Biochemistry: Biological Molecules, Enzymes and Metabolism
Molecules, catalysts, energy
Biochemistry items reward precise bookkeeping: which bond, which compartment, how many ATP, and which factor limits the rate. Vague answers such as the enzyme speeds up the reaction lose most of the credit.
Core rules
- Carbohydrates: glycosidic bonds; starch (plant storage, α-glucose), glycogen (animal storage, branched), cellulose (structural, β-1,4, indigestible), chitin.
- Lipids: ester bonds between glycerol and fatty acids; saturated (no C=C, solid) vs unsaturated; phospholipids are amphipathic; steroids have four fused rings.
- Proteins: peptide bonds; primary to quaternary structure; hydrogen, ionic, hydrophobic and disulfide interactions set tertiary shape; denaturation destroys shape, not peptide bonds.
- Nucleic acids: phosphodiester bonds; 5-prime to 3-prime directionality.
- Enzymes: lower activation energy, are not consumed; active-site specificity and induced fit; temperature and pH optima; substrate saturation gives Vmax; Km is the substrate concentration at half Vmax, so low Km means high affinity; competitive inhibitors raise Km, noncompetitive inhibitors lower Vmax; allosteric and feedback inhibition; cofactors and coenzymes such as NAD⁺.
- Respiration: glycolysis in the cytoplasm (net 2 ATP, 2 NADH, 2 pyruvate); Krebs cycle in the matrix (per glucose: 6 NADH, 2 FADH₂, 2 ATP); electron transport chain on the inner membrane with chemiosmosis, about 30–32 ATP; fermentation regenerates NAD⁺.
- Photosynthesis: light reactions on the thylakoid (water split, O₂ released, ATP and NADPH made); Calvin cycle in the stroma, RuBisCO fixes CO₂.
Worked example
Activity rises about twofold per 10 °C up to the optimum, then falls sharply. Reasoning: beyond the optimum, hydrogen and ionic interactions break, the active site loses complementary shape, and substrate no longer binds - the fall is denaturation, not slower collisions.
Marks lost
Saying enzymes lower ΔG or are used up; quoting 36 ATP for Krebs alone; placing the Calvin cycle on the thylakoid; treating a low Km as low affinity.