NUTR.400.PRO.FSVIT

Card Set Information

Author:
jsohl
ID:
145451
Filename:
NUTR.400.PRO.FSVIT
Updated:
2012-04-03 22:36:41
Tags:
400 protein
Folders:

Description:
Nutritional biochemistry - proteins & fat soluble vitamins
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user jsohl on FreezingBlue Flashcards. What would you like to do?


  1. What will a noncompetitive inhibitor do to Vmax & Km?
    • Decrease Vmax
    • Km stays the same
  2. What will a competitive inhibitor do to Vmax & Km?
    • Vmax stays the same
    • Km increases
  3. Km
    • Michaelis constant
    • indicates the concentration of substrate needed to reach 1/2 Vmax
    • inversely proportional to enzyme's affinity
  4. configuration of amino acids
    L
  5. classification of amino acids
    • nonpolar
    • polar - uncharged, acidic (low pKa), basic (high pKa)
  6. pKa
    deprotonates above this point
  7. What 2 amino acids are only ketogenic?
    • leucine
    • lysine
  8. Glucogenic amino acids enter TCA as...
    • pyruvate
    • alpha ketoglutarate
    • succinyl CoA
    • fumarate
    • oxaloacetate
  9. Ketogenic amino acids can be metabolized into...
    • acetyl CoA (for energy metabolism or FA synthesis)
    • acetoacetate (ketone body - can be used outside liver for energy production)
  10. enzyme & substrates involved in oxidative deamination
    • E= glutamate dehydrogenase for either direction
    • glutamate + NAD+ -> alpha-ketoglutarate +NH3(+NADH)
    • activated by ADP (low energy), high glutamate & alpha-ketoglutarate levels
    • OR
    • alpha-ketoglutarate + NADPH + NH3->glutamate+ NADP+
    • activated by high ammonia levels
  11. transamination
    • mechanism of creation of nonessential amino acids
    • removes amino acid group (transfers ammonia/amine)
    • a.a. + alpha-keto acid -> alpha-keto acid + a.a.
  12. synthesis of nonessential amino acids
    • amidation (glutamate -> asparganine)
    • removal/addition of CH3 (glycine -> serine)
    • cyclization (glutamate -> proline)
    • homocysteine & serine ->cysteine
    • phe -> tyr
  13. Urea Cycle
    • most tissues: glutamate + NH3 -> glutamine
    • (E= glutamine synthase)
    • skeletal muscle:
    • transamination of pyruvate + glutamate->alanine
    • (E= ALT = alanine aminotransferase)
    • free NH3 is cleaved from glutamine/alanine after delivery

    • free NH3 + CO2 + 2 ATP from mitochondria
    • + Asparate's NH3 in cytosol
    • (asprartate from AST acting on glutamate + oxaloacetate)
    • = urea (cleaved from arganine) - diffuses from liver to blood - excreted by kidneys & a small amount in feces
  14. amino acids are precursors for
    • porphyrins (that bind metal ions - FE++) including heme
    • catecholamines
    • -dopamine & norepinephrine - neurotransmitters
    • -norepinephrine & epinephrine - hormones
    • histamine
    • serotonin
    • phosphocreatine - energy storage in muscle
    • melanin
    • carnitine - line between protein & fat metabolism
  15. synthesis of S-Adenosylmethionine
    • met is precursor of SAM
    • universal methyl group donor
    • met resynthesized using methyl group from N5MTHF
    • this creates homocysteine- associated with CVD
    • homocysteine is converted to cysteine by serine & B 6,9,12
  16. primary structure of proteins
    • covalent peptide bond - usually in trans configuration
    • no free rotation
    • carboxyl - amino
  17. secondary structure of proteins
    • formed by H bonds
    • alpha helix
    • B pleated sheet
    • can be arranged in parallel or antiparallel configuration
    • nonpolar groups found in phospholipid bilayer
    • ex. barrel - channel
  18. tertiary structure of proteins
    • > 200 aas
    • disulfide (covalent) bonds
    • ionic interactions
    • H bonds
    • hydrophobic interactions
    • low energy state
    • begins folding during synthesis w/ help of cheperones
    • enhances solubility in water
  19. denaturation
    unfolding of secondary & tertiary structures
  20. quaternary structure of proteins
    • 2 or more polypeptide chains
    • ionic bonds, H bonds, hydrophobic interactions
  21. Heme
    • complex of protoporphyrin IX & Fe3+
    • can support redox catalysts, electron transport (cytochromes in ETC), oxygen transport (hemoglobin, myoglobin)
  22. myoglobin
    • in heart & skeletal muscle
    • reservoir & carrier for O2 within myocyte
    • transports O2 to the mitochondria for ETC
    • O2 release is stimulated by buildup of CO2 & lactate
    • single polypeptide folded into 8 stretches of alpha-helix (A-H)
    • heme group in between helix E & F
  23. hemoglobin
    • 2 alpha & 2 beta chains w/ helical structure
    • can hold 4 O2s
    • cooperativity
    • ALLOSTERIC EFFECTS
    • T(tense) form release O2 - once 1 becomes tense, the rest become more tense
    • low pH (from lactic acid) & high pCO2 - lower affinity
    • 2,3 bisphosphoglycerate increases as O2 levels decrease, so 2,3 BPG causes less affinity for O2 (good normally) - response to hypoxia or chronic anemia(not good)
  24. R form has high affinity for O2 - increases as each group binds
    high pH &low pCO2 - higher affinity for O2
  25. collagen
    • triple helix
    • lots of proline & glycine (every 3rd aa is gly)
    • tropocollagen -> disulfide bridges must be cleaved to form collagen
  26. elastin
    • fibrous protein
    • tropoelastin-> elastin + glycoprotein microfibrils = elastin
    • (alveoli, artery walls, elastic ligaments)
  27. cofactor
    inorganic metal ion
  28. prosthetic group
    • organic, covalently bound to enzyme
    • ex. vitamin
    • phosphate
    • biotin
  29. coenzyme
    organic with transient interactions with enzyme
  30. apoenzyme
    inactive enzyme (w/o non-protein groups bound)
  31. holoenzyme
    active enzyme (w/ non-protein component(s))
  32. most enzymes show _________
    • Michaelis-Menten kinetics
    • (as opposed to allosteric w/ sigmoidal curve)
  33. factors affecting reaction velocity
    • substrate concentration
    • temperature
    • pH
  34. regulation of enzyme activity
    • allosteric - (effectors) bind noncovalently - homotropic (substrate is usually activitor) vs. heterotropic (component other than substrate activates or inhibits)
    • covalent modification - phosphorylation (protein kinases), dephosphorylation (phosphatases)
    • induction & repression - by modulation of gene transcription
  35. protein degradation
    • acid hydrolases (endocytosis)
    • ubiquitin-proteasome mechanism - tagged w/ ubiquinin (ubiquinitation), cytosolic, barrel-shaped proteosome recognizes, proteases of proteosome cleave to short polypeptide fragments then aas, ubiquitin is recycled
  36. protein digestion in stomach
    • HCl - denatures
    • pepsinogen -> pepsin - cleave to polypeptides & aas
  37. protein digestion by pancreatic enzymes
    • zymogens -(activated by trypsin)-> proteases
    • enteropeptidase activates trypsinogen->trypsin - Arg, Lys
    • chymotrypsin - Leu, Met, Trp, Tyr, Phe
    • pro--->elastase - Gly, Ala, Ser
    • pro---->carboxypeptidase A - Val, Ala, Iso, Leu (nonpolar)
    • pro---->carboxypeptidase B - Arg, Lys
  38. small intestine protein digestion
    • EXOPEPTIDASES:
    • aminopeptidases - cleave N-terminal residue from oligopeptides
    • tri & dipeptidases
  39. absorption of AAs
    • free aas absorbed by Na+ dependent transporter
    • di & tri peptides by H+ linked transporter - then get hydrolyzed inside enterocytes
  40. cystinuria
    • proximal tubule can't reabsorb COAL (cystine, ala, ornithine, and lys) (works wih Na/K pump)
    • precipitation of stones
  41. PKU
    • phenylketonuria
    • mutation in phe hydroxylase gene or tetrhydrobiopterin
    • phe accumulates - retardation, odor
    • lack tyr - hypopigmentation
  42. MSUD
    • maple syrup urine disease
    • deficiency in branched-chain alpha keto acid dehydrogenase (which breaks down leu, iso, val)
    • toxic to brain
  43. albinism
    defect in tyr metabolism
  44. homocystinuria
    • high levels of homocystine & met in plasma & urine
    • low levels of cystine in plasma & urine
    • premature arterial disease due to oxidative damage, inflammation, endothelial dysfunction
    • restrict met intake
    • supplement w/ B6, B12 & folate (B9)
  45. hyperammonemia
    • decreased capacity of urea cycle caused by liver disease or genetic deficiency
    • neurotoxic
    • low protein diet, drugs that bind AAs
  46. porphyria
    • defect in heme synthesis
    • skin eruptions
  47. jaundice
    • deposition of bilirubin in skin (product of heme degredation)
    • hemolytic - associated w/ anemia - can't be excreted from gut quick enough
    • hepatocellular - damaged liver
    • obstructive - of bile duct
    • neonatal - bilirubin glucuronyltransferase low at birth
  48. protein misfolding
    • 1. amyloidoses - amyloid (B-pleated sheet) accumulation - neurotoxic- Alzheimers
    • 2. prion disease - infectious form of protein (PrP/prion) is an altered version of the normal form (normal has a-helices & PrP has b-pleated sheets)
  49. emphysema
    • deficiency of elastase
    • w/out it, immune cells can't get through tight junctions
  50. Forms of vitamin A
    • retinol & retinal (reversible rxn)
    • formation of retinoic acid (CO-OH) by oxidation of retinol is irreversible
  51. Provitamin A Compounds
    • some carotenoids - cooking makes them easier to absorb
    • beta carotene - makes 2 retinal --> retinols, but less bioavailable (9-22% absorption)
    • alpha carotene
    • cryptoxantin - oranges/tangerines
    • (lycopene, lutein, & zeaxathin have no Vitamin A activity, but are antioxidants)
  52. Which vitamins have a major role as antioxidants?
    E & C
  53. Which vitamins have a major role as coenzymes?
    B
  54. Which vitamins have a major role in vision?
    A - retinal
  55. Which vitamins have a major role in blood clotting?
    K
  56. Which vitamins have a major role in bone health?
    D & K
  57. tocopherol
    Vitamin E
  58. retinol
    Vitamin A
  59. calcitriol
    Vitamin D
  60. phylloquinone, menaquinones
    • Vitamin K
    • phylloquinone - K1-plant sources - major source/ most biologicallly active
    • menaquinones-K2 - animal sources & gut
    • menadione - K3 - synthetic
  61. a-tocopherol
    Vitamin E
  62. Vitamin A transport
    • retinol is reesterified & secreted in chylomicrons & lymph
    • taken up by liver
    • RBP, retinol-binding protein, transports retinyl esters to extrahepatic tissues where they attach to specific receptors
    • cellular RBP carries retinol in cytosol
  63. Vitamin A & gene transcription
    • rentinoic acid binds to retinoic acid receptor (RAR) in nucleus
    • RA-RAR complex is a transcription factor that interacts with retinoic acid response elements (RAREs)
    • transcription of genes that function in:
    • embryonic development (essential for spermatogenesis & preventing fetal resorption)
    • cell proliferation
    • cell differentiation - ex. epithelial goblet cells (lack of vitamin A leads to dry mucous membranes, prone to infection)
    • immune functions (epithelial cell growth & T lymphocytes)
    • bone growth
  64. Vitamin A form involved in transcription
    Retinoic Acid
  65. Vitamin A & Night Vision
    retinol transported to retina --> cis-retinal + opsin --> rhodopsin + light --> trans-retinal + nerve impulse

    trans-retinal recycled by conversion to trans-retinol then cis-retinol then trans-retinal

    • amount of rhodopsin increases in dim light as more cis-retinal binds to opsin
    • rhodopsin is broken down when light is turned on
    • depends on amount of Vitamin A that is available - not alot, then can't adjust quickly to bright or dark
  66. Vitamin A & Color Vision
    iodopsin, violet pigment
  67. signs of vitamin A toxicity
    • dry, pruritic skin
    • enlarged & cirrhotic liver
    • rise in intercranial pressure in the brain
    • congenital malformations
  68. Vitamin A in Cancer Therapy
    • trans retinoic acid improves survival for acute promyelocytic leukemia where there is translocation between genes that normally help WBCs mature
    • this is because RA receptor gene is affected by translocation
  69. dietary forms of vitamin D
    • D2 - ergocalciferol - plants
    • D3 - cholecaciferol - animals
  70. vitamin D synthesis
    • 1. Skin: UV rays convert 7-dehydrocholesterol to cholecalciferol (D3)
    • 2. Liver: D3 is hydroxylated to calcidiol (predominant form in plasma & storage form in liver) - requires NADPH
    • 3. Kidney: Calcidiol is hydroxylated to calcitriol - requires NADPH

    activated by low plasma phophate or low Ca2+
  71. function of calcitriol
    • BINDS TO VITAMIN D RECEPTOR FORMING CALCITRIOL VDR COMPLEX
    • THIS BINDS TO VDREs to promote mineral metabolism, immune response, cancer regulation...
    • maintaining homeostasis through transcription regulation
    • bones/teeth
    • blood clotting/wound healing
    • nerve transmission that controls blood pressure
    • macronutrient energy metabolism (gluconeogenesis)
    • membrane transport
    • muscle contraction
  72. calcium absorption in small intestine
    • stimulated by calcitriol by increasing binding of Ca2+ to calmodulin & increasing sythesis of calbindin & Ca2+ ATPase
    • lumen - through Ca channel - binds to calmodulin then to calbindin then leaves enterocyte through Ca2+ATPase
  73. When blood Ca2+ drops...
    • PTH stimulates kidneys to produce more calcitriol from calcidiol - which increases intestinal absorption, proximal tubule reabsorption (by increasing transcription of transporters), and stimulates resorption of bone by activating osteoclases
    • PTH stimulates osteoclasts
    • PTH signal kidneys to slow Ca2+ excretion, but increase phosphate excretion
  74. When blood Ca2+ is high...
    • PTH in the blood drops
    • Kidneys produce little/no calcitriol
    • synthesis of Ca2+ transporters in small intesting & kidney decrease
    • calcitonin secretion from thyroid gland is increased, inhibiting osteoclasts & acvating osteoblasts to use blood Ca2+ to mineralize bone
  75. rickets
    • low absorption of dietary Ca2+ due to vitamin D deficiency
    • skeletal deformities due to incomplete mineralization resulting in soft, pliable bones
    • adult form = osteomalacia - often seen in individuals with diseases of organs involving vitamin D production / absorption
    • mutations in VDR gene or 25-hydroxy-cholecalciferol 1-hydroxylase gene
    • renal rickets - calcitriol can be administered
  76. hypoparathyroidism
    • low blood Ca2+ levels
    • high phosphate levels - PTH stimulates phosphate secretion
    • treatments = vitamin D + PTH
  77. vitamin D toxicity
    • UL = 100 mcg = 4000IU
    • hypercalcemia
    • Ca2+ deposits in soft tissues (heart, lungs). blood vessels
    • CNS (loss of appetite, nausea...)
    • loss of bone mass - unbalanced bone resorption = decalcification
  78. function of vitamin K
    • posttranslational modification - carboxylation
    • blood coagulation, bone mineralization, cell growth & proliferation
    • cofactor for v-gluamyl carboxylase that catalyzes carboxylation of glutamic acid residues -> v-carboxyglutamic acid (Gla)
    • Gla domains have high affinity for Ca2+
  79. vitamin K cycle
    • glutamate is carboxylated with the help of vitamin K to form Gla with Ca2+ attached
    • the oxidized vitamin K then needs to be recycled by epoxide reductase & NADH to form its reduced form
    • short half life
  80. What drug is used as an anticoagulant? How does it work?
    • warfarin- inhibits epoxide reductase from reducing/recycling vitamin K
    • dicumarol from sweet clover also inhibits clotting
  81. How does vitamin K play a role in blood clotting?
    • it aids in carboxylation forming Gla in the precursors that form mature clotting factors II, VII, IX, and X leading to fibrin
    • prethrombin -> prothrombin (+ thromboplastin from intrinsic or extrinsic pathway) -> thrombin ->which turns fibrinogen into fibrin
    • prothrombin-Ca2+ complex weakly binds to phospholipids on platelets which increases the rate of proteolytic conversion of prothrombin to thrombin
    • Ca2+ provides binding opportunity & it is there because vitamin K carboxylated precursors forming the Gla
  82. Vitamin K's role in Bone Mineralization
    • assists with formation of Gla residues enhancing Ca2+ binding capacity of osteocalcin which is secreted by osteoblasts for bone mineralization
    • plus at least 2 other bone proteins require vitamin K for carboxylation
  83. What VitaminK-dependent protein regulates cell growth?
    • Gas6
    • found in nervous system, heart, lungs, stomach, kidneys & cartilage
    • cell-signaling, cell adhesion, proliferation, protection agains apoptosis, platelet signaling
  84. Vitamin K deficiency
    • rare, but is possible with fat malabsorption and extended antiobiotic use
    • prothrombinemia is a side effect - nosebleeds, gums bleed, blood in urine & stool
    • decreased bone density
    • newborns get vitamin K injection for protection from brain hemorrhage
    • mega doses of vitamin A hamper intestinal absorption
    • mega doses of vitamin E block K-depended clotting factors
  85. Vitamin K overdose
    • rare - body excretes it rapidly
    • hemolytic anemia, esp in newborns
  86. Forms of vitamin E
    • tocopherols (alpha, beta, gamma, & delta) - saturated
    • tocotrionols (alpha, beta, gamma, & delta) - unsaturated
    • 90% is stored in adipose
    • 10% in plasma membranes
  87. functions of vitamin E
    • antioxidant
    • stabilization of cell membranes
    • pollution oxidative damage protection in lungs
    • DNA/cancer
    • protect against peroxidation / CVD
    • protection of liver, breast, muscle, mainenance of B-carotene
  88. vitamin E in cell membranes
    • alpha tocopherol prevents free radical damage to PUFA in cell membranes
    • PUFAs are susceptible to peroxidation
    • forms a stable free radical
    • tocopherol accepts electron stabilizing free radical - recycled by ascorbic acid - recycled by GSH - recycled by NADPH
  89. vitamin E deficiency
    • very rare - premature infants / fat-malabsorption syndromes
    • hemolytic anemia - insufficient protection of RBCs
    • cataracts - oxidation in lense of eye
    • CVD
    • decline in immune function
  90. vitamin E toxicity
    • least toxic fat soluble vitamin
    • high doses counter vitamin K's blood clotting mechanism

What would you like to do?

Home > Flashcards > Print Preview