bio 2 ch.9

how C-H bonds are source of energy for cellular respiration

• high potential energy covalent bond

• high stable bond formed when oxidized

NAD+

• oxidized

• electron acceptor (empty)

• extract 2 electron & 1 H+ during glycosis & krebs cycle

NADH

• reduced

• Electron donor

• deliver electron to Complex 1 of ETC. power heavy proton pumping, 2.5-3 atp

FAD

• oxidized

• electron acceptor bound to Krebs cycle (complex II)

• extract 2 electron & 2 H+ from lower energy substrate that NAD+ cannot oxidize

FADH2

• reduced

• delivers electron to Complex II of ETC, bypass Complex I, pumps fewprotoen & low energy return of 1.5-2 ATP

NADH ATP production

2.5 ATP

FADH2 ATP production

1,5 ATP

Glycosis

Location: cytosol

Reactants & Products: 1 glucose, 2 NAD+, 2 ADP + 2 Pi & 2Pyruvate, 2 NADH, 2 net ATP

Substrates for next reaction: pyruvate goes to pyruvate oxidation, NADH goes to ETC(fermentation)

O2 Effect: unaffected by O2, run both aerobic(Acety CoA, Kreb cycle) & anaerobic (lactic acid)

Inhibition Effect: glucose breakdown stops entirely, drop total cell ATP yield to zero unless alternative

fermentation

Location:cytosol

Reactants & Products: 2 Pyruvate, 2 NADH (glycolysis) & 2 Lactate/Ethanol + 2 CO2(yeast), 2 NAD+

Substrates for next reaction: NAD+ cycles back to keep glycolysis running

O2 Effect: only when no/little O2

Inhibition Effect: blocked under anaerobic conditions, NAD+ cannot regenerate, holds glycolysis & kills ATP production from glucose

Pyruvate oxidation

Location: Mitochondrial Matrix

Reactants & Products: 2 Pyruvate, 2 CoA, 2 NAD+ & 2 Acetyl-CoA, 2 CO2, 2 NADH

Substrates for next reaction: Acetyl - CoA enters Krebs cycle, NADH goes to ETC

O2 Effect:Require O2 indirectly, without O2, ETC halts → backup of NADH & lack of available NAD+

Inhibition Effect: stops link to aerobic respiration, shift cell to fermentation, drop ATP yielf to 2 net ATP per glucose

Citric acid cycle

Location: mitochondrial matrix

Reactants & Products: 2Acetyl-CoA, 6 NAD+, 2 FAD, 2 ADP + 2Pi & 4CO2, 6NADH, 2FADH2, 2ATP/GRP

Substrates for next reaction: NADH & FADH2 to ETC

O2 Effect: Strictly aerobic, require O2 to clear NADH & FADH2 back into empty NAD+ & FAD

Inhibition Effect: aerobic respiration halts, bulk source of electron carrier drops, ATP tield down to 2 net ATP (glycolysis/fermentation)

Electron Transport

Location: inner mitochondrial membrane (cristae)

Reactants & Products: 10 NADH, 2 FADH2, 6O2 & 10NAD+, 2FAD, 6H2O, Proton H+ gradient

Substrates for next reaction: Proton H+ for ATP synthase, NAD+/FAD return to earlier stages

O2 Effect: Strictly aerobic, without O2 chain stops

Inhibition Effect: no electron flow, proton gradient not established, drop oxidative ATP yield to 0

Oxidative phosphorylation

Location: inner mitochondrial membrane/matrix

Reactants & Products: Proton H+, ADP + Pi & ATP, H+ ions return to matrix

Substrates for next reaction: ATP export to cytoplasm power cellular work

O2 Effect: strictly aerobic, reliant on ETC (stops without O2)

Inhibition Effect: If ATP production blocked, aerobic ATP generation drop to 0

Effect of inhibition at Complex I

NADH cannot donate electrons

ATP drops significantly

FADH2 still feed electrons into Complex II

Effect of inhibition at Complex II

FADH2 cannot donate electrons

ATP drops slightly

NADH still feed electrons to Complex I, maintain most proton gradient

Effect of inhibition at Coenzyme Q

Shuts down electron collection from Complex I & Complex II

ATP production crash near 0 (no electron reach rest of chain)

Effect of inhibition at Complex IV

prevents electron from leaving chain onto O2

entire ETC locks up

Aerobic ATP production completely stops

Ion transport function of ATP synthase

Act as channel protein for facilitated diffusion, allows H+ protons flow down their electrochemical gradient from inter membrane space back into mitochondrial matrix

Enzyme functions of ATP synthase

Molecular rotary motor, passage of proton forces internal rotor to spin, changing the conformation of catalytic know in the matrix to squeeze ADP & pi together into ATP

Direct source of energy for specific reaction that synthesizes ATP

Proton Motice Force (PMF)/Electrochemical H+ Gradient. Kinetic energy of proton flow down their concentration gradient drive the reaction

Changes in ATP synthesis if H+ concentration gradient changes

Increase gradient (more H+ outside): Speeds up rotation of ATP synthase → increase ATP synthesis

Decrease/destroy gradient: motor stops spinning → ATP synthesis drops to 0, energy lost as heat

How properties of respiratory surfaces affect gas diffusion rate

Large Surface Area (A) : provide max space (increase) (tiny millions of alveoli)

Thin (low) Barrier (x): single cell layer thick to minimize denominator (increase)

Large concentration gradient (C2 - C1) : difference high, increase

Moist: prevent cell membrane from collapsing

physical limitation of extracting oxygen from water

Oxygen content: low in water, must extract volume of water

Density: high in water, push dense fluid across respiratory surfaces require huge muscle power

Viscosity(thick/sticky): high in water, harder to move through gills

Qs

Amount of substance diffused

D(diffusion coefficient, constant determine by gas molecule)

directly proportional

A (Surface Area)

Directly proportional

C2 - C1 (Concentration difference)

Directly proportional

X (Diffusion distance/membrane thickness)

Inversely proportional

t = Time

Directly proportional