TRICARBOXYLIC ACID CYCLE (TCA) Flashcards
(18 cards)
where does TCA occur
mitochondria
What is the functon of TCA
Pathway for the terminal oxidation of
carbohydrates, fatty acids and amino acids. Also, the starting point for the synthesis of glucose and non-essential amino acids.
Process of TCA
- Acetyl CoA (2C) reacts with oxoalacetate (4C) -> citrate synthase -> citrate (6C)
- releases 3 NADH, 1 FADH2, 2 CO2, 1GTP
- CO2 breathed out
- GTP easily turned into ATP
- NADH and FADH -> oxidative phosphorylation
What is the ATP yeild from TCA overall?
- NADH = 2.5 ATPS each (x3 = 7.5 ATP)
- FADH2 = 1.5 ATP
- phosphorylation succinate thiokinase = 1 ATp
TOTAL = 10ATP
where does oxidative phosphorylation occur
- inner membrane of mitochondria (bilayer)
What is the function of substrate shuttles?
transfer of electrons (most important purpose) (NADH) and carbons between the cytosol and mitochondria. -> needed for TCA cycle/phosphorylation
explain the GLYCEROPHOSPHATE SHUTTLE
- glycerol 3-phosphate dehydrogenase steals electron from NADH converting dihydroxyacetone phosphate into glycerol 3-phosphate -> freely permeable
- Glycerol 3-phosphate in mitochondrion donates electron to FAD, forming FADH2 and Dihydroxyacetone phosphate (enzyme glycerol 3-phosphate dehydrogenase needed) -> reversal of first step but with FAD -> FADH2 in mitochondrion
- Dihydroxyacetone phosphate moves back into cytosol to be used again with NADH
- FADH2 yields 1.5 ATP
explain MALATE/ASPARTATE SHUTTLE:
- NADH to NAD+ beside oxaloacetate to malate using malate dehydrogenase in cytosol
- to transport malate inside mitochondrion, a-KG transporter swaps malate (into mito) for a-keto glutarate (into cytosol)
- malate loses electron -> added too NAD+ to form
- NADH -> forms oxaloacetate (enzyme malate dehydrogenase)
NADH in mito goes into respiratory chain - oxaloacetate not freely permeable so steals amine group from glutamate in mito, becomes a-KG and glutamate becomes aspartate
- glutamate/aspartate transporter swaps glutamate (in cytosol) for aspartate (in mito), then a-KG now in cytosol can be converted back to oxaloacetate beside aspartate (cytosol) back to glutamate (cyto)
- NADH yeilds 2.5 ATP
how much ATP is generated from one unit of glucose overall (glycolysis and TCA) if O2 supplied
- Glycolysis = 2
- Substrate shuttle = 2.5 x 2 = 5
- Pyruvate dehydrogenase = 2.5 x 2 = 5 (produces NADH when creating acetyl coA = 2.5 ATP each)
- TCA cycle = 10 x 2 = 20
TOTAL = 32 (30 if glycerophsopate shuttle used)
Note: ignore ATP cost of pyruvate transport and shuttle operation (about 1 ATP)
Anaerobic vs aerobic glucose catabolism
- Anaerobic metabolism: 2 ATP/glucose
- Aerobic metabolism: 30-32 ATP/glucose
- aerobic metabolism is far more productive/efficient in terms of ATP
- Anaerobic glycolysis can yield ATP 10x faster than TCA
where do malate/aspartate ad glycerophosphate shuttles occur
malate = cytosol and mitochondrial matrix (bidirectional)
glycero = cytosol and inner mitochondal membrane (unidirectional)
What is the Pentose phosphate pathway needed for?
- An oxidative pathway the proceeds NADPH for reductive synthesis (eg for fatty acid synthesis and steroid hormone synthesis) -> storing fat
- A non oxidative pathway that produces ribose-5-phosphate for synthesis of nucleotides -> making DNA and RNA components
*NADPH provides reducing power for fatty acid and steroid biosynthesis
*Ribose residues for nucleotide/nucleic acid synthesis
location of PPP
cytosol of all cells
summary of PPP steps
3 glucose 6-phosphate, 6 NADP+ —> 3CO2, 2 glucose 6-phosphate, glyceraldhyde 3-phosphate, 6 NADPH+, 6H+
electron acceptor in PPP
NAPD+
What are the 2 phases of PPP
- Oxidative
- NON REVERSIBLE DEHYDROGENATION and decarboxylation reactions
- Dehydrogenations
- produce NADPH and ribulose 5- phosphate - Non oxidative
- REVERSIBLE series of reactions
- Ribulose 5-phosphate
converted back to glucose 6-
phosphate
- Avenue for producing ribose
Why is it important that the non-oxidative phase be reversible (PPP)
- if organism doesn’t need more fat synthesis, then simply reverse non-oxidative pathway to produce backbone without needing to produce NADPH
how is PPP regulated
entire pathway regulated by presence of NADPH -> if more than needed, product inhibits glucose 6-ohosphatte dehydrogenase which forms NADPH from glucose 6-phosphate
- aloosteric inhibition
