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Metabolism
all the chemical reactions in a living cell to sustain life
Metabolic Pathways
a series of biochemical reactions in cells that are catalyzed by an enzyme
Catabolism
the process of breaking down compounds into smaller molecules to release energy
Anabolism
the process of using energy to make larger compounds
Endergonic Reactions
non-spontaneous, requires energy to occur
Exergonic Reactions
spontaneous, occurs on their own
e.g. ATP hydrolysis
Coupled Reactions
pairing an endergonic reaction with an exergonic reaction to drive the endergonic one
e.g. ATP hydrolysis releases free energy which can be used by another reaction
Redox Reactions
transfer of electrons between substances using cofactors
“reduction-oxiation” reactions
Oxidation
loss of electrons
Reduction
gain of electrons
Cofactor
inorganic compound needed by an enzyme to catalyze a reaction
Coenzyme
organic molecule needed by enzyme to catalyze a reaction
e.g. NAD+/NADH functioning as an electron carrier/acceptor for oxidation of energy rich molecules
ADP & ATP
energy storing/releasing molecules
ADP - energy poor, ATP - energy rich
adding Pi stores energy, removing Pi releases energy
energy used for photosynthesis, protein synthesis, active transport, muscle contractions
Substrate-Level Phosphorylation
phosphate removed from substrate to phosphorylate ADP → ATP
Oxidative Phosphorylation
oxidizes NADH and FADH2 to create gradient for ATP synthesis
Aerobic Respiration
needs O2
Anaerobic Respiration
does not need O2
Cellular Respiration
break down glucose in presence of oxygen
C6H12O6 + O2 → CO2 + H2O + ATP
energy released in small, controlled steps → 36/38 ATP made
Matrix
space within the inner membrane of the mitochondria
lower [H+] than intermembrane space
ADP + Pi enters ATP synthase and exits as ATP from matrix
Cristae
folds of the mitochondrial inner membrane
Intermembrane Space
space between outer and inner membrane
higher [H+] than mitochondrial matrix
Glycolysis
net equation: 1 glucose → 2 ATP + 2 NADH
2 NADH → 2 FADH2 in eukaryotes (since mitochondrial inner membrane is impermeable to NADH, needs energy to shuttle)
Pyruvate Oxidation
Net products per 1 glucose: 2 NADH
Krebs Cycle
net products: 6 NADH, 2 FADH2, 2 ATP
Electron Transport Chain (ETC)
uses free energy from electrons transferred by NADH and FADH2 to pump H+ to intermembrane space
electrochemical gradient is created → chemical potential energy
36/38 H+ are pumped
oxygen is final electron acceptor
Chemiosmosis
1 H+ pumped → 1 ATP made in matrix via ATP synthase
ATP synthase spins from chemical potential energy
Fermentation
occurs in anaerobic conditions
alternative to oxidize NADH since ETC is not working (no oxygen = no final acceptor to oxidize)
inefficient ATP synthesis (2 ATP vs 36/38 ATP)
Alcohol Fermentation
NADH is oxidized by acetylaldehyde to make NAD+
acetylaldehyde is reduced to ethanol (ethyl alcohol)
Lactic Acid Fermentation
pyruvate oxidizes NADH to form NAD+
pyruvate is reduced to lactic acid (lactate)
Phosphofructokinase (PFK)
main control in glycolysis
converts F6P to F1,6BP via phosphorylation
extra ADP → binds to allosteric site to increase enzyme activity
extra ADP → binds to same allosteric site as ADP to decrease enzyme activity
extra citrate → binds to different allosteric site as ADP to decrease enzyme activity
Pyruvate Dehydrogenase
main control in pyruvate oxidation
pyruvate + NAD+
extra NADH binds to active site to compete against NAD+ → decrease enzyme activity
Mobile Carriers
transports electrons between enzymes (complexes)
e.g. Ubiquinone (Q) and Cytochrome C (C)
Deamination
removal of a amino group from an amino acid
amino → ammonia → urea
organic acid → molecule in cellular respiration
Leucine
becomes acetyl-CoA after undergoing deamination
Alanine
becomes pyruvate after undergoing deamination
Proline
becomes α-ketoglutarate after undergoing deamination
Beta-Oxidation
occurs in mitochondria
fatty acids (triglycerides/free fatty acid tails) are broken into acetyl-CoA
1 β-oxidation → 1 acetyl-CoA, 1 NADH, 1 FADH2
Glycerol
becomes glucose via gluconeogenesis
becomes DHAP with help of enzymes → G3P (DHAP is unstable)
Gluconeogenesis
making glucose from non-carbohydrate precursors
Friederich’s Ataxia
autosomal recessive → mutation in FXN gene → less frataxin production
lack of ATP made, loss of movement (neurological, cardiovascular, muscular)
Frataxin
a protein responsible for making iron-sulfur clusters
important for ETC to prevent accumulation of iron
iron accumulation → oxidative stress and ETC damage
Omaveloloxone
treatment for Friederich’s Ataxia
activates Nrf2 pathways → increases antioxidants → lowers oxidative stress & inflammation
Cyanide Poisoning
cyanide binds to and inhibits cytochrome oxidase complex
prevents oxidation of the complex → can’t pass electrons to oxygen → obstructs ETC
lack of ATP production
dizziness, restlessness, rapid/slow breathing