Krebs Etc Notes
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Krebs Etc Revision
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metabolic reactions catabolic reactions- breakdown of compounds to release energy and usually involves oxidation
-biologically reduced forms of carbon- fatty acids-palmitic acid
-oxidised to release energy
-invitro- oxidation occurs in one step, complete conversion of the substrate into carbon dioxide and water- energy is released as heat and light
-biological oxidation- oxidation occurs in a step wise process- substrate can be partially or completely oxidised- source of energy is Anabolic reactions- biosynthesis of complex compounds using small precursors consumes energy-reduction ATP
-adensine, ribose, triphosphate- releases a lot of energy as it has 2 phosphoanhydride bonds- hydrolysed
-Hydrolysed into ADP and AMP- releases energy - 7.3 kcal/mol, 30.5 Kj/mol
-energy can be coupled for energy requiring reactions- thermodynamically unfavourable reactions can be coupled with the hydrolysis of ATP to form favourable reactions Compounds with high phosphyrl transfer potential can couple carbon oxidation with ATP synthesis. The energy released from the carbon oxidation is used to form high phosphyrl transfer potential compounds whose cleavage is coupled with ATP synthesis. Glyceraldehyde-3-phosphate is oxidised to 1,3, biphosphage glycerate, electrons released reduce NAD. Metabolic reactions- controlled
-supply meets demand, forward reactions and reverse reactions don't occur at the same time- there is no futile cycling short term affecting enzyme activity- reversible allosteric control, reversible covalent modification. Hormones control the metabolic activity on a wide range of tissue by controlling the reversible modifications Long term control the amount of enzyme present- level of transcription can be controlled
Cycles between organs
-cori cycle- skeletal muscle gives lactate to the liver which converts it to glucose and then returns it to the muscle where it produces ATP
CITRIC ACID CYCLE
-final common pathway for the oxidation of fuel molecules- carbohydrates, fatty acids, amino acids- acetyl coA
-acetyl Coa- 3NADH, 1FADH2, ATP, CoASH
Cycle- small number of intermediates are required to oxidise the acetyl coAintermediates, reforemed, oxidise more ATP, spin the cycle faster Cycle- if we block the cycle using malanote at succinate dehydrogenase, for every molecule of ATP hydrolysed, one molecule of oxaloacetate needs to be added. Entry compound of the TCA cycle is acetyl CoA
-acetyl CoA is synthesised from oxidation of pyruvate, fatty acids, amino acids
-pyruvate is oxidised into acetyl coA by pyruvate dehydrogenase. This enzyme is inactivated by pyruvate dehydrogenase kinase which is activated by ATP, acetyl coA. Inhibition of pyruvate dehydrogenase is relieved through dephosphorylation by phosphoprotein phosphatase. Oxidation of other intermediates Oxidation of other substrates can be converted into one of the TCA cycles intermediates where it is oxidised, NADH, ATP- fatty acids, amino acids, enter the cycle as acetyl coA- alpha keto glutarate can be formed by glutamate, histidine, proline, glycine, arginine
-succinyl coA- odd chain fatty acids, propionyl coA -valine, isoleucine, methionine Oxaloacetate- asparagines, aspartate, Biosynthesis of other intermediates
-Krebs cycle- intermediates also as starting molecules for the biosynthesis of other molecules- citrate is used fatty acids- citrate leaves the mitochondria where it is cleaved into the oxaloacetate and acetyl CoA- the Acetyl CoA is then carboxylated to malonyl coA
-alpha ketoglutarate- glutamate and other amino acids
-succinyl coA- porphyrins and haem
-oxaloacetate- asparagines, aspartate (makes urea) glucose
-however if the intermediates were used for biosynthesis it could deplete the concentrations- oxidation of acetyl coa Anapleurotic reactions are used to prevent this occurring- balance- glutamate is transaminated to form alpha ketoglutarate And aspartate is transaminated to form oxaloaceate Anapleurotic reaction 2: Pyruvate carboxylase
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