Biochemistry 2 Flashcards
oxidation
- gain oxygen
- lose hydrogen
- lose electrons
reduction
- lose oxygen
- gain hydrogen
- gain electrons
where does glycolysis occur?
is oxygen needed?
- cytosol
- no
where does the PDC/Krebs cycle occur
is oxygen needed?
- cytosol (prokaryotes)
- mitochondrial matrix (eukaryotes)
- indirectly needed
where does the ETC/Ox phos occur?
is oxygen needed?
- cytosol (prokaryotes)
- inner mitochondrial membrane (eukaryotes)
- yes directly
enzyme that converts glucose to glucose-6-phosphate
regulation
- hexokinase
- ATP used
(-) G-6-P
enzyme that converts fructose-6-phosphate to fructose-1,6-bisphosphate
regulation
- PFK-1
- first committed step
- ATP used
(-) ATP, Citrate
(+) AMP, F-2,6-bisP
enzyme that converts phosphoenolpyruvate to pyruvate
- pyruvate kinase
PDC
- 2 pyruvate put in
- 2 acetyl CoA come out; produce 2 NADH and release CO2
- oxidize pyruvate
- reduce NAD+
Krebs
- oxidative decarboxylation reactions
- acetyl-CoA reacts with oxaloacetate - forms citrate with loss of CoA
- 3 NADH, 1 FADH2 are produced per acetyl-CoA
- 3 CO2 lost.
2 goals of ETC
- oxidize (empty) the electron carriers
- make usable energy (ATP)
process of ETC
- NADH oxidized at NADH dehydrogenase
- FADH2 oxidized at coenzyme Q. Electrons from NADH in glycolysis also sent here.
- electrons flow through cytc reductase, cytc, and cytc oxidase.
- hydrogens pumped across inner membrane into outer membrane so matrix becomes more basic
- hydrogens flow through ATP synthase to generate ATP.
number of ATP per NADH
number of ATP per FADH2
- 2.5
- 1.5 (also for NADH from glycolysis)
number of ATP produced in glycolysis
- 4 ATP total
- 2 ATP needed at beginning
- 2 ATP net
number of ATP produced in prokaryotes
32
number of ATP produced in eukaryotes
30
how many hydrogens to produce ATP
- 4
- 3 per turn
- 1 to bring Pi in.
fermentation purpose
- regenerates NAD+ (oxidize it)
- reduce pyruvate
- allows glycolysis to continue in absence of oxygen.
fermentation process
- pyruvate reduced to ethanol (yeast) or lactic acid (muscle)
- NAD+ produced.
- CO2 released.
lactic acid in fermentation
- lactate transported to liver to make pyruvate.
problems with fermentation
- toxic end products
- not enough ATP leads to loss of total energy.
gluconeogenesis
- pyruvate back to glucose
- when dietary sources of glucose are unavailable and liver is out of glucose and glycogen.
- occurs in the liver
enzyme that converts pyruvate to OAA
- pyruvate carboxylase
- 2 ATP used
enzyme that converts OAA to PEP
- pyruvate carboxykinase
- 2 GTP used
enzyme that converts f-1,6-bisp to f-6-p
- f-1,6-bisphosphatase
- Pi released
enzyme that converts g-6-p to glucose
- g-6-phosphatase
- Pi released
regulation of f-1,6-bisphosphotase
(-) AMP, F-2,6-Bpase
(+) ATP
gluconeogenesis requires
- 4 ATP
- 2 GTP
- 2 NADH
hormonal regulation of insulin
- blood glucose high
- stimulates F-2,6-BisP levels
- stimulates PFK
- stimulates glycolysis
hormonal regulation of glucagon
- blood glucose low
- inhibits F-2,6-BisP levels
- inhibits PFK
- inhibits glycolysis
glycogenesis
- formation of glycogen
- stored in liver and lesser in skeletal muscle
process of glycogenesis
- glucose to glucose-6-phosphate (by hexokinase) use 1 ATP
- glucose-6-phosphate to glucose-1-phosphate (by phosphoglucomutase)
- glucose-1-phosphate to glycogen (glycogen synthase)
- use of 1 UTP
- under control of insulin
glycogenolysis
- breakdown of glycogen
- use of glucagon and epinephrine
process of glycogenolysis
- glycogen to glucose-1-phosphate (glycogen phosphorylase)
- glucose-1-phosphate - glucose-6-phosphate (phosphoglucomutase)
- glucose-6-phosphate to glucose by glucose-6-phosphatase
- under control of glucagon
pentose phosphate pathway phases
- oxidative
- nonoxidative
oxidative phase
- G6P broken down into ribulose-5-phosphate and 2 NADPH by glucose-6-phosphate dehydrogenase..
- NADPH feeds back
- irreversible.
nonoxidative phase
- Ribulose-5-phosphate and other carbons broken down to F-6-P and GAP (glycolytic intermediates)
- also formed ribose-5-phosphate
role of NADPH
- reducing power for anabolic reactions (e.g., fatty acid synthesis)
- reducing power to eliminate free radicals like during detoxification in the liver
- inability to generate NADPH (G6PDH deficiency) leads to oxidative damage to RBCs and anemia.
role of ribulose-5-phosphate
- synthesize nucleotides
- RNA converted to deoxyribose for DNA.
breakdown of triglycerides
- broken down into 2 fatty acids and a monoglyceride.
- 3 fatty acids and 1 glycerol
fatty acid conversion to acyl-CoA
fatty acid activation in beta oxidation
- begins at outer mitochondrial membrane
- conversion of fatty acid to acyl-CoA using acyl-CoA synthetase
- costs 2 ATP
beta oxidation of fatty acids
- 4 reactions to cleave bond between alpha and beta carbons to free acetyl-CoA and generate FADH2 and NADH
- use dehydrogenase to add double bond
- use thiolase to cleave
- each round cleaves a 2 carbon acetyl-CoA
- final round cleaves a 4 carbon acetyl-CoA
calculate the number of times through the cycle
(#carbons/2) - 1 = that many NADH, FADH2
+1 = that many acetyl-CoA
beta oxidation of unsaturated fats
- isomerize the double bond in an additional step if the double bond is in the wrong position.
- then same thing.
fatty acid synthesis starting material
- acetyl-coA + bicarbonate -> malonyl CoA
- use of 2 ATP
- by acetyl-CoA carboxylase
activation of fatty acid synthesis
- acetyl-CoA + ACP -> acetyl-ACP + CoA (shifted to another part of the enzyme)
- malonyl-CoA + ACP -> malonyl-ACP + CoA
elongation of fatty acid synthesis
- combine acetyl-ACP and malonyl-ACP
- use of 2 NADPH from PPP to provide energy.
- addition and loss of CO2 drives unfavorable reactions.
- For every 2 carbons you add, you need 2 NADPH
location of fatty acid oxidation
- mitochondrial matrix
fatty acid oxidation linked to
- CoA
coenzymes in fatty acid oxidation
- NAD+, FAD
energy cost in fatty acid oxidation
- 2 ATP
location of fatty acid synthesis
- cytosol
fatty acid synthesis linked to
- acyl carrier protein
fatty acid synthesis coenzymes
- NADPH
energy cost in fatty acid synthesis
lots of ATP to convert acetyl-CoA to malonyl-CoA
ketogenesis
- during long term starvation, blood glucose levels fall
- fatty acids oxidized to form acetyl-CoA
- levels of acetyl-CoA increase
- some feeds into Krebs
- others react to form ketone bodies
formation of ketone bodies
- two acetyl-CoA combine to form acetoacetate
- aceteoacetate broken down into hydroxybutyrate and acetone.
type I diabetes
- no insulin. glucose can’t get into cell
- patient relies on fatty acid oxidation for acetyl-CoA
- so many acetyl-CoA. some converted to ketone bodies.
- DKA - fatigue, confusion, fruity breathe (acetone)
ketone bodies
- soluble in blood
- cross blood bran barrier
- reconverted to acetyl-CoA for fuel
- brain cannot use fats as fuel
- very acidic.
glucose high
- make ATP in glycolysis
- stored as glycogen
- acetyl CoA from PDC make fatty acids
glucose low
- break down glycogen
- gluconeogenesis
starved state (all glycogen stores used)
- fatty acid breakdown
- free fatty acids - Beta oxidation - acetyl-coA - (Krebs and ketone bodies)
- glycerol - gluconeogenesis
what can pass easily through the blood-brain barrier
- small, hydrophobic molecules.
- charged things do not cross membranes.
if you lose carbon as CO2
- you will generate a reduced electron carrier such as NADH.
primary source of brain during starvation
- ketone bodies being converted to acetyl-CoA
protein catabolism
- break down protein from diet into individual amino aids using proteases
- individual amino acids broken into amino group and carbon skeleton
- individual amino acids can be used for protein synthesis.
amino group used for
- nitrogenous compounds (bases in DNA or RNA)
- urea cycle (waste product via kidneys)
- happening in liver
carbon skeleton used for
- glucogenic amino acids (used to generate glucose in gluconeogenesis)
- ketogenic amino acids (lysine and leucine) - converted into acetyl CoA for ketogenesis or Krebs
