Term
| Superoxide: Sources (3); properties of superoxide; where it is produced (3 places). |
|
Definition
O2-
Electron leakage, cytochrome P450 enzymes, Respiratory burst - NADPH oxidase.
Properties: Not lipid soluble (can't leave where it was made). Can be produced in mitochondria, cytosol, Vacuole. |
|
|
Term
| Hydrogen peroxide: Sources (2); Places where it's produced (3) |
|
Definition
H2O2
Ascorbate, Activity of Superoxide dismutase.
Not lipid soluble.
Mitochondria, cytosol, and vacuole. |
|
|
Term
| Hydroxyl Radical: Sources (4); Properties (2) |
|
Definition
-Haber-Weiss reaction
-Other electrons and protons
-Fenton reaction
-Major initiator of lipid per-oxidation (made from hydrogen peroxide)
-Lipid soluble (moves anywhere it wants)
-VERY dangerous; whatever it encounters fist will be it's e- donor. |
|
|
Term
| Lipid Peroxides; Initiation, propagation, Termination. |
|
Definition
OH (hydroxyl radical) interacts with normal lipid. (OH- starts reaction)
Initiation:(normal lipid) LH + OH- ----> (lipid radical) L- + H2O
Propagation: L- + O2 = (lipid peroxyl radical)LOO-
Loo- + LH = LOOH + L- (this is a chain reaction)
Termination: Antioxidant interacts to stop chain reaction (usually Vit. E) |
|
|
Term
| Endogenous antioxidant defense (7): |
|
Definition
-Elimination of superoxide: Superoxide Dismutase. (turns into hydroxyl radical)
-Elimation of hydrogen peroxide:
Catalase
Glutathione Peroxidase
(becomes hydroxyl radical)
-Elimination of lipid peroxides:
Glutathione peroxidase
(comes from hydroxyl radical)
-Elimination of hydroxyl radical: -Glutathione
Other endogenous antioxidants: lipoic acid, uric acid, CoQ10 |
|
|
Term
| Exogenous antioxidant defense (4): |
|
Definition
Elimination of:
Superoxide: Vitamin C
Hydrogen Peroxide: Vitamin C
Hydroxyl Radical: Vitamin C
Lipid Peroxide: Vitamin E, Carotinoids, CoQ10. |
|
|
Term
| Superoxide dismutase enzymes (3): where are they found and name which co-factor each are dependent on? |
|
Definition
-Extracellular (Cu and Zn)
-Cytosolic (Cu and Zn)
-Mitochondrial (Manganese dependent) |
|
|
Term
| Glutathione peroxidase reaction and co-enzymes. |
|
Definition
H2O2 + 2 GSH ------> 2H2O + GSSG
Needs: FAD, Selenium, NADPH
(There is another kind of glutathione peroxidase that takes care of lipid peroxides that are found in lipid membrane.)
LOOH + 2GSH---> LOH + H2O + GSSG |
|
|
Term
|
Definition
|
|
Term
| Digestion and absorption, and transport of Vitamin E: |
|
Definition
Duodenum and jejunum
Requires pancreatic esterases, bile acids
Transfer into enterocyte not well understood
All forms absorbed and secreted from enterocyte in chylomicrons (via LPL can be transported from chylomicrons to peripheral tissue)
a-tocopherol transport protein (Alpha-TTP): -Preferentially transfers a-tocopherol between liposomes and microsomes
-Role in delivering a-tocopherol to VLDL
Can be transported to HDL via tissues
Highest affinity for Alpha-tocopherol
Then: Beta-tocopherol (38%)
Gamma-tocopherol (9%)
delta-tocopherol (2%)
Tocopherol associated protein (TAP):
-Cytosolic protein in liver (and brain and prostate) of unknown function |
|
|
Term
| Metabolism and Excretion of Vitamin E: |
|
Definition
Storage –
• Largest concentration in adipose tissue
o In fat droplets, not membranes
o Smaller amounts in liver, brain, lung, heart, and muscle
Excretion -
Urine - Various glucuronic acid conjugated metabolites
Most vitamin E excreted by fecal route
Low absorption
Excess hepatic vitamin E excreted in bile (a-ttp chooses a-tocopherol and the rest is excreted with bile)
Skin |
|
|
Term
| Riboflavin coenzymes remain bound to their enzymes during the oxidation-reduction reactions and the complexes are called |
|
Definition
|
|
Term
| Which of the water soluble vitamins is found widely distributed in all plant and animal foods, which makes a deficiency unlikely? |
|
Definition
|
|
Term
| Because vitamin B6 is involved in heme synthesis, a deficiency symptom is |
|
Definition
hypochromic, microcytic anemia
This is because B6 is involved in the first stage of heme synthesis. |
|
|
Term
Name the vitamins required for proper functioning of the pyruvate dehydrogenase multienzyme complex.
Then name the substrate and the product of this reaction. |
|
Definition
Niacin, Riboflavin, Thiamin(TPP) and Pantothenic acid (CoA)
Pyruvate ---> Acetyl CoA (kind assumed we already knew this?! but whatev) |
|
|
Term
| List 4 important roles/functions of vitamin C. (including it's obvious role) (5). |
|
Definition
Collagen synthesis
Carnitine synthesis
Neurotransmitter synthesis (norepinephrine, serotonin)
Hormone production (calcitonin, CCK, oxytocin, GHRF, and more)
(Pssssttt: plus it's an antioxidant, bet you didn't know that ^^) |
|
|
Term
|
Definition
Awkward Man Hug (in my opinion--it's intentional :)
douche (according to Google)
Tim would beat both of these guys http://www.youtube.com/watch?v=Fad6eZTDikA&ob=av3e |
|
|
Term
| What types of vitamin E are most prevalent in our diet (2)? |
|
Definition
| a-Tocopherol and gamma-Tocopherol |
|
|
Term
| Functions of Vitamin E (7): |
|
Definition
Antioxidant (a-tocopherol):
-Cardiovascular disease
-Cancer
-Cataracts
-Alzheimer's disease
Non-antioxidant (a-tocopherol, y-tocopherol)
-Cell signaling
-Inflammation
-Gene expression |
|
|
Term
| Cellular uptake of Vitamin E (HDL, VLDL, LDL): |
|
Definition
HDL - Selective lipid uptake and efflux
VLDL - Uptake facilitated by LPL
LDL - Receptor-mediated uptake |
|
|
Term
| Vitamin E deficiency (who is at risk): |
|
Definition
Very rare in humans
Neurological symptoms – impaired balance and coordination (ataxia), skeletal myopathy, hemolytic anemia
Who's at risk?
a-TTP dysfunction due to genetic defects
Ataxia with vitamin E deficiency (AVED)
Severe malnutrition
Fat malabsorption syndromes (CF, cholestasis, abetalipoproteinemia) |
|
|
Term
|
Definition
No harmful effects reported in numerous supplementation studies (400 – 800 mg a-tocopherol equivalents per day)
Few side effects in adults taking < 2000 mg a-tocopherol daily
Animal studies – high vitamin E intake interferes with absorption and/or function of vitamins A & K
UL set with avoidance of hemorrhage in mind = 1000 mg |
|
|
Term
| What is the difference between synthetic and natural Vitamin E? |
|
Definition
Natural Vitamin E: RRR-a-tocopherol
Synthetic: SRR-a-tocopherol (position 2 of side chain is S instead of R) |
|
|
Term
|
Definition
| ascorbic acid(Reduced), dehydroascorbic acid (Oxidized) |
|
|
Term
| Absorption and transport and where Vitamin C is found (14): |
|
Definition
Absorption:
-Carrier mediated, active transport
-Sodium coupled Vitamin C Transporters (SVCT1)
-Throughout small intestine
-Absorption rate varies
12 grams (high intake) 16%
<20 mg (low intake) 98%
30-180 mg (usual intakes) 70-95%
-Dehydroascorbate more readily absorbed than ascorbate via GLUT transporters
-Reduced back to ascorbate in enterocyte by dehydroascorbate reductase
Transport:
-Found free as ascorbate
-~5% as dehydroascorbate – rapid uptake via GLUT-1,-2 or -4 transporters
-Ascorbate taken into cells requires SVCT 2.
-Body pool – 1500 mg (half life:8 to 40 days)
-Tissue concentrations of ascorbate exceed circulating concentrations
-Highest concentrations - adrenal gland, pituitary gland, retina
-Intermediate concentrations - liver, lungs, kidneys, pancreas, white blood cells
-Smallest concentrations - muscles, red blood cells |
|
|
Term
|
Definition
-Vitamin C excreted intact or as dehydroascorbate
Or other metabolites
Oxidation reactions mainly in liver, also kidney
-Excreted via urine |
|
|
Term
| What is Scurvy and what are the signs of scurvy (10 symptoms)? and who is at risk(4)? |
|
Definition
Of course Vit C deficiency!
Early – weakness, fatigue
bleeding gums, bruising, impaired wound/fracture healing, joint pain, hyperkeratosis of hair follicles
Depression
Increased risk – elderly, poor dietary intake, diabetes, smokers
(10-12 mg/d prevents scurvy) |
|
|
Term
|
Definition
| UL = 2 g/d; set to avoid risk of GI distress |
|
|
Term
|
Definition
Whole and enriched grains, nuts, yeast (esp. brewer’s yeast), meats (esp. pork), legumes.
Plant sources: Free thiamin
Animal sources: Phosphorylated (mainly TPP) |
|
|
Term
|
Definition
-Primarily in jejunum
-Phosphatases hydrolyze phosphate groups from TPP and TMP prior to absorption
-Active transport at low concentrations
-Thiamin transporters 1 & 2
-Also carrier mediated egress from enterocyte
-Passive diffusion when intakes high but not significant |
|
|
Term
| Inhibitors of absorption and bioavailability of Thiamin: |
|
Definition
Thiaminases - found in raw fish
Anti-thiamin factors: -Ethanol
-tea, coffee, blueberries, and red cabbage.
-Losses with cooking and handling (pH, heat, oxidation, radiation) |
|
|
Term
| Thiamin: Transport and Metabolism in Liver and where it's found in high concentrations (5) |
|
Definition
-In liver free thiamin phosphorylated to TPP
-Transported mainly as TPP
Found in high concentrations in skeletal muscles, heart, liver, kidney and brain.
-Also found as free thiamin, albumin bound, or as TMP
(Body pool of thiamin ~30 mg, but not readily stored.) |
|
|
Term
|
Definition
| Thiamin and its metabolites excreted in urine |
|
|
Term
| Thiamins 3 main functions: |
|
Definition
1 – Energy transformation (co-enzyme)
2 – Synthesis of NADPH and ribose (co-enzyme of Transketolase in pentose phosphate shunt)(Ribose required for nucleic acid synthesis)
3 – Non-coenzyme functions – nerve conduction and neurotransmitter function
(TTP and TPP present in neuronal cell membranes) |
|
|
Term
| Thiamin's role in energy transformation (which enzymes requires TPP? (3)) |
|
Definition
-Pyruvate Dehydrogenase
-a-ketoglutarate DH
-Branched chain a-keto acid DH
-In all cases, thiamin has same activity within active site, oxidative decarboxylation of substrate |
|
|
Term
| Dry beriberi Symptoms (9ish): |
|
Definition
-Peripheral neuropathy
-Weakness, weight loss, apathy, confusion
-Nerve degeneration and loss of nerve transmission
-Gastrointestinal tract distress
-Poor arm/leg coordination
-Extreme muscle wasting
THIAMIN DEFICIENCY |
|
|
Term
| Wet beriberi symptoms (4) |
|
Definition
Dry beriberi +
–Edema
–Enlarged heart
–Congestive heart failure |
|
|
Term
| Wernicke-Korsakoff Syndrome: What are the symptoms (4)? What is this and who does it affect (7)? |
|
Definition
| • Characteristics -Paralysis of eye muscles -Ataxia -Confusion and apathy -Loss of short term memory Cerebral beriberi Who is at risk for this? • Mainly in alcoholics o but also chronic dialysis, pregnancy, IV glucose infusion in people with marginal deficiency o Diminished thiamin absorption o Increased thiamin excretion o Poor quality diet |
|
|
Term
| What can be some Causes of Deficiency for Thiamin? |
|
Definition
• Inadequate intake
o Esp. high carbohydrate intake with low thiamin
o High intake of thiaminase containing foods
o Infants breastfed by thiamin deficient moms
• Decreased absorption
o Ethanol
o Folate deficiency
o Intestinal resection |
|
|
Term
| Assessment of thiamin status |
|
Definition
| RBC Transketolase activity |
|
|
Term
| What is Riboflavin's structure, and what are the two active coenzyme forms? |
|
Definition
-Nitrogenous ringed structure with sugar
alcohol side chain
-Active in coenzyme forms FAD and FMN |
|
|
Term
| Food sources of Riboflavin: |
|
Definition
Widely distributed – milk, cheeses, eggs,
fatty fishes, broccoli, green leafy vegetables,
enriched cereals, meats and legumes
(unstable to light, that's why it's good to keep milk in a non-see through container). |
|
|
Term
| Absorption of Riboflavin: |
|
Definition
•Mainly found as FAD in foods (requires proteases and phosphatases to free from FAD)
o(exceptions - found free in fortified foods, dairy products and eggs)
•Absorbed as free riboflavin
•Active transport in jejunum
•Phosphorylated in enterocyte, dephosphorylated to get out
•Seems to be an upper limit on absorption of ~30 mg |
|
|
Term
| Transport, metabolism, and excretion of Riboflavin (3): |
|
Definition
• Transported mainly as free riboflavin
• Transported into cells as free riboflavin
• Excreted in urine as free riboflavin and metabolites |
|
|
Term
| Riboflavin Functions (3): |
|
Definition
(REDOX reactions)
1-Interactions with Niacin, B6 and folate. (Riboflavin plays a role in folate metabolism. Used in methylene THF reductase).
2-Energy Production
-Electron Transport Chain
-Pyruvate DH
-FA oxidation
3-Antioxidant activity
-Glutathione recycling (used specifically in Glutathione Reductase as a co-factor to the enzyme.) |
|
|
Term
| What is Ariboflavinosis and what are the symptoms (6)? And who is at risk (6)? |
|
Definition
Riboflavin deficiency!
-Rare, but poor dietary intake in general predisposes one to deficiency
-Cheilosis (vertical fissure in the lips)
-Angular stomatitis
-Glossitis
-Photophobia
-Dermatitis (flaking)
-Anemia
-Newborns treated for hyperbilirubinemia by phototherapy (riboflavin is unstable to light)
-Lactose intolerance
-Hypothyroidism
-Anorexia
-Chronic alcoholism
-Trauma, stress (meaning metabolic stress) |
|
|
Term
| Assessment of riboflavin status: |
|
Definition
| Red blood cell glutathione reductase activity. |
|
|
Term
|
Definition
| Biocytin (biotinyllysine) form in which we find biotin bound to lysine residues of carboxylase enzymes |
|
|
Term
| Digestion, absorption, transport and metabolism of Biotin (6): |
|
Definition
-Proteolytic enzymes - yield free biotin, biocytin, biotinyl peptides
-Biotinidase (made by enterocytes)- Hydrolysis of biocytin to yield free biotin and lysine. Gives free biotin for the enterocytes to absorb.
-Sodium dependent facilitated transport in jejunum and ileum; shares carrier with pantothenic acid (sodium dependent multivitamin transporter, SMVT)
-Transported in circulation as free (80%) and protein bound
-Transported into cells by active, carrier mediated transport
-Free biotin excreted in urine |
|
|
Term
Functions of biotin (4):
Specific enzymes that use biotin (4): |
|
Definition
-ATP dependent carboxylations and carboxyl-group exchange.
Other (non-coenzyme)functions:
-responsible for synthesis of HMG CoA (cholesterol synthesis).
-Biotinylation of histones - Regulate gene expression.
-Critical in degregation of leucine to acetyl CoA (TCA cycle or FA) (LOOK THIS UP, my notes are unclear about if this is a non-enzymatic thing that biotin does)
Enzymes:
-Acetyl CoA Carboxylase
Acetyl CoA---> Malonyl CoA
-Pyruvate Carboxylase
Pyruvate---> OAA
Propionyl CoA carboxylase
Propionyl CoA--->Methylmalonyl CoA
-Methylcrotonyl CoA carboxylase
3-methylcrotonyl CoA-->3-methylglutaconyl CoA
In this last reaction, if Biotin is deficient, instead of making 3-methylglutaconyl CoA, the body will make and secrete 3-hydroxyisovaleric acid in the urine. This will determine biotin status in the body. |
|
|
Term
| Deficiency symptoms of Biotin (11ish): |
|
Definition
Rare
-Dermatitis – scaly red rash around eyes, nose, mouth, genital area (raccoon eyes and round (moon) face appearance).
-Depression, lethargy, hallucinations, numbness & tingling (paresthesia)
-Alopecia (loss of hair) |
|
|
Term
| Who's at risk for biotin deficiency (9): |
|
Definition
-Biotinidase deficiency
-Reduced intestinal absorption
-Reduced recycling
-Increased excretion
-Holocarboxylase synthetase deficiency
-Prolonged raw egg white consumption
(Signs begin after weeks to years because of recycling of biotin)
-Parenteral nutrition without biotin supplementation
-Long term anticonvulsant therapy – may compete for absorption, increase excretion, and/or displace biotin from biotinidase.
-Pregnancy |
|
|
Term
| Assessment of biotin status: |
|
Definition
-Urinary biotin & metabolites
*3-hydroxyisovaleric acid
Levels increase within 2 weeks on biotin deficient diet |
|
|
Term
|
Definition
Widespread in foods – egg yolk, soybeans, yeast, peanut butter, legumes, nuts, whole grains.
Synthesized by colonic bacteria and we can absorb some of what’s made.
-Unclear what the contribution is to our needs |
|
|
Term
| What are the Vitamers of Pyridoxine and how are they activated? |
|
Definition
Pyridoxine (PN)
Pyridoxal (PL)
Pyridoxamine (PM)
They are activated by phosphorylation and become PNP, PLP, PMP but only PLP is the coenzyme form & is the most biologically active |
|
|
Term
| Describe the Absorption of Vitamin B-6 (6) |
|
Definition
Absorb about 75% depending on glycoside content of food
Poorly absorbed in glycoside form
Better absorbed from vegetables, meat, fish and dairy than from grains
Absorbed by passive diffusion in jejunum
Phosphorylation Trapping Occurs
Evidence suggests a carrier mediated pathway |
|
|
Term
| Describe the transportation of B-6 |
|
Definition
Mainly albumin-bound PLP
Must be in non-phosphorylated form (PL) to enter cell
Membrane phosphatase activity cleaves P
Carrier mediated
Trapped in cell by rephosphorylation |
|
|
Term
| Where is B-6 Mostly stored? |
|
Definition
| Mainly found in muscle (PLP bound to glycogen phosphorylase) --remember enzyme name |
|
|
Term
| Draw the interconversion of the three vitamers of b-6 |
|
Definition
| Pyridoxine Phosphate –Pyridoxine Phosphate Oxidase→ Pyrioxal Phosphate ←Pyridoxine Phosphate Oxidase→ Pyridoxamine Phosphate |
|
|
Term
|
Definition
Excreted in the urine as 4-pyridoxic acid
All tissues can oxidize PL to 4-pyridoxic acid |
|
|
Term
|
Definition
AA Metabolism:
Transamination and deamination – reactions that generate carbon skeletons for synthesis of new amino acids or for entry into energy producing pathways; catabolism of amino acids
Decarboxylation reactions - neurotransmitter synthesis
Trans- and de-sulfhydration – cysteine synthesis from homocysteine
--
Glycogenolysis and Gluconeogenesis:
Coenzyme in glycogen phosphorylase
Transamination of gluconeogenic amino acids
--
Heme synthesis:
delta-aminolevulinate synthase occurs in mitochondria
First step in heme synthesis:
glycine + succinyl CoA --Delta-aminolevulinic acid synthase – requires b6→ Delta amino-levulinic acid (ALA) |
|
|
Term
| Deficiency facts and symptoms of B6: (12) |
|
Definition
Deficiencies are Rare Symptoms include: Fatigue, depression, confusion, glossitis, angular stomatitis, cheilosis, irritability
Mouth problems due to Niacin production from tryptophan requiring b-6
Riboflavin deficiency can lead to a functional b-6 deficiency Anemia, neurological problems can be mistaken for iron deficiency anemia When heme is not made, RBCs are smaller – pink/pale
Hyperhomocysteinemia |
|
|
Term
| Who is at risk for b-6 deficiency (6) |
|
Definition
Inadequate intake
Isoniazid treatment--also penicillamine, corticosteroids, anticonvulsant therapies
Alcohol can impair conversion of PN and PM to PLP and may increase metabolism of PLP |
|
|
Term
|
Definition
Daily 1000mg can cause concern
Can result in peripheral neuropathy in chronic doses > 500 mg/d
Symptoms – peripheral neuropathy
UL 100 mg/d |
|
|
Term
| Assessment of B6 status (3) |
|
Definition
Direct measure of plasma PLP
Urine 4-pyridoxic acid
Erythrocyte transaminase activity |
|
|
Term
|
Definition
Found in protein-rich foods whole grains, legumes, nuts, chicken, fish, beef, eggs; also bananas, potatoes
Stable to heat but not to oxidation and UV light |
|
|
Term
| What are the two forms of niacin, and are they interconvertable? |
|
Definition
Nicotinic acid (potent lipid lowering agent when used pharmaceutically; has potential for liver damage) and nicotinamide/niacinamide (does not have these effects)
no direct conversion between but indirectly – NA → NAD → Nam |
|
|
Term
| What are the active co-enzyme forms of niacin? |
|
Definition
|
|
Term
| What are the exogenous and endogenous sources of niacin? |
|
Definition
Exogenous
Foods: Fish, meats, poultry, enriched grains, cereals, peanuts, seeds, legumes
Plant sources – NA
Animal sources – NAD and NADP, Nam
In some plant foods (corn) niacin bound to complex carbohydrates or peptides making it unavailable - niacytins
Endogenous
We can synthesize it from tryptophan
60 mg tryptophan yields 1 mg niacin
Conversion requires vitamin B6, riboflavin and iron |
|
|
Term
| Absorption, transport, metabolism and excretion of b-3 (6) |
|
Definition
| • Facilitated uptake in jejunum • Absorbed as NA and Nam • Transported mainly as Nam • Transported into cells as Nam, trapped there by conversion to NAD or NADP • Metabolized in liver and excreted in urine NAD and NADP are degraded to nam, oxidized in liver, metabolites excreted in urine NA and Nam reabsorbed by kidneys |
|
|
Term
|
Definition
Co-enzyme functions: redox reactions
Transfer of electrons in catabolic reactions and the electron transport chain (NAD) – therefore intimately involved in energy production
Redox active
NAD/NADH + H+, NADP/NADPH + H+
NAD ~ catabolic pathways
NADP ~ anabolic pathways
Oxidative reactions/pathways requiring NAD:
Glycolysis
Pyruvate dehydrogenase complex
Oxidation of acetyl CoA
β-oxidation
Oxidation of ethanol
Reductive reactions/pathways requiring NADPH:
Fatty acid synthesis
Cholesterol and steroid hormone synthesis
Synthesis of deoxyribonucleotides
Interconversions of folate derivatives
Regeneration of glutathione (glutathione reductase) and thioredoxin
Cholesterol lowering – nicotinic acid only, mechanism not completely defined but known to reduce VLDL production. Reduced VLDL synthesis related to reduced mobilization of fatty acids from adipocytes
Substrate Functions:
NAD is substrate for ADP-ribose polymerase (Poly ADP Ribose Polymerase PARP) and ADP-ribose cyclase enzymes
DNA repair
Cell division
Regulation of gene expression |
|
|
Term
| What are the four D's of Pellagra? |
|
Definition
Diarrhea (general GI distress), Dermatitis, Dementia, Death
Occur in no particular order |
|
|
Term
| How long does it take to develop a b3 deficiency? |
|
Definition
| On average takes a month of no B-3 to develop |
|
|
Term
| How is pellagra dermatitis distinct? (4) |
|
Definition
• Symmetrical, well demarcated redness & scaling
• Primarily in areas exposed to light, heat or mechanical trauma
• Seasonal exacerbations
• Thickened hyper-pigmented skin in chronic lesions |
|
|
Term
| Describe the symptoms associated with the GI changes and Dementia of pellagra (15) |
|
Definition
GI changes – inflammation in mouth, mucosa (like ariboflavinosis or vitamin B6 deficiency), intestinal mucosa (diarrhea OR constipation), cheilosis, glossitis
Dementia – early – muscle weakness, twitching, burning sensation, leads to depression, apprehension, memory loss, paranoia, delirium, hallucinations, violent behavior |
|
|
Term
| Describe the toxicity of b-3 (15) |
|
Definition
Nicotinic acid in pharmacologic doses can result in severe flushing
Additional side effects include burning, itching, headache, heartburn, nausea, vomiting, hepatotoxicity, impaired glucose tolerance
Nicotinamide – nausea, vomiting, hepatotoxicity (much less frequent/rare)
Upper Limit set at 35 mg/d in adults based on flushing reaction.
Hepatotoxicity is much higher. Therapeutic cholesterol amount is 3g.
Occurs from supplementation and fortification alone (not from food) |
|
|
Term
| How are niacin levels assessed? |
|
Definition
| Commonly assessed by measuring levels of urinary metabolites of Nam |
|
|
Term
| Digestion, absorption, transport and metabolism of PA (6) |
|
Definition
85% of PA in foods is bound as part of CoA – Phosphatase and pyrophosphatase activities yield free PA via hydrolyzation
Free pantohtenic acid absorbed using active transport (sodium dependent multivitamin transporter, SMVT)
40-60% absorbed
Transported mainly as CoA in RBC, some free PA too
Actively transported into cells
Excreted in urine as PA
No metabolites identified |
|
|
Term
|
Definition
Part of Coenzyme A and Acyl carrier protein
CoA – in energy production; Part of PDH and a-ketogluterate DH and BCaKADH
Also needed for synthesis of cholesterol, ketone bodies, CoQ10, acetylcholine, phospholipids, sphingomyelin, triglycerides
Acyl carrier protein – required for fatty acid synthesis |
|
|
Term
| Deficiency and Toxicity of PA |
|
Definition
Deficiency – rare
“Burning feet syndrome”
Fatigue, weakness, depression, sleep disturbances, ataxia, vomiting
Toxicity – none |
|
|
Term
|
Definition
|
|
Term
|
Definition
Found in almost all foods – good sources – avocado, bran, broccoli, whole grains, legumes, eggs, mushrooms, and more
Unstable in heat, acid, and alkali conditions |
|
|
Term
| What is the haber-weiss reaction? |
|
Definition
| H2O2 + O2 → O2 + OH- + OH- |
|
|
Term
| What is the fenton reaction? |
|
Definition
|
|
Term
| What is the respiratory burst? |
|
Definition
| NADPH oxidase – purposely creates a burst of oxidation to kill a cell (immunologically) |
|
|
Term
|
Definition
| 2O2- + 2H+ --> H2O2 + O 2 |
|
|
Term
|
Definition
|
|
Term
|
Definition
Average dietary energy intake (kcal) to maintain energy balance in a healthy adult
Based on age, gender, weight, height, level of physical activity |
|
|
Term
|
Definition
The average daily intake level of a nutrient that will meet the needs of half of the healthy people in a particular category
Used to determine the Recommended Dietary Allowance (RDA) of a nutrient |
|
|
Term
|
Definition
| The average daily intake level required to meet the needs of 97 – 98% of healthy people in a particular category |
|
|
Term
|
Definition
Recommended average daily intake level for a nutrient
Used when the RDA is not yet established: vitamin K, fluoride
Based off of “healthy people’s” intake |
|
|
Term
| Vitamin E absorption rate |
|
Definition
|
|
Term
| What drug can be dangerous in combination with vitamin E? |
|
Definition
|
|
Term
|
Definition
plant oils: canola, olive, sunflower, safflower, cottonseed, wheat germ oil
(for γ-tocopherol – soybean and corn oils high), nuts avocado |
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Term
| What enzyme do humans lack to produce their own vitamin c? |
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Definition
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Term
| What 6 reactions require b-6 for DEcarboxylation |
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Definition
Serine --decarboxylation--> ethanolamine --> Acetylcholine
Tyrosine --> Dopa --decarboxylation--> dopamine --> epinephrine
typtophan --> 5-HT --decarboxylation--> serotonin
histidine --decarboxylation--> histamine
glutamic acid --decarboxylation--> gamma aminobutryric acid (GABA)
cysteine --> cysteine sulfinic acid --decarboxylation--> taurine |
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Term
| Name the vitamins required for proper functioning of the pyruvate dehydrogenase of the pyruvate DH multienzyme complex: |
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Definition
| Pantothenic Acid, Niacin, Riboflavin, Thiamin. |
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Term
| What are the substrate and product of the pyruvate DH multienzyme complex: |
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Definition
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Term
| What 2 reactions is vitamin c required in carnitine synthesis? |
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Definition
-Trimethyl liysine dioxygenase (hydroxylase
4-butryobetaine hydroxylase
reactions also utilize a-ketoglutarate, o2, and Iron |
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Term
| In what way does vit c assist in tyrosine production from phenylalanine? |
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Definition
Phenylalanine hydroxylase (phenylalanine to tyrosine)
In liver and kidneys
Requires O2 and tetrahydrobiopterin
Vitamin C regenerates tetrahydrobiopterin |
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Term
| What four neurotransmitters require vit c for their production and how? |
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Definition
Dopamine mono-oxygenase (Copper)
makes norepinephrine from dopamine (which can also then become epinephrine)
directly requires vit c
--
Tryptophan mono-oxygenase (requires tetrahydrobiopterin and is recycled via vit c) makes serotonin (which can then become melotonin as well) |
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Term
| What is the role of scvt2? |
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Definition
| General tissue cells use/require this to uptake vit c |
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Term
| How does vit c assist in collagen synthesis? |
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Definition
Post-translational hydroxylation
Ferrous (2+) & Ferric (3+) Iron
(vitamin c is not a coenzyme in this way) |
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Term
| Where do you find High concentrations (3), intermediate concentrations (5) and low concentrations (2) of Vit. C? |
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Definition
-Highest concentrations - adrenal gland, pituitary gland, retina
-Intermediate concentrations - liver, lungs, kidneys, pancreas, white blood cells
-Smallest concentrations - muscles, red blood cells |
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Term
| What is the importance of methylcrotonyl CoA carboxylase for Biotin? |
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Definition
Methylcrotonyl CoA carboxylase is an enzyme that is biotin dependent and if biotin is not available the substrate will accumulate (substrate being 3-methylcrotonyl CoA) and will be turned into 3-hydroxyisovaleric acid and excreted in the urine.
You can see if someone is Biotin deficient if they have an accumulation of this metabolite in the urine. |
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Term
| What is the role of flavokinase? |
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Definition
| Phosphorylates Flavin in FMN |
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Term
| What is the role of FAD synthetase? |
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Definition
| The adenylation of riboflavin to form FAD |
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Term
| How is riboflavin absorbed into the liver? |
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Definition
| energy dependent, carrier mediated absorption, there it is reconverted to FMN and FAD |
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