Carbohydrate: monosaccharide (e.g., glucose), energy & structural (cellulose); Lipid: glycerol + fatty acids (no true monomer), energy storage / membranes / hormones; Protein: amino acid, structure / catalysis / transport; Nucleic acid: nucleotide (sugar + phosphate + base), information storage (DNA) / expression (RNA).
B. Phosphate-containing head is polar/charged (hydrophilic); two fatty-acid tails are non-polar (hydrophobic). This amphipathic property drives bilayer formation.
B. Enzymes provide an alternate pathway with lower E_a so more substrate molecules have enough energy to react at body temperature. They do not change ΔG or K_eq.
V_max = horizontal asymptote; rate when all sites occupied. K_m = [S] at v = ½V_max; lower K_m means higher affinity. Saturation region = plateau where adding [S] no longer increases rate (rate-limited by enzyme amount).
B. Heat disrupts H-bonds and hydrophobic interactions that hold tertiary structure; the active site collapses (denaturation). Primary sequence is intact (peptide bonds are covalent and stable).
Phospholipid bilayer (semipermeable barrier); cholesterol (fluidity buffer); integral/transmembrane proteins (transport, receptors); peripheral proteins (signaling, structure); glycoproteins/glycolipids (cell recognition, immunity).
v = 100·[S]/(2+[S]). At [S]=2: v = 100·2/4 = 50 µmol/min. At [S]=4: v = 100·4/6 ≈ 66.7 µmol/min. At [S]=20: v = 100·20/22 ≈ 90.9 µmol/min (approaching V_max).
IV: temperature (e.g., 0, 20, 37, 60, 80 °C). DV: rate of starch breakdown (time for iodine test to stop turning blue-black, or absorbance over time). Controlled: amylase concentration, starch concentration, pH (buffer), volume, mixing. Hypothesis: rate increases up to ~37 °C optimum then declines as enzyme denatures. Replicate ≥3 trials/condition; plot rate vs T.
Without I: hyperbolic curve to V_max with K_m = some value. With non-competitive I: lower V_max (because some enzyme molecules are inactive regardless of [S]); K_m unchanged (the enzymes that remain active have unchanged affinity). The curve plateaus at lower height. (Contrast with competitive: same V_max, higher apparent K_m.)
Lock-and-key (Fischer, 1894): rigid active site fits one substrate exactly. Induced-fit (Koshland, 1958): active site is flexible — substrate binding induces a conformational change that brings catalytic residues into optimal alignment, stabilizes the transition state, and lowers E_a. Induced-fit better explains promiscuous enzymes and allosteric regulation.
Phospholipid: glycerol backbone, phosphate head (polar), 2 fatty acid tails (non-polar). Bilayer with heads outward, tails inward. Cholesterol nestled among tails. Integral (transmembrane) proteins span the bilayer; peripheral proteins on one face only. Glycolipids and glycoproteins on extracellular side carry oligosaccharide chains for cell recognition.
Simple diffusion: no ATP, with gradient, example O₂/CO₂. Facilitated diffusion: no ATP, with gradient, requires channel/carrier protein, example glucose via GLUT, water via aquaporin. Active transport: ATP required, against gradient, example Na+/K+ ATPase pumping 3 Na+ out / 2 K+ in.
Lactase, a brush-border enzyme on small intestine villi, hydrolyzes lactose → glucose + galactose for absorption. Deficient lactase means lactose persists, drawing water osmotically (diarrhea) and is fermented by colon bacteria producing H₂, CO₂, methane (gas, cramps). Oral lactase supplement provides exogenous enzyme that hydrolyzes lactose before bacteria can ferment it.
0.9% NaCl matches blood plasma osmolarity (~300 mOsm), so RBCs experience no net water movement and remain normal. Pure water (hypotonic) → water rushes into RBCs → swell & hemolyse. 5% NaCl (hypertonic) → water leaves RBCs → crenate (shrivel), losing function. Isotonic prevents both.
(i) Partial hydrogenation of vegetable oils converts cis-double bonds (kinked) to trans (straight), increasing shelf life and giving spreadable texture. (ii) Trans tails pack like saturated fats, raising melting point. (iii) Trans-fats raise LDL ("bad") cholesterol and lower HDL ("good"), accelerating atherosclerosis and heart-disease risk; hence regulatory limits.