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152 Cards in this Set
- Front
- Back
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Sources of vitamin C |
Fruits and vegetables, citrus fruit and juices. Easily degradable during long storage |
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Absorption of vitamin C |
reduced form is absorbed by sodium dependent cotransporters SVCT1 and SVCT2 |
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oxidation of Vitamin C |
occurs prior to absorption. absorption of oxidized form is also common, through facilitated diffusion and glucose transporters GLUT 1 and GLUT 3 |
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absorption efficiency of vitamin c |
efficiency decreases with intake from about 95% down to about 15% |
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vitamin c reduction to ascorbate in enterocytes... |
done by dehydroascorbate reductase
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** Ascorbate regeneration is very important with redundant mechanisms |
* |
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electron sources in ascorbate regeneration |
dihydrolipic acid, NADPH, NADH, glutathione (GSH), thioredoxin |
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functions and mechanisms of vitamin c |
collagen syn (3 enzymes) carnitine syn (2 enzymes) tyrosine syn and catabolism (1 enzyme) Neurotransmitter syn-norepinephrine and serotonine (1 enzyme)
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Name the oxidized and reduced forms of vitamin c |
oxidized-ascorbic acid reduced-dehydroascorbic acid |
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What ion is needed for absorption of reduced vitamin c? |
sodium |
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how is oxidized vitamin c absorbed |
absorbed by glut 1 and 3 (glucose transmitters)
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what is the primary cofactor used by dehydroascorbate reductase? |
glutothiamine |
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Reduction (Loss or gain) or electrons and loss of gain of hydrogens? |
gain and gain |
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what 2 amino acids are hydroxylated by ASC- dependent hydroxylation of collagen? |
proline and lysine |
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What is the metal involved in the hydroxylation of collagen? |
iron |
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antioxidant activity of vitamin C |
ascorbate is the bodies primary water-soluble antioxidant -ascorbate +OH=semihydroascorbate +H2O -ascorbate +O2=dehydroascorbate +H20 -ascorbate +H2O2=dehydroascorbate +2H2O |
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pro-oxidant activity of vitamin C |
at high concentrations, ASC reduces free copper and iron (especially with iron) |
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common cold and vitamin c |
generally no effect- all hype |
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Cancer and vitamin C |
Vitamin c rich foods have positive effect against upper GI cancers -acting as an antioxidant, preventing mutation and nitrosamine formation **VIT C rich foods are MUCH better than supplement |
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Vitamin C and Cardiovascular disease
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1 serving of fruit and veg per day decreases CVD by 4% -ASC inhibits monocyte adhesion, early step in arteriosclerosis -lowers LDL oxidation -lowers oxidative damage in smokers -supplements do not reduce CVD risk
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Vitamin C and cataracts |
antioxidant prevents clouding in eyes unclear is its from ASC alone
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vitamin c interactions with other nutrients |
iron promotes nonhdme iron absorption, but causes destruction of ASC -extra ASC and free iron may lead to free radical damage
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Metabolism and excretion of vitamin c |
renal threshold > ~1.2 mg/L in plasma or a daily intake of >500 mg -excreted as ASC or oxidized to dehydroascorbate (then to 2,3 diketogulonic acid, then excreted)
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Vitamin C RDA |
men- 90 mg women- 75 mg pregnancy-100 mg lactation- 120 mg +35 mg for smokers |
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vitamin c deficiency |
scurvy, can be fatal failure to cross link collagen
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vitamin c toxicity |
UL= 2g/ day concern about oxalate and kidney stones |
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Assessment of nutriture |
plasma and serum concentrations normal- .2-1.2 mg/L deficient <.2 mg/L
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What is most likely to be deficient in Vitamin C |
smokers people not eating fruit and vege elderly homeless
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of ascorbate's many biological activities, which pathway is most susceptible to deficiency? |
hydroxylation of collagen because it is where we see pathological effects of deficiency |
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what is measured in the urine that reflects collagen turnover |
hydroxy lysine |
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a street person admitted for surgery is released to a shelter too soon and the wound fails to heal, why? |
without ascorbate, collegian synthesis doesn't work and therefore won't heal |
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Thiamine |
vitamin B1 |
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sources of thiamine |
pork, legumes, germ, enriched flour- have to be deficient in a lot of things to be deficient in thiamine |
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what is the first vitamin |
thiamine |
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what are some anti-thiamine factors? |
raw fish, tea, tannis |
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what breaks down thiamine? |
thiamin-ase |
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where is thiamine absorbed and how? |
jejunum, by carries ThTr1 and ThTr2 (thiamine transporter 1 and 2) -passive absorption with high intake
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what interferes with thiamine absorption |
ethonol |
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where is thiamine phosphorylated? |
in an enterocyte, TDP and metabolic trapping (brings thiamine into enterocyte and doesn't recognize TDP and traps thiamine)
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Thiamine transport |
in blood free and bound to albumin, or as thiamine monophosphate |
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coenzyme roles of thiamine |
energy transformation (oxidative decarboxylases)- pyruvate, alpha ketogluterate, transketolases -synthesis of pentoses and NADPH |
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non-coenzyme roles of thiamine |
membrane and nerve conduction |
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metabolism and excretion of thiamine |
excreted intact or catabolized, saturable reabsorption means blood excess is excreted |
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thiamin RDA |
men-1.2 mg women- 1.1 mg more for preg, lactation, alcoholics, high cho consumption, renal patients, PEIN (protein, energy malnutrition) -total body stores- 30 mg 1/2 life is 2 weeks |
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thiamine deficiency |
beriberi (dry or wet) -wenicke-karsakoff in alcoholics -alcoholics -possible genetic causes -alcohol interferes with thiamin absorption, liver metabolism and storage
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thiamine toxicity |
little danger with oral intake, no UL
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assessment of nutriture of thiamine |
measuring erythrocyte transketolase activity in whole body -measuring thiamine and TDP in blood urine |
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how is riboflavin activated |
in blood and tissues- not too metabolic |
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riboflavin |
5 carbons- almost a sugar (ribo) 3 ring structure (flavin)` |
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sources of riboflavin |
milk, diary, eggs, meat, legumes, greens
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digestion, absorption, transport and storage |
-ingested riboflavin as FAD, FMN and riboflavin is freed from phosphate by intestinal phosphates prior to absorption -absorbed by saturated, energy dependent carrier mechanisms in duodenum -highly efficient - 95%
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How is riboflavin absorption impared |
by alcohol and diffusion |
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how is riboflavin phosphorylated |
to FMN in enterocytes (metabolic trapping) and then dephosphorylated back to riboflavin for transport into the plasma
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what is riboflavin often attached to during transportion |
proteins such as albumin |
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functions and mechanisms of action of riboflavin |
flavoproteins-oxidation/ reduction reaction -electron transport chain -decarboxylation of pyruvate -glutathione reductase |
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riboflavin excretion |
primary in urine, small amounts in feces -fluorescent marker in urine (yellow urine)
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RDA riboflavin |
men-1.3 mg women 1.1 mg preg 1.4 mg lactation 1.6 mg
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riboflavin toxicity |
none reported, no UL |
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deficiency of riboflavin |
no clear deficiency disease -still common in poor countries with no milk or meat -possible in alcoholics, contributor to wernicke korsakoff syndrome -secondary deficiency due to birth control pills, diabetes, trauma and stress |
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assessment of nutriture of riboflavin |
measuring activity of erythrocyte glutathione reductase with or without added FAD
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Riboflavin concept map?! |
! |
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Niacin |
smallest vitamin |
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history of niacin |
pellagra was first documented in 1735 in spain and was common in europe in the 1800s -pellagra broke out in the SE US in 1906 among poor rural folks who ate a lot of corn products -experimented with priosoners |
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where is pellagra still common? |
africa and asia |
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sources of niacin |
fish, meats, grains, seeds, legumes, enriched flours
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synthesis of niacin |
in the liver from tryptophan, about 1 mg niacin from 60 mg of tryptophan intakes |
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absorption of niacin |
in the small intestine and stomach -NA dependent carrier mediated diffusion -passive diffusion when consumed in excess |
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transportation of niacin |
primarily as nicotinamide and also nicotinic acid to a lesser extent |
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oxidative reactions in niacin |
glycolysis, pyruvate dehdryogenase, citric acid cycle, beta oxidation of fatty acids
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reductive biosynthesis of niacin |
fatty acid synthesis, regeneration of glutathiamine, cholesterol synthesis |
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metabolism and excretion of niacin |
NAD/NADP degraded to nicotinamide and ADP-ribose -methylated and oxidized before excretion -little niacin is excreted, efficient kidney reabsorbtion |
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Niacin RDA |
men- 16 mg NE women 14 mg NE 1 NE= 1 mg or 60 mg of tryptophan |
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niacin deficiency |
pellegra -corn treated with lye-water or lime-water releases niacin -alcoholics are at risk for deficiency -four D's- dermatitis dementia, diarrhea, death |
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assessment of nutriture |
-measuring urinary metabolites <.8 g/day=deficiency ration of NAD to NADP <1.0 means deficiency -not measured in serum -probably a combo of measures taken together is best strategy
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Niacin oddities |
smalles vitamin -bound in corn by released by lime -from tryptophan -megadoses treat CHO- especially low HDL, itchy side effects -not measured in blood
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niacin toxicity |
large doses used to treat hypercholesterolemia -side effects with does >1 g per day UL=35 mg |
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pantothenic acid functions and mechanisms of actions |
component of coenzyme A acetyl coA key junction in energy metabolism- entry way to TCA cycle -nutrient metabolism for energy -prosthetic group for acyl carrier protein- fatty acid syn -acetylation of prot, sugar, drugs
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metabolism and excretion of pantothenic acid |
excreted intact in urine, small amount in feces ~2-5 mg excreted per day
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adequate intake of pantothenic acid |
adults- 5 mg preg- 6 mg lactation- 7 mg |
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deficiency and experimental of pantothenic acid |
possible contributor to wenicke- karsakorf |
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pantothenic acid toxicity |
non reported unsubstantiated anti-agin claims for mega doses |
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assessments of nutriture |
blood concentrations are a poor measurement urinary pantothenate excretion <1mg per day=poor |
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sources of biotin |
widely distributed in foods like liver, cereal, legumes, nuts made by bacteria in large intestine
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digestion of biotin |
protein bound digestion by proteolytic enzymes |
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absorption of biotin |
for food: absorbed primarily in jejunum, followed by ilium
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transport of biotin |
uses the sodium-depended multivitamin transporter (SMVT)
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what prevents absorption of biotin |
avidin, in raw eggs, binds to biotin and prevents absorption -cooking eggs denatures avidin and releases biotin |
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functions and mechanisms of action of biotin |
coenzyme roles in transferring activated CO2 -pyruvate carboxylase -acetyle coA carboxylase -propinyle coA corboxylase -beta-methylcrotonyle coA carboxylase |
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no co-enzyme roles of biotin |
cell proliferation, gene silencing and DNA repair gene expression and cell signaling |
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metabolism and excretion of biotin |
biotin holocarboxylases catabolyzed to biotin oligopeptide and the biocytin -biocytin degraded to lysine and biotin -biotin and metabolites excreted in urine -biotine from bacteria that is not absorbed excreted in feces |
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sources of folate |
mushrooms, many green vegetables, peanuts, legumes, lentils, fruits, liver, fortified flour
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what is folium latin for? |
leaf |
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what is the stable oxidized form of folate (used in supplements) |
folic acid folate=reduced form found in food |
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digestion of folate |
polyglutamate forms are hydrolyzed to mono glutamate form in intestine |
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absorption of folate |
absorbed with folate binding receptors, protein coupled folate transporters (PCFT) |
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transport of folate |
transported as reduced form, tetrahydrofolate (THF) |
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storage of folate |
body has 20 mg, 1/2 in liver |
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functions and mechanisms of action of folate |
cofactor as the polyglutamate form single carbon transfer amino acid metabolism (histidine, serine, glycine, methionine, cysteine)
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what other deficiency would cause a folate deficiency?` |
b12 |
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functions of folate |
methionine cycle ...... research |
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b12 deficiency and folate |
methionine synthase slows down 5-methyl THF and homocysteine build up, "methyl folate trap" -limits folate for other activities such as thymidine sythesis |
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folate deficinecy |
homocysteine builds pup in a cell and causes blood toxin
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folate interactions with other nutrients |
vitamin b12 deficiency of either b12 or folate leads to lack of thmidine and increased homocysteine
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excretion of folate |
in urine and feces |
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RDA of folate |
adults- 400 micrograms preg 600 micro. lactations 500 micro. |
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folate and neural tube deffects |
in embryo, neural tube closes at ~ 4 weeks folate deficiency slows and disrupts DNA syn a deficiency of folate in pre conceptual period leads to increase in NTD's, including spina bifida
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prevention of NTD and folate deficiency |
pre-conception, 400 micrograms of folic acid reduces NTD 2/3.
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folate and cardiovascular disease |
high serum homocysteine is a risk factor -multiple trials using folate supplementation lower homocysteine but not CVD risk |
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folate and caner |
deficiency may contribute to colon cancer through decreased methylation of DNA and through lack of thymidine - |
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methotrexate and folate |
a chemotheraputic agent that inhibits DHF reductase -blocks thymidine syn. and inhibits DNA syn. -stops cell division, especially of rapidly growing cells like cancer cells -extra folate in diet over comes this
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alzheimers and dementia and folate |
homocysteine and low folate are risk factors -no trials really prove |
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osteoporosis and folate |
stroke prevention study shows folate reduced fractures by 80 percents -homocysteine is known to disrupt collagen cross-linking |
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a person with plasma folate is low but RBC level is normal, why? |
have not eaten fruits or vege in the past few days |
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oxidized form of folate |
folic acid |
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reduced form of folate with 4 hydrogen |
THF |
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primary biochem. role of folate |
methylation |
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folate important in syn. of what DNA base |
thionadione |
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what chemo. agent inhibits folate reduction |
methotraxate |
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B12 |
cobalamin |
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sources of b12 |
animal products, liver, made exclusively by bacteria |
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b12 in the stomach |
releases from proteins by acid and proteases bind to R proteins (haptocorrins) |
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b12 in the duodenum |
r proteins hydrolyzed- free cobalamin binds to intrinsic factor (syn in stomach lining) |
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b12 in the illeum |
absorbed via binding with b12 intrinsic factor receptors (cubilins) -binds to transcobalamin II for transport |
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enterohepatic circulation of b12 |
secretion of about 5 micrograms per day in the bile -reabsorbed in the illeum |
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transport of b12 |
in blood, bound to 1 of 3 transcobalamins -TCII- main proteins that carries newly absorbed cobalamin -TCI and TCII- exact functions unknown
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storage of b12 |
can be stored and retained in the body for long periods, even years. -about 3 mg is stored in the body, mostly in the liver |
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functions of b12 |
critical to methyl group metabolism -conversion of homocysteine to methionin -conversion of L-methylmalonyl coA to succinyl coA -critical to myelination of nerves |
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metabolism and excretion of b12 |
.1 percent per day excreted in bile, bound to IF -recycled by enterohepatic circulation |
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RDA b12 |
adults- 2.4 micro preg- 2.6 micro lactating- 2.8 micro |
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deficiency of b12 |
megablastic macrocytic anemia -also neuropathy -usually causes by inadequate absorption by loss of stomach acid and loss of IF -pernicious anemia is an autoimmune attack on stomach cells that make IF
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what mineral is at the center of b12 |
cobalt |
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name the autoimmune disease that destroys the cells that make IF |
pernicious anemia |
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what is extrinsic factor |
b12 |
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what organisms make up b12 |
bacteria |
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name the proteins in the stomach that 1st bound to b12 |
R protein -intrinsic factor |
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name the proteins that transport b12 to the illium |
transcoblamins |
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how long can b12 be stored in the liver? |
years |
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name 1 enzyme with b12 as prosthetic groups |
methyanine sythase |
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name 2 metabolites measured in serum or urine that assess b12 status |
homocysteine and methylmalonic acid |
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who is at risk of a b12 deficiency |
elderly |
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what nutrient, in excess, can make b12 defieicny |
folate |
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sources of b6 |
meats, liver, whole grains, vegetables, some fruit, nuts |
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absorption of b6 |
passive diffusion in jejunom |
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b6 dephosphorylated to |
PN (most stable), PL or PM |
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absorption efficiency of b6 |
75% |
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functions of b6 |
very versatile |
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coenzyme of amino acid metabolism of b6 |
transamination, decarboxylation, transulfhydration and desulfhydration |
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**know transaination of b6 |
! |
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metabolism of b6 |
4-pyridoxic acid- metabolite (excreted in urine) excess intake is readily excreted |
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deficiency of b6 |
rare but more likely in elderly, alcoholics, people on certain drugs -dermatitis and microcytic anemia -elderly and alcoholics have increase breakdown of PLP -contributes to high blood homocysteine |
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toxicity of b6 |
sensory and peripheral neuropathy UL= 100 mg
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assessment of nutriture of b6 |
plasma PLP concentrations <20 nmol/L deficient -xanthurenic acid excretion following tryptophan loading -erthryocyte transaminate activity before and after adding PLP
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