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MCAT Rapid Review

Bio/Biochem — Rapid Review

Biological & Biochemical Foundations of Living Systems. Amino acids, enzymes, metabolism, molecular biology, genetics, cell biology, and physiology — a dense last-week cram sheet. Print or save as PDF.

Original study material for review only — not a substitute for a full course or clinical/scientific reference. Verify high-stakes details against primary sources.

MAP The Section at a Glance

  • 59 questions, 95 min. Content mix (approx.): Biochem ~25%, Biology ~65%, plus gen/organic chem in a biological context.
  • Heavy on experiments, figures, and data interpretation — reason from the passage.
Central themes: structure→function, energy flow, information flow (DNA→RNA→protein), homeostasis and feedback.
Amino-acid focus: nine amino acids are essential (must come from diet): histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine. For the exam, prioritize the charge/polarity classes below — they drive most questions, not the essential list.

BC Biochemistry — Amino Acids & Proteins

Amino Acid Classes (20)

By R-group
ClassMembers
NonpolarGly, Ala, Val, Leu, Ile, Pro, Met, Phe, Trp
Polar unchargedSer, Thr, Cys, Tyr, Asn, Gln
Acidic (−)Asp, Glu
Basic (+)Lys, Arg, His
AromaticPhe, Tyr, Trp (UV 280 nm)
SpecialGly (achiral, flexible), Pro (kink), Cys (disulfide)

Charge & pI

  • All (except Gly) are L, chiral. Zwitterion at physiologic pH.
  • pI = pH of net-zero charge. Below pI → protonated (+); above pI → (−).
  • Titratable groups: α-COOH (~2), α-NH₃⁺ (~9–10), plus side chains (Asp/Glu ~4, His ~6, Cys ~8, Lys ~10.5, Arg ~12.5).

Protein Structure

LevelDefined by
Primaryaa sequence (peptide bonds)
Secondaryα-helix, β-sheet (backbone H-bonds)
Tertiary3-D fold (R-group interactions, disulfides)
Quaternarymultiple subunits
Denaturation (heat, pH, urea) disrupts 2°–4° but not 1°. Chaperones aid folding.

Enzymes

  • Lower activation energy; don't change ΔG or Keq.
  • Models: lock-and-key, induced fit.
  • Cofactors (metals), coenzymes (organic, e.g. NAD⁺, FAD from vitamins).
  • Regulation: allosteric, feedback inhibition, covalent (phosphorylation), zymogens.

Enzyme Kinetics

Michaelis–Menten v = V_max[S]/(K_m+[S])
K_m = [S] at ½V_max (↓K_m = ↑affinity)
Lineweaver–Burk: 1/v vs 1/[S] (linear)
Inhibition
TypeV_maxK_m
Competitive—↑
Noncompetitive↓—
Uncompetitive↓↓
Mixed↓↑/↓

Cooperativity & Hemoglobin

  • Allosteric/cooperative binders (hemoglobin) give a sigmoidal (S-shaped) curve, not hyperbolic — binding one ligand raises affinity for the next.
  • Hemoglobin (cooperative, 4 subunits) vs myoglobin (hyperbolic, 1 subunit, higher affinity).
  • Right shift = ↓ O₂ affinity, unloads to tissue: ↑CO₂, ↓pH (Bohr effect), ↑temperature, ↑2,3-BPG.

Biomolecules

  • Carbs: mono/di/polysaccharides; glycosidic bonds; glycogen (branched storage), cellulose (β, structural).
  • Lipids: triglycerides (storage), phospholipids (membranes, amphipathic), steroids (cholesterol → hormones), fat-soluble vitamins (ADEK).
  • Nucleic acids: nucleotide = sugar + phosphate + base; A-T(U), G-C; antiparallel.
[substrate] → reaction rate v V_max competitive (↑K_m) noncompetitive (↓V_max) ½V_max → K_m at this [S]
Fig 1. Michaelis–Menten kinetics. K_m is the substrate concentration giving half of V_max (lower K_m = higher affinity). Competitive inhibitors are overcome by more substrate (same V_max, higher apparent K_m); noncompetitive inhibitors lower V_max regardless of substrate (K_m unchanged).

MET Metabolism & Bioenergetics

Glucose Oxidation Map

Aerobic yields per glucose
StageLocationYield
Glycolysiscytosol2 ATP, 2 NADH, 2 pyruvate
Pyruvate → acetyl-CoAmito matrix2 NADH (×2 pyr)
TCA (×2 turns)matrix6 NADH, 2 FADH₂, 2 GTP
ETC / Ox-phosinner membraneNADH≈2.5, FADH₂≈1.5 ATP
Total≈30–32 ATP

Key Regulation

  • Glycolysis rate-limiting: PFK-1 (activated by AMP/F-2,6-BP; inhibited by ATP/citrate).
  • TCA rate-limiting: isocitrate dehydrogenase.
  • Insulin → storage (glycogenesis, lipogenesis); glucagon/epi → breakdown (glycogenolysis, gluconeogenesis).

Other Pathways

  • Anaerobic: pyruvate → lactate (regenerates NAD⁺); only 2 ATP.
  • Gluconeogenesis: liver; reverses glycolysis at 3 irreversible steps.
  • β-oxidation: fatty acids → acetyl-CoA (lots of ATP); occurs in mito.
  • Ketogenesis: fasting/low-carb, from acetyl-CoA (liver).
  • PPP: makes NADPH + ribose-5-P (biosynthesis, not ATP).

ETC & Chemiosmosis

  • NADH enters at complex I, FADH₂ at complex II; e⁻ flow drives H⁺ pumping at complexes I, III, IV (complex II does not pump) → proton gradient.
  • ATP synthase (complex V) uses H⁺ flow to make ATP. O₂ = final e⁻ acceptor → H₂O.
  • Uncouplers (e.g., dinitrophenol) dissipate gradient → heat, no ATP.
Glucose Glycolysis2 ATP,2 NADH Pyruvate Acetyl-CoA→ TCA cycle TCANADH,FADH₂ ETC≈30-32ATP anaerobic: pyruvate → lactate (2 ATP only)
Fig 2. Aerobic glucose oxidation. Glycolysis (cytosol) → pyruvate → acetyl-CoA → TCA cycle (mitochondrial matrix) feeds electron carriers into the electron transport chain, where oxidative phosphorylation yields the bulk of ATP. Without O₂, pyruvate is reduced to lactate to regenerate NAD⁺.

MB Molecular Biology & Genetics

Central Dogma

  • Replication (S phase): semiconservative; helicase, primase, DNA pol (5′→3′), leading vs lagging (Okazaki), ligase, telomerase.
  • Transcription (nucleus): RNA pol II; pre-mRNA → 5′ cap, poly-A tail, splicing (introns out, exons kept).
  • Translation (ribosome): initiation (AUG=Met), elongation, termination (stop codons UAA/UAG/UGA); tRNA anticodons.

Mutations

TypeEffect
Silentsame aa (degeneracy)
Missensedifferent aa
Nonsensepremature stop
Frameshiftinsertion/deletion (not ×3)

Gene Regulation

  • Prokaryote: operons (lac = inducible; trp = repressible).
  • Eukaryote: transcription factors, enhancers/silencers, epigenetics (DNA methylation ↓, histone acetylation ↑ expression).

Biotechnology

  • PCR = amplify DNA (denature, anneal, extend). Gel = separate by size (− → +).
  • Blots: Southern (DNA), Northern (RNA), Western (protein).
  • Sanger sequencing; recombinant DNA (restriction enzymes, plasmids); CRISPR.

Mendelian Genetics

  • Dominant/recessive; Punnett squares; incomplete dominance, codominance.
  • X-linked recessive: affects males more; carrier mothers.
  • Autosomal recessive: skips generations; consanguinity.

Hardy–Weinberg

p + q = 1
p² + 2pq + q² = 1
p²=homozygous dominant, 2pq=heterozygous, q²=homozygous recessive. Assumes no selection, mutation, migration, drift; random mating; large population.
DNA mRNA Protein transcription translation replication
Fig 3. The central dogma. DNA is replicated and transcribed to mRNA (nucleus); mRNA is translated to protein at the ribosome. The genetic code is degenerate (multiple codons per amino acid) and read in non-overlapping triplets from a start (AUG) to a stop codon.

CELL Cell Biology & Physiology

Organelles

  • Nucleus (DNA), mitochondria (ATP, own DNA), rough ER (protein synth), smooth ER (lipids, detox), Golgi (modify/ship), lysosome (digest), peroxisome (β-oxidation, H₂O₂).
  • Cytoskeleton: microfilaments (actin), intermediate, microtubules (mitosis, transport).

Membrane Transport

TypeEnergy
Simple/facilitated diffusionnone (down gradient)
Primary active (Na⁺/K⁺ ATPase)ATP
Secondary activeion gradient
Osmosis (water)none
Na⁺/K⁺ ATPase: 3 Na⁺ out, 2 K⁺ in per ATP.

Cell Cycle

  • G₁ → S (DNA copy) → G₂ → M (mitosis: PMAT) → cytokinesis.
  • Checkpoints (G₁/S, G₂/M) gate progression; p53 guards; cyclins/CDKs drive.
  • Meiosis: 2 divisions → 4 haploid gametes; crossing over (prophase I) → diversity.

Signaling & Endocrine

  • Peptide hormones → surface receptors → 2nd messengers (cAMP), fast.
  • Steroid hormones → cross membrane → intracellular receptors → gene transcription, slow.
  • Feedback: mostly negative (e.g., HPA axis).

Neuron & Action Potential

  • Resting ~ −70 mV (Na⁺/K⁺ ATPase + K⁺ leak).
  • Depolarize (Na⁺ in) → repolarize (K⁺ out) → hyperpolarize → refractory.
  • All-or-none; saltatory conduction (myelin, nodes of Ranvier).

Systems Snapshot

  • Circulatory: heart → arteries → capillaries → veins; left heart systemic, right pulmonary.
  • Respiratory: gas exchange at alveoli; O₂/CO₂ diffusion.
  • Renal: nephron — filter (glomerulus), reabsorb, secrete; regulates volume, pH, electrolytes.
  • Digestive: mechanical + enzymatic; absorption in small intestine.
  • Immune: innate (fast, nonspecific) + adaptive (B cells/antibodies, T cells).
+40 −70 time → resting −70 mV threshold ~−55 depol. (Na⁺ in) repol. (K⁺ out) ↓ hyperpolarize
Fig 4. Action potential. A stimulus reaching threshold (~−55 mV) opens voltage-gated Na⁺ channels (rapid depolarization); K⁺ channels then open to repolarize, briefly overshooting to hyperpolarization. The refractory period ensures one-way propagation.