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biochem
midterm
| substrate | products | Cofactors, Coupled Rxn, ETC | Control Mechanism | enzymes |
|---|---|---|---|---|
| pyruvate (in anaerobic) | Lactate and Alanine | 1. NADH ----> NAD 2.Transamination reaction between amino acid form and keto form. Alanine trasnaminates to gluamate which becomes alphaketogluterate. Nees Pyridoxal phosphate. (OTC is Pryidoxidine) | oxygen. lack of O2 causes pyruvate to form lactate and alanine. | lactate dehydrogenase |
| GLUT 1 | erythrocytes | (blank) | (blank) | (blank) |
| GLUT 2 | liver and pancreas | (blank) | (blank) | (blank) |
| GLUT 3 | brain | (blank) | (blank) | (blank) |
| GLUT 4 | skeletal muscle and apipose tissue | (blank) | (blank) | (blank) |
| GLUT 5 | small intestine | (blank) | (blank) | (blank) |
| what stimulates PFK1? | unphosphrylated PFK2 | (blank) | (blank) | (blank) |
| Is phosphotase is phosphorylated, it is | ACTIVE | (blank) | (blank) | (blank) |
| if PFK2 is phosphorylated, it is | NOT active, not producing PFK1 | (blank) | (blank) | (blank) |
| what happens to phosphotase when it is active | stays there until it's needed. Interacts with another dimer and degrades into cell. | (blank) | (blank) | (blank) |
| What typically promotes phosphoylation? | glucagon | (blank) | (blank) | (blank) |
| When ratio is high (high insulin), what now happens in regards to PFK? | low glucagon, glucose into cell, Phosphorylation does not occur, PFK 2 active, PFK1 upregulated by fructo 26 bisP | (blank) | (blank) | (blank) |
| There are PFK I and PFK II. Same substrate, different product. What does 2,6 do??? | This stimulates, upregulates PFK1, otherwise you would have a toxicity of fruc 6 phosphate. (then makes sorbitol…extra glucose).So it builds up PFK I. To then continue pathway. | (blank) | (blank) | (blank) |
| when glucagon receptor is stimulated what happens? | adenolyne cyclase + ATP = cAMP, stimulating protein Kinase A, phosphorylating PFK 2 | (blank) | (blank) | (blank) |
| mtDNA | Ring structure. Unchanged. | (blank) | (blank) | (blank) |
| mtRNA | Does own transcription, translation, cell division. | (blank) | (blank) | (blank) |
| in regards to PDH, the pyruvate attaches where? | on outer surface of mitochondria | (blank) | (blank) | (blank) |
| where does PDH complex take place | inner surface of outer membrane of mito | (blank) | (blank) | (blank) |
| pyruvate (PDH complex) | hydroxyethyl (from ethanolthiaminepyrophosphate)+ CO2 | thiamine.(thiamine pyrophosphate), This attaches to E1 so it can accept pyruvate. | controlled by ATP/ADP and NADH/NAD ratio | pyruvate decarboylase |
| What is the first vitamin associated with PDH | Thiamine (inactive form), Thiamine pyrophosphate (active form) | (blank) | (blank) | (blank) |
| hydroxyethyl | 2H+ + acetyl CoA | 1. CoA 2. interediates: acetyolipamide, dihydrolipamide | activated by lysil residue | dihydrolipoyltransacetalase |
| what stimulates E enzymes to be reactive? | cortisol (cortocortisoids) | (blank) | (blank) | (blank) |
| Coenzyme A : active form of | panothenic acid. | (blank) | (blank) | (blank) |
| how does CoA work in E2? | □ Kicks acetyl group off of acetyolipoamide and transfers it to matrix of Mito in which TCA cycle occurs. | (blank) | (blank) | (blank) |
| 2H | NADH | Riboflavin (FAD). protons attach and make FADH2 as intermediate. Coupled rxn with NAD. ReDox. Niacin. FADH2 gives protons to NAD to form NADH. | FAD activites E3 | dihydrolioplydehydrogenase |
| What is the first vitamin associated with E1? What is its active form? | thiamine, thiamine pyrophosphate | (blank) | (blank) | (blank) |
| where did the hydroxyethyl in E1 and E2 comes from/. (what molecule?) | ethanolthiaminepyrophosphate (hydroxyethylthiaminepyophosphate) | (blank) | (blank) | (blank) |
| which one of the vitamins would you need to properly consume for make PDH | thiamine, lipoic acid (OTC is alpha lipoic acid), panthothenic acid, riboflavin, niacin) | (blank) | (blank) | (blank) |
| how do you reverse vitamin difeciencies in mitochondria? | build up pyruvate and lactate, reduce carbs, increase vitamins, feed with lipids | (blank) | (blank) | (blank) |
| Why feed with lipids when vitamin defeicient? | because lipid metabolism does not occur in PDH. | (blank) | (blank) | (blank) |
| The PDH is regulated by | stimulation by inhibition | (blank) | (blank) | (blank) |
| what is the first regulation of carbohydrate metabolism in Mitochondria | PDH complex | (blank) | (blank) | (blank) |
| when the E are not phosphylated are they active or inactive? | active | (blank) | (blank) | (blank) |
| What does Kinase do? | only adds Phosphates | (blank) | (blank) | (blank) |
| What enzyme adds phosphates to PDH to make it Inactive? | protein kinase | (blank) | (blank) | (blank) |
| when phosphoryated, E2 is active or inactive? | inactive | (blank) | (blank) | (blank) |
| NADH/NAD is low, there is higher proportion of NAD+, this INHIBITS or ACTIVATES protein kinase. | inhibits (lacking energy, so it inhibits pK from phosphorylating and therefore inactiving enzyme. We want it active, so we want to inhibit Pk. | (blank) | (blank) | (blank) |
| If ATP is high, NADH high. What happens in PDH? | do not inhibit enzyme, phosphorylate enzyme and make inactive (via Protein Kinase) | (blank) | (blank) | (blank) |
| What stimulates PDH other than NAD and ATP ratios? | Insulin, Norepi, epi, cortisol | (blank) | (blank) | (blank) |
| What vitamins and minerals are needed for epinephrine synthesis? | Vitamin C, Copper | (blank) | (blank) | (blank) |
| Tyrosine | norepinephrine | Vitamin C. Intermediates are 3,4 dihydroxypheylalanine (DOPA) and Dopamine, copper | cortisol in adrenal medulla | 1. tyrosine hydroxlase 2. DOPA decarboxylase 3. Dopamine Beta hydroxylase |
| norepinephrine | epineprine | SAM-E | cortisol in adenal medulla | Phenylethanolamine N Methyl transferase |
| what does a lack of copper affect? | reduced absorbtion in the gut, formation of epinephrine, Ldopa and melanin production. | (blank) | (blank) | (blank) |
| What are the defects in PDH? (conditions) | Lactic Acidosis, Neurological disorders, high pyruvate in serum, high alanine in serum. | (blank) | (blank) | (blank) |
| How would glucogenic Amino acids be affected if there was a defect in PDH? | they would end at Pyruvate. No other pathways for them to take other than PDH | (blank) | (blank) | (blank) |
| What would happen to ketogenic AA if a defect occured in PDH | nothing. They would go onto Krebs by entering into mitochondria from another point. They do not require PDH. | (blank) | (blank) | (blank) |
| TCA cycle occurs where? | matrix of Mitochondria. | (blank) | (blank) | (blank) |
| Acetyl CoA (from E2) + Oxaloacetate | Citrate | 1. exergonic condensation reaction. 2. COA-SH is liberated into matrix | Inhibitors: ATP, NADH (high energy) 2. Succinyl CoA (end result of FA breakdown) 3. therefore, activated by ADP,NAD+ and low Succinyl CoA levels. | Citrate Synthase |
| Citrate | Isocitrate | Intemediate: cis-aconitate 2. both a dehydration and hyration rxn. | inhibited by flourocitrate (rat Poison) | cis-aconitase |
| Isocitrate | CO2 + NADH (3 ATP)+ alpha Ketogluterate | trytophan/niacin 2. this is oxidative decarboxylation | activation: ADP, Ca+. inhibited: ATP, NADH. | isocitrate dehydrogenase |
| What reaction in TCA cycle first produced ATP? | Isocitrate (reaction 3) | (blank) | (blank) | (blank) |
| alpha ketogluterate | succinyl CoA + CO2 + NADH (3ATP) | Niacin, Riboflavin, thiamine, alpha lipoic acid. | Inhibited: Succinyl CoA (feedback), NADH, ATP | alphaketogluterate dehydrogenase complex. Contains tightly bound Tpp,lipoamide, FAD. |
| Succinyl CoA | Succinate + ATP | Coupled Reaction: 1. GDP + Pi --> GTP 2. ADP + Pi ---> ATP catalyzed by Nucleotidediphosphate | not a control point. | Succinate thiokinase (kinase) (synthase) |
| what reaction in TCA is by substrate level phosphorylation? | Reaction 5, Succinyl CoA --> Succinate. | (blank) | (blank) | (blank) |
| What s the only step where ATP is directly produced (in TCA?) | Succinyl CoA to Succinate | (blank) | (blank) | (blank) |
| Succinate | Fumerate | FADH2 (2ATP) 2. oxidation rxn | Iron in porphyrin ring facilitates rxn. Covalently binds to FAD. Inhibited by Copper and Zinc??? | succinate dehydrogenase |
| Fumerate | Malate | Hydration Rxn, isoergonic. | (blank) | Fumerase |
| Malate | Oxaloacetate + NADH (3ATP) | NAD (niacin). Slightly endergonic (favors Malate) | (blank) | malate dehydrogenase |
| How much energy produced from TCA cycle? What steps? | 12 total per round!. 3 from isocitrate dH, 3 from alphaketoglut DH, 1 from succinate synthase, 2 from succinate DH, 3 from malate DH | (blank) | (blank) | (blank) |
| How many ATP produced in the entire mitochondria from one mole of glucose? | 3 (PDH) + 12(TCA) times 2 (6 carbon) ---> 30 total in mitochondria. | (blank) | (blank) | (blank) |
| how many theo ATP from one mole o glucose in TCA cycle? | 24 (12 x2) | (blank) | (blank) | (blank) |
| how many moles of CO2 produced in Mitochondria. Where from? (overall) | 2 in PDH (E1) + 4 in TCA. Total 6 per one mole of glucose. | (blank) | (blank) | (blank) |
| What is Alphaketo form of gluterate? | alphaketogluterate | (blank) | (blank) | (blank) |
| Alpha keto form of Aspertate? | Oxaloacetate | (blank) | (blank) | (blank) |
| Alpha keto form of alanine? | Pyruvate | (blank) | (blank) | (blank) |
| Amphibolic | involved in catabolic and anabolic processes | (blank) | (blank) | (blank) |
| Anapleurotic Reactions | Increase concentrations of TCA cycle intermediates. | (blank) | (blank) | (blank) |
| IS NAD in cytosol? Does it always produce ATP? | Yes, No | (blank) | (blank) | (blank) |
| How do we pull NAD from cytosol to form ATP? | Malate Apartate Shuttle and glycertae phosphate shuttle | (blank) | (blank) | (blank) |
| Which shuttle, Malate or Glyerate would be used if energy is plentiful? Why? | Glycerate. Produces less energy than malate. | (blank) | (blank) | (blank) |
| Malate Shuttle: NADH + Oxaloacetate in Cytosol. | Malate | pyrodoxial phosphate | NADH cytosolic level | Malate dehydrogenase |
| Malate shuttle: Malate inside mito | Oxaloacetate + NADH | pyrodoxial phosphate | -- | malate dehydrogenase |
| Malate Shuttle: Oxaloacetate inside Mito | Aspartate | glutamate ----> Alphaketogluterate via aminotranspherase | -- | Aminotranspherase |
| Malate Shuttle: aspartate in cytosol | Oxaloacetate | alphaketoglurate --> glutamate | -- | Aminotransferase |
| Glycerate Shuttle: dihydroxyacetone phosphate + NADH in Cytosol | Glycerol 3 phosphate + NAD+ | pyrodoxial phosphate? | -- | Glycerol 3 phosphate dehydrogenase |
| Glycerate shuttle: Glycerol 3 phosphate in Mito | Dihydroxuacetone phosphate | FAD ----> FADH2 | -- | Glycerol 3 phosphate dehydrogenase |
| Explain the fate of NAD in ETS (general overview) | NAD enters at complex 1. H+ go to complex 3 to form ATP, then to complex 4 to produce ATP, then to complex 5 to produce ATP. | (blank) | (blank) | (blank) |
| Explain the fate of FAD in ETS (general overview) | Enters at complex 2 and goes to 3 and 4 and 5. Produces 2 ATP | (blank) | (blank) | (blank) |
| What complex in ETS makes water? What elements are involved? | complex 4. Copper and Iron. | (blank) | (blank) | (blank) |
| Enzymes of Complex 1 in ETS | NADH dehydrogenase or NADH coenzyme Q reductase | (blank) | (blank) | (blank) |
| Complex 2 in ETS enzymes | Succinate Dehydrogenase or succinate coenzyme Q reductase | (blank) | (blank) | (blank) |
| Complex 3 enzymes in ETS | Cytochrome C - coenzyme Q oxidoreductase | (blank) | (blank) | (blank) |
| Complex 4 enzymes for ETS | Cytochrome oxidase (copper) | Copper | (blank) | (blank) |
| Complex 5 enzymes for ETS | ATP synthase | (blank) | (blank) | (blank) |
| Inhibitors of Complex 1 ETS | insecticides, barbituates, antibiotics. | (blank) | (blank) | (blank) |
| NAD in ETS | Coenzyme Q10 (ubiquinone) | FMN (riboflavin) | (blank) | (blank) |
| describe struture of complex 5 | see notes for diagram. alpha and beta sections, concentration gradient, H+ pass through F0 and F1 to stimulate Pi + ADP ---> ATP. Turns as H+ pass. | (blank) | (blank) | (blank) |
| coupling | Whenever a H+ is going through the Core (the Gamma) of the ATP synthetase. | (blank) | (blank) | (blank) |
| un coupling | When H+ is diverted away from Gamma Region. H+ are produced, but won't produce ATP. | (blank) | (blank) | (blank) |
| inhibitors of complex 2 | antibiotics and insecticides. | (blank) | (blank) | (blank) |
| inhibitors of complex 3 | antibiotics (some) | (blank) | (blank) | (blank) |
| Inhibitors of complex 4 | H2S, Cyanide, Azide, CO | (blank) | (blank) | (blank) |
| what vitamins are associated with ETS? | Riboflavin (FMN and FAD), Niacin | (blank) | (blank) | (blank) |
| high insulin in blood: What happens to PFK2? | 1. glu into cell. 2. Fruc 6 Phosphate ---> (ATP + Mg) Fruc 2,6 bisphosphate. 3. Stimulates PFK1 in glycolitic pathway so breakdown of glu can continue. When modulated, PFK2 slows production of fructo 26 bP and pathways slows. | (blank) | (blank) | (blank) |
| when glucagon binds to cells of mitochondrial membane, what is stimulated? | Adenolyne cyclase and ATP to form CAMP. This turns on Protein Kinase A, whch stimulates with ATP to phosphorylate PFK2. PFK2 is now inhibited and breakdown of glucose is slowed. | (blank) | (blank) | (blank) |
| active form of panothenic acid? | Coenzyme A | (blank) | (blank) | (blank) |
| how many ATP and ow many CO2 are produced in PDH complex? | 1 NADH (3 ATP) and 1 CO2. For glucose mole, would be DOUBLE! | (blank) | (blank) | (blank) |
| If ATP is high, then Ca+ is ______? | LOW | (blank) | (blank) | (blank) |
| What does Ca+ stimulate in PDH? | phosphotases to come off the PDH complex to make ACTIVE to get ATP production. ATP low, Ca+ high….remove PH makes it active. | (blank) | (blank) | (blank) |
Created by:
tpingel