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Biochem Cluster II
review information about biochem cluster II
| Question | Answer |
|---|---|
| enzymes that hydrolyze phosphoesters | phosphatases (also, hydrolases and esterases) |
| steps in pathways that are the targets of regulation (irreversible or reversible) | irreversible |
| insulin stimulates _______ and inhibits _______ | glycolysis, gluconeogenesis |
| glucagon stimulates _______ and inhibits _______ | gluconeogenesis, glycolysis |
| the most complex allosteric control in glycolysis/gluconeogenesis happens at these enzymes | phosphofructokinase (glycolysis) and fructose-1,6-bisphosphatase (gluconeogenesis) |
| The ETC is coupled to the formation of ATP from ADP and Pi in the mitochondria by… | a chemiosmotic gradient |
| The key enzyme in the synthesis of a strand of glycogen is… | glycogen synthase |
| Hydrogen cyanide gas is toxic in large part because it inhibits… | the passage of a pair of electrons through one of the proteins complexes of the ETC |
| Glycolysis INHIBITED by… | ATP,NADH |
| Glycolysis STIMULATED by… | AMP |
| Gluconeogenesis inhibited by… | AMP |
| Gluconeogenesis STIMULATED by… | ATP, NADH ?? |
| Though gluconeogenesis is a/an _______ pathway, it still uses _____, not _____ like most anabolic pathways | anabolic; NADH, NADPH |
| The pentose phosphate pathway takes place in…(5) | liver, mammary glands, testes, adipose tissue, adrenal cortex |
| The source of energy for glycogen synthesis | UTP (UDP-glucose) |
| Functions of the pentose phosphate pathway | interconvert monosaccharides, secondary route for glucose oxidation-->NADPH, production of pentose sugars (mainly ribose), catabolism of pentoses --> 3/6C sugars for glycolysis |
| The two parts of the pentose phosphate pathway | oxidative (sugars --> NADPH) and non-oxidative (differently sized monosaccharides --> F6P or glyceraldehyde-3-phosphates |
| ETC is located WITHIN the… | INNER mitochondrial membrane |
| Which way are protons pumped in the mitochondria? Which way do they flow after this concentration gradient is formed? | FROM the matrix TO the intermembrane space; THEN back TO the matrix FROM the intermembrane sapce |
| Name two transmembrane proteins involved in the ETC | coenzyme Q and cytochrome C |
| The most evolutionarily conserved protein | cytochrome C! |
| The only organs where glucose-6-phosphatase exists | liver and kidneys |
| Most common entry point for PPP | G6P (glucose-6-phosphate), then ox-decarb to ribulose-5-phosphate --> R5P |
| Glycogen is stored in the ¬¬______ of liver cells and the ¬¬______ of muscle cells | cytoplasm, sarcoplasm |
| Committed step of glycolysis | conversion of G6P to F6P (aldose-ketose isomerization by isomerase) |
| Glycolysis occurs in the ¬¬¬¬_______ | cytoplasm |
| TCA cycle occurs in the _______ | mitochondria (matrix) |
| Alpha-keto glutarate can be made into ¬¬¬______ | glutamic acid |
| Oxaloacetate (OAA) can be made into this amino acid | aspartic acid |
| Phosphatases in gluconeogenesis break the phosphoesters bonds by a _______ reaction | hydrolysis |
| Possible sources of carbon for gluconeogenesis | glucogenic amino acids (MAJOR), lactate from muscle cells, glycerol from triacylglycerols or membrane phospholipids |
| Glucose units in glycogen are connected at the (?,?) position and branched at the (?,?) position | 1,4 and 1,6 |
| Branching of glycogen gives what benefits? (3) | increased energy capacity, easier/faster to split bonds, increased solubility |
| Glucagon and epinephrine STIMULATE _____ ______ and INHIBIT _____ ______ | glycogen breakdown, glycogen synthesis |
| Insulin STIMULATES _____ _____ and INHIBITS _____ _____ | glycogen synthesis, glycogen breakdown |
| Insulin and glucagon are released from what organ? | pancreas |
| Do insulin and glucagon directly bind to cellular enzymes? | NO! (they are “second messengers”) |
| Possible symptoms with problems in LIVER glycogen metabolism | increased glycogen concentrations, enlargement of liver (hepatomegaly), abnormally structured glycogen, or low blood glucose levels |
| Possible symptoms with problems in MUSCLE glycogen metabolism | abnormally structured glycogen, inability to maintain long-term, strenuous exercise |
| Galactosemia is caused by… | deficiency of an epimerase enzyme that converted galactose to useable glucose |
| Treatment of galactosemia is simply… | elimination of as much galactose as possible in diet |
| In gluconeogenesis, pyruvate is shuttled out of mitochondria in the form of… | malate |
| Balanced equation for glycolysis…GO! | glucose + 2 ATP + 4 ADP + 4 Pi + 2 NAD+ --> 2 pyruvate + 2 ATP + 2 NADH |
| Balanced equation for gluconeogenesis…GO! | 2 pyruvate + 4 ATP + 2 GTP + 2 NADH --> glucose + 4 ADP + 2 GDP + 2 NAD+ + 6 Pi |
| Balanced equation for TCA cycle…GO! | acetyl CoA + FAD + 3 NAD+ + GDP + Pi --> 3 NADH + FADH2 + GTP + 2 CO2 + CoA |
| Glycolysis costs __ ATP and generates NET of __ ATP, __ NADH | 2, 2, 2 |
| Gluconeogenesis costs __ ATP, __ GTP, and __ NADH, for a total of __ net nucleoside triphosphates used and generates _____ | 4, 2, 2, 12 ATP equivalents, a free glucose |
| TCA produces what forms of energy and how many of each? How much ATP equivalents is that? | 1 FADH2, 3 NADH, 1 GTP for a total of 12 ATP equivalents |
| Fatty acids are activated (attached to ____) in ¬¬the _____ by the enzyme _____. They are now called ____ | CoA, cytosol, thiokinase, fatty acyl CoAs |
| Fatty acyl CoA can cross the _____ but need to be attached to ______ by the enzyme ______ in order to cross the _____ | outer mitochondrial membrane, carnitine acyl transferase, inner mitochondrial membrane |
| Number of acetyl CoA molecules required to produce a molecule of cholesterol | 18 |
| Number of ATP gained from β-oxidation of palmitate | 131 (35 from just degradation, 96 from acetyl CoA --> TCA cycle |
| In times of severe stress or untreated diabetes, the liver turns to _____ for energy | fatty acid β-oxidation |
| Excess _____ from ______ is converted into ketone bodies in the liver | acetyl CoA, fatty acid β-oxidation |
| Why does acetyl CoA build up and lead to ketone body synthesis? | the molecule oxaloacetate (OAA), which would normally be combined with acetyl CoA in the TCA cycle to produce CO2 and reduced coenzymes-->energy in ETC, is not available because it is being used by gluconeogenesis!! |
| _____ can spontaneously decarboxylate to form acetone | acetoacetate |
| True or false: Under periods of extended stress, organs such as the heart and skeletal muscle, and to some extent the brain can oxidize ketone bodies for fuel | TRUE |
| Fatty acid synthesis occurs in the ¬¬______ | cytosol |
| The separation of fatty acid synthesis and fatty acid degradation into two different cellular compartments is a form of _________ | regulation |
| Pyruvate can be carboxylated to ______ by the enzyme ______ and decarboxylated to ______ by the enzyme _______ | oxaloacetate, pyruvate carboxylase; acetyl CoA, pyruvate dehydrogenase |
| The committed step of fatty acid synthesis is… | the carboxylation (activation) of acetyl CoA to form MALONYL CoA |
| Major enzyme complex of fatty acid synthesis; has two identical subunits | fatty acid synthase |
| The condensation energy to form the bond that extends the growing fatty acid chain comes from… | the release of the recently added terminal carbonyl group of MALONYL CoA as carbon dioxide |
| The enzyme that forms malonyl CoA from acetyl CoA is called… | acetyl CoA carboxylase |
| Through simple fatty acid synthesis, humans can create (?:?) fatty acids, but with help from the ______ in the cell’s ¬¬_______ ________, it can be extended/unsaturated to (?:?) | 16:0, microsomes, endoplasmic reticulum, 18:1 |
| Omega-3 fatty acids are ______ fatty acids abundant in _____ and proven to have ________ benefits | essential, fish, cardiovascular |
| Omega-6 fatty acids are ______ fatty acids, notably precursors for ________ _____, which is the precursor for a group of signaling molecules called ________, which include (4 things) | essential, arachidonic acid, eicosanoids; leukotrienes, prostaglandins, prostacyclins, and thromboxanes |
| Concerning fatty acid synth/deg, insulin stimulates ______ | synthesis |
| Concerning fatty acid synth/deg, glucagon stimulates ______ | degradation |
| Two primary sites for allosteric control of FA synth/deg are (enzymes) ________ | acetyl CoA carboxylase, carnitine acyl transferase |
| Main stimulator of acetyl CoA carboxylase | citrate (precursor to acetyl CoA release for FA SYNTHESIS) |
| Main inhibitor of acetyl CoA carboxylase | palmitoyl CoA (activated FA, represents FA BREAKDOWN) |
| Main inhibitor of carnitine acyl transferase | malonyl CoA (committed step of FA SYNTHESIS inhibits a key step in FA BREAKDOWN) |
| Triglyceride and phospholipid synthesis uses _TP as an energy source | C (CTP!) |
| The point at which triglyceride and phospholipid synthesis pathways diverge is at the formation of _______ | phosphatidate (diacylglycerol-3-phosphate; glycerol with 2 FA and a phosphate) |
| Replacement of the phosphocholine head group in sphingolipids with a MONOSACCHARIDE creates a ______ | cerebroside |
| Replacement of the phosphocholine head group in sphingolipids with an OLIGOSACCHARIDE creates a ______ | ganglioside |
| Statins are _______ ________ of the enzyme ________ ________, which in responsible for the committed step of ________ _________, the formation of ________ from _________ | COMPETITIVE inhibitors, HMG-CoA Reductase, cholesterol synthesis; mevalonate, HMG-CoA |
| HMG-CoA Reductase is regulated by the addition and removal of ________ groups, which is regulated by the two hormones ________ and _________ | phosphate; insulin, glucagon |
| Mevalonate is converted to intermediates called ______ _______, which include _____ and _____, compounds of (?) carbons | isoprenoid units; IPPP, DMAPP, 5 |
| 5-carbon compounds are polymerized into a (?)-carbon chain called _______, which is converted to ______, the first compound in cholesterol synthesis to have the characteristic ring system | 30, squalene, lanosterol |
| Lanosterol is converted by _______ to _______, which contains (?) carbons | microsomes, cholesterol, 27 |
| In all, it takes (?) acetyl CoA units to make a molecule of cholesterol | 18 |
| True or false: humans possess a pathway for cholesterol degradation | FALSE |
| ___ binds to ___ receptors on the liver and is taken up through _______ _______ | LDL, LDL, receptor-mediated endocytosis |
| In order to increase excretion, cholesterol is oxidized into ____ _____ and ____ ____ by _______ | bile salts, bile acids; microsomes |
| (?)% of cholesterol excreted into the bile duct is eventually reabsorbed because intestinal bacteria unconjugate it in a process called _______ _______ | 95, enterohepatic cycling |
| Fats from the diet are packaged into _______, a type of _______ that eventually end up in the _____ | chylomicrons, lipoprotein, liver |
| The _____ packages endogenously synthesized lipids into _____, a type of _______ that carries lipids to ______ _______ | liver, VLDLs, lipoprotein, peripheral tissues |
| This lipoprotein picks up excess cholesterol and lipids in the blood, transforming from ____ to ____ and eventually to ____, at which point it is taken back up by the _____ | HDL, IDL, LDL, liver |
| The lower a lipoprotein gets in density, the more _____ it contains and the _______ its lipid:protein ratio becomes | lipid, higher |
| Positive risk factors for coronary heart disease (7) | men over 45, women over 55, family history, smoking, HTN, HDL below 35 mg/dL, and diabetes |
| The only accepted NEGATIVE risk factor for coronary heart disease | HDL levels over 60 mg/dL |
| Tay-Sachs disease, common in _______ _____, is attributed to the inability to break off the _________ head group of sphingolipids, which leads to a _____ of lipids in the brain | Ashkenazi Jews, oligosaccharide, buildup |
| Symptoms of Tay-Sachs disease include…(4) | enlargement of head, blindness, retardation, early death |
| Gaucher disease causes a buildup of _________ in ________ | glucocerebrosides, organs besides the brain |
| Krabbe disease causes a buildup of ________ in the _______ and is usually fatal? (T/F) | galactocerebrosides, TRUE |
| The first step in amino acid breakdown is the _______ of the ______ group by enzymes called ________, which require the coenzyme ________ | removal, amine, transaminases, pyridoxal 5’-phosphate |
| The removed amine groups are transferred to an acceptor molecule that is a/an ________ | alpha-ketoacid |
| After the removal of the amine group, the amino acid is now a/an ________, and the receptor molecule is now a/an _________ | alpha-ketoacid, amino acid! |
| The only 2 purely ketogenic amino acids are…? | leucine and lysine |
| OAA can be aminated to form ______ | aspartate |
| The urea cycle converts the toxic by-product _____ into _____, which is very water soluble and can be easily excreted from the body | ammonia, urea |
| (T/F) One can live with a complete block of the urea cycle | FALSE |
| One turn of the urea cycle uses (?) carbon dioxide(s) and (?) amine group(s) | 1, 2 |
| Where do the 2 amine groups of urea come from? | 1 from amine group of aspartate, 1 from carbamoyl phosphate (made from a free ammonia and a CO2) |
| Symptoms of hyperammonemia (2) | lethargy, developmental impairment |
| Phenylketonuria is caused by the lack of the enzyme that breaks down __________, causing byproducts called _______ to build up and cause _______ _______ | phenylalanine, phenylketones, mental retardation |
| The inability to metabolize the carbon skeletons of the three branched amino acids _____, ______, and _____, causes a buildup of their ketoacid forms, which causes ______ of the blood and a sweet smell in the urine is called __________ | leucine, isoleucine, valine; acidosis, maple syrup urine disease |
| The inability to degrade tyrosine leads to a non-threatening urine disease called ________, where the urine appears black in color | alkaptonuria |
| The ____ test tests the renal clearance of urea, and abnormal results may be indicative of…(3) | BUN, infection, damage, and/or renal carcinoma |
| Proper kidney functioning can be determined by the ____-to-_______ ratio | BUN, creatinine |
| Very high levels of creatine or its breakdown product, creatinine, could be indicative of… | muscle tissue necrosis |
| Creatinine clearance is a good measurement of the _______ _______ _______ (???) | glomerular filtration rate, GFR |
| The carbon skeletons of amino acids are derived from _________ of the central metabolic pathways, including (3) | intermediates, glycolysis, TCA cycle, PPP |
| The amine group of all amino acids that are synthesized de novo is derived directly or indirectly from the amine group of ______, whose side chain can be further aminated to form _______ | glutamate, glutamine |
| The amine groups from ______ are transferred by enzymes called ________ to _______ to form new amino acids | glutamate, transaminases, alpha-ketoacids |
| Transaminases, notably ____ and _____, are especially abundant in the ______, and their presence in the blood indicates… | liver; ALT, AST; cirrhosis, viral infection, or other chronic liver disorders |
| The amino acid _________ has been somewhat linked to coronary heart disease and is made from _______, which is made from ________ | homocysteine, cysteine, methionine |
| Some other important biomolecules made from amino acids include… | serotonin, creatine, sphingosine, porphyrin ring systems, purine/pyrimidines |
| There are (?) essential amino acids | 9 |
| This many amino acids can be synthesized “de novo” | 8 |
| This many amino acids are created through “salvage” pathways | 3 |
| Purines are synthesized as _________ and attached to a scaffold of ______ | nucleotides, ribose-5’-phosphate |
| Pyrimidines are synthesized as ______ ______ | free bases |
| The first purine (nucleotide) synthesized de novo and its base | inosine-5’-monophosphate (IMP), base: hypoxanthine |
| The first pyrimidine (free base) synthesized de novo | orotic acid (orotate) |
| The first pyrimidine (nucleotide) synthesized de novo | uridine-5’-monophosphate (UMP) |
| IMP can be converted to ___ using GTP or ___ using ATP depending on cell needs | AMP, GMP |
| Purine synthesis uses…(4) | glycine, glutamine side chain, aspartate amine group, formyl groups |
| Pyrimidine synthesis uses…(2) | aspartate, carbamoyl phosphate |
| Patients with orotic aciduria cannot form _____, so it becomes essential to diet; they also have a buildup of ______, which causes (2) | uridine-5'-monophosphate, orotic acid; slow, stunted growth, blood cell deficiencies |
| _____ is converted into all of the pyrimidine nucleotides needed by the cell | uridine-5’-monophosphate |
| Deoxyribonucleotides are converted from the _______ form of _________ by the enzyme ________ _______ | DIphosphate, ribonucleotides, ribonucleotide REDUCTase |
| Although they are not used in DNA, _______ must be produced and reduced to make thymidine deoxyribonucleotides | uridine deoxyribonucleotides |
| The monophosphate form of __________ is the substrate for thymidylate synthase | deoxy-uridine-5’-monophosphate |
| The two DNA synthesis enzymes targeted by anticancer drugs are _______ and ________ | ribonucleotide reductase and thymidylate synthase |
| The anticancer drug hydroxyurea inhibits the enzyme ________ | ribonucleotide reductase |
| The anticancer drugs 5-fluorouracil and Tomudex inhibit the enzyme ________ | thymidylate synthase |
| Nucleotides ingested in the diet are first converted to their _______ form by _______ enzymes. Then, the glycosidic linkages between the base and the monosaccharide are hydrolyzed by __________ enzymes, different ones for purines and pyrimidines | nucleoSIDE, phosphatases, phosphorylase |
| The monosaccharide released during nucleotide breakdown is… | ribose-1-phosphate |
| Pyrimidine bases are broken down in pathways that release very ________ products that easily excreted in the urine | water-soluble |
| The ultimate product of PURINE degradation is ___ ___, notably INSOLUBLE in water | uric acid |
| The hypoxanthine released from AMP/IMP and the guanine from GMP are both converted to ______, which is then oxidized to ____ ____ by the enzyme ______ _______ | xanthine, uric acid, xanthine oxidase |
| If uric acid levels get too high, this is called _________ and could result in crystallized uric acid depositing in joints, especially in the _________, causing a condition known as ______ | hyperuricemia, extremities, gout |
| Gout can progress to _____ _______ if inflammatory reactions are triggered | gouty arthritis |
| Patients with gout are usually treated with _______, a competitive inhibitor of the enzyme _____ _____, preventing the conversion of _______ to uric acid; this is good since _______ is much more easily excreted | allopurinol, xanthine oxidase, xanthine, xanthine |
| Concerning PURINE salvage pathways, ____ can be formed from free adenine and phosphoribosyl pyrophosphate, and ___ and ___ can be formed from free hypoxanthine and guanine | AMP; GMP, IMP |
| Concerning PYRIMIDINE salvage pathways, the action of the ________ enzyme must be reversed by reacting a pyrimidine with _______ to create a nucleoSIDE, then using special nucleoside kinases to create the _________ | phosphorylase, ribose-1-phosphate, nucleotide |
| Children with a deficiency in the _____ enzyme have extremely high uric acid levels and are considered to have a disease known as ________, which causes extreme self-mutilation | HGPRT, Lesch-Nyhan syndrome |
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