in cells that break down existing complex macromolecules into simpler components, releasing energy.

Energy Coupling

The pairing of an endergonic reaction with an exergonic reaction (such as ATP hydrolysis) to make the combined net $\Delta G$ negative.

Adenosine Triphosphate (ATP)

The primary energy currency of the cell, which undergoes exergonic hydrolysis into $ADP + P_i$ ($\Delta G = -7.3\,\text{kcal/mol}$) to drive cellular work.

Activation Energy ($E_a$)

The minimum energy input required for reactant molecules to reach the high-energy transition state and initiate a chemical reaction.

Transition State

A high-energy, unstable intermediate molecular conformation that has higher free energy than either the reactants or the products.

Catalyst

A substance that speeds up the rate of a chemical reaction by lowering the activation energy without being consumed, permanently altered, or changing $\Delta G$ or chemical equilibrium.

Enzymes

Biological catalysts, typically proteins, that speed up biological reactions by lowering activation energy without being consumed or permanently altered.

Ribozymes

Catalytic RNA molecules that can function as biological catalysts to accelerate specific biochemical reactions.

Active Site

The specific region on an enzyme where substrate molecules bind based on precise compatibility of shape, chemical groups, and the positions of those chemical groups.

Enzyme Saturation

The condition where all active sites of an enzyme population are occupied by substrate, causing the reaction rate to plateau at $V_{\max}$.

$$V_{\max}$$

The maximum reaction rate achievable by an enzymatic reaction, occurring when the enzyme is completely saturated with substrate.

$K_m$ (Michaelis Constant)

The substrate concentration at which the reaction velocity equals $\frac{1}{2}\,V_{\max}$; it serves as an inverse measure of the enzyme's affinity for its substrate.

Competitive Inhibitor

An inhibitor that competes with the substrate by binding directly to the active site, physically blocking substrate binding.

Noncompetitive Inhibitor

An inhibitor that binds to an allosteric site separate from the active site, inducing a conformational change that impedes substrate binding or catalysis.

Allosteric Site

A regulatory site on an enzyme distinct from the active site where effector molecules bind to alter the enzyme's shape and activity.

Cyclooxygenase (COX)

An enzyme that catalyzes the conversion of arachidonic acid to prostaglandin $H_2$, a precursor for prostaglandins that mediate fever, inflammation, and pain.

COX-1

A cyclooxygenase isoform that synthesizes prostaglandins involved in protecting the stomach lining and promoting platelet activation.

COX-2

A cyclooxygenase isoform induced during inflammatory responses that synthesizes prostaglandins promoting inflammation, pain, and fever.

Aspirin (Acetylsalicylate)

A drug that irreversibly inactivates both COX-1 and COX-2 by transferring an acetyl group to a residue inside the active site.

Ibuprofen (Motrin)

A non-steroidal anti-inflammatory drug that acts as a competitive inhibitor of both COX-1 and COX-2.

Naproxen (Aleve)

A pain reliever and anti-inflammatory medication that acts as a noncompetitive inhibitor of both COX-1 and COX-2.

Acetaminophen (Tylenol)

An analgesic that does not bind to the COX active site, appears multimodal, preferentially inhibits COX-2, and is the leading cause of acute liver failure in the United States when overdosed.