Microminerals Flashcards
1
Q
iron distribution in the body
A
65% as part of hemoglobin
10% in myoglobin
1-5% as part of enzymes
20% in storage
2
Q
two categories of sources for iron
A
heme iron
non-heme iron
3
Q
sources of heme iron
A
heme iron is contained within a porphryin structure and is derived from hemoglobin and myoglobin so is only find in animal products
meat, fish, poultry, oysters, clams
4
Q
sources of non-heme iron
A
meat
beans, dark green leafy veggies, dried fruits
blackstrap molasses
enriched foods fortified with iron
5
Q
which minerals are microminerals?
A
iron copper zinc selenium chromium iodine manganese molybdenum (Mo) fluoride boron silicon vanadium (V)
6
Q
chemical forms of iron in the body
A
2 stable forms are:
ferric (Fe3+) and ferrous (Fe2+) iron
7
Q
digestion of heme iron
A
heme iron is hydrolyzed from hemoglobin or myoglobin by proteases in the stomach and SI
8
Q
digestion of non-heme iron
A
- non-heme iron is hyrolyzed from food components by HCl and proteases in the stomach releasing iron in the Fe3+ form
- some of it is reduced to Fe2+ by low pH of the stomach but it may complex to FeOH3 in the alkaline environment of the SI an and be poorly absorbed
9
Q
duodenal cytochrome b
A
acts as a ferric reductase
reduces Fe3+ to Fe2+ in the duodenum and improves solubility and absorption
10
Q
what is needed as a cofactor for duodenal cytochrome b/ferric reductase?
A
vitamin C is required for it so it can help absorption of non-heme iron
11
Q
absorption of heme iron
A
- absorbed throughout the SI but absorbed most in the duodenum by the carrier protein HCP1 (heme carrier protein 1)
- then, once absorbed heme is hydrolyzed by heme oxygenase to give inorganic Fe2+ and a porphyrin ring
12
Q
what percentage of heme iron is absorbed?
what percentage of non-heme e iron is absorbed?
A
15-35% of heme iron is absorbed
2-20% of non-heme iron is absorbed
13
Q
absorption of non-heme iron
A
any Fe2+ is absorbed via the DMT1 (divalent mineral transporter 1), stimulated by low iron stores
iron present in the Fe3+ form is reduced to Fe2+
14
Q
factors that enhance absorption of non-heme iron
A
- vitamin C
- other organic acids (malic, citric, tartaric, lactic acids)
- meat, fish, poultry
- low iron status
15
Q
factors that inhibit iron absorption
A
phytic acids (phytases) polyphenols oxalates phosvitin (found in egg yolks) other minerals (calcium, zinc, copper, manganese) soy, wheat, egg, whey, casein protein herbal teas: peppermint, green tea, linden flower and chamomile rapid transit time decreased stomach acidity
16
Q
what does hepcidin do?
A
when iron stores are high or adequate, hepcidin is released from the liver which promotes the degradation of ferroportin which decreases the transport of iron across the membrane of the enterocyte
- also, low levels of hepcidin cause increased ferroportin levels
17
Q
actions of mobilferrin, ferroportin, and transferrin
A
- mobilferrin transports iron through enterocytes
- ferroportin is required to transport iron across the basolateral membrane
- transferrin transports iron in the blood while in the Fe3+ form
18
Q
how is Fe2+ iron converted into Fe3+ iron before it enters the bloodstream?
A
with either of:
- hephaestin
- ceruloplasmin
19
Q
where is iron stored in the body?
A
60% stored in lover
also stores in bone marrow and spleen
20
Q
storage proteins for iron?
A
- ferritin - primary storage protein for iron
- hemosiderin - a degradation product of ferritin
21
Q
when do levels of hemosiderin increase?
A
during iron overload
22
Q
why is iron turnover so high?
A
because the dietary intake cannot meet the daily needs of the body so iron is constantly recycling its stores from degradation of ferritin, hemoglobin, and hemosiderin
23
Q
functions of iron in the body
A
- oxygen transport and storage
- electron transport and energy metabolism
- some iron-dependant enzymes
24
Q
what are some examples of iron-dependant enzymes?
A
- peroxidases (catalyse, myeloperosidase, thyroperosidase)
- ribonucleotide reductase
- tyrosine hyroxylase
- monooxygenases
25
3 levels of iron deficiency
1. storage iron depletion
2. early functional iron deficiency
3. iron-deficiency anemia
26
symptoms of iron deficiency
most result from associated anemia (fatigue, tachycardia, arrhythmias, dyspnea on exertion)
other symptoms:
- cold intolerance
- poor concentration, mood disturbances
- angular stomatitis and atrophic glossitis
- alopecia and brittle and spoon shaped nails
27
who is at increased risk of iron deficiency?
```
infants, young children, adolescents
menstruating females
pregnancy
chronic blood loss
parasitic infections
hypochlorhydria
gastric bypass surgery and faster GI transit time
celiac disease
vegetarians, vegans
regular intense exercise
```
28
clinical indications for iron
restless leg syndrome
29
adverse effects of iron supplementation
```
constipation or occasionally diarrhea
dark tarry stools
nausea and vomiting
epigastric pain
generally they are tolerated better when taken in smaller doses divided with food
```
30
who has higher risk of chronic iron toxicity?
hemochromatosis - increased absorption in the intestines caused by a genetic mutation
thalassemia or sideroblastic anemia
alcoholic cirrhosis
31
nutrient interactions of iron
- vitamin C - enhances absorption of non-heme iron
- copper - both hephaestin and ceruloplasmin are copper-dependent enzymes and required to mobilize iron from tissues
- calcium, zinc, copper, manganese - non-heme iron and these divalent minerals compete for a common absorptive pathway
- lead - iron deficiency increases led absorption which inhibits incorporation of iron into heme
32
what oxidation states of copper are found in the body?
Cu1+
| Cu2+
33
sources of copper
```
organ meats
shellfish
whole grains
nuts and seeds
it's in a wide variety of foods
```
34
how is copper released from its organic components during digestion?
HCl and pepsin in the stomach
| proteolytic enzymes in the SI
35
absorption of copper in the body
| - what enzyme is involved
most Cu2+ is reduced to Cu1+ by the enzyme copper reductase
36
what methods are used in copper absorption?
- active carrier mediated transport by CTR1 (copper transporter 1) and DMT1 (divalent mineral transporter) in low concentrations of copper
- nonsaturable passive diffusion in high concentrations of copper
37
factors that enhance copper absorption
```
amino acids (especially histidine and methionine)
organic acids (HCl, citric, lactic, malic, acetic)
low copper status
```
38
factors that inhibit copper absorption
phytates
vitamin C and cystiene
other minerals (zinc, iron, molybdenum, calcium, phosphorous)
hypochlorhydria or excessive use of antacids
39
transport of copper in the body
- enters circulation from enterocytes via transport protein ATP7A
- bound primarily to albumin in hepatic portal circulation
- in liver, binds to ceruloplasmin to be transported to other tissues as needed
40
where is copper stored in the body?
liver, brain, kidneys
| bound to various proteins (thionine, forming metallothionine)
41
function of copper in the body
as a cofactor for various copper-dependent enzymes
| also angiogenesis and production of neutrophils
42
what enzymes use copper as a cofactor?
- feroxidases (ceruloplasmin and hephaestin)
- copper-zinc SOD
- cytochrome C oxidase
- lysys oxidase
- dopamine monoxygenase (aka dopamine beta-hydroxylase)
- tyrosinase
43
when is there increased risk of copper deficiency?
- high supplemental zinc intakes (50mg/day for extended period of time)
- Menkes disease - recessive genetic disorder that results in mutations of the copper transport gene ATP7A
- frequent use of antacids
- infants fed exclusively cow's milk based formula
44
signs and symptoms of copper deficiency
- microcytic, hypochromic anemia not responsive to iron supplementation
- neutropenia and subsequent impaired immune function
- deterioration of the neurological system
- hypopigmentation of skin and hair, kinky hair
45
clinical indications for copper supplementation
only for treating or preventing a copper deficiency
46
which form of copper should not be used as a supplement?
cupric oxide - has shown to be unavailable for absorption through the digestive tract
47
symptoms of copper toxicity
general
acute
chronic toxicity
N & V
constipation
for doses of 2mg or more (supplemental)
acute toxicity (much higher dose needed): abdominal pain, diarrhea, N&V
chronic toxicity: causes liver and kidney damage and eventually death
48
what is Wilson's disease?
a genetic disorder of copper metabolism resulting in defective biliary copper excretion and so copper accumulates in the liver, brain, kidneys, cornea, spleen
49
nutrient interactions of copper
- iron
- zinc
- molybdenum
50
how does copper affect iron levels in the body?
- prolonged copper deficiency can cause secondary/functional iron deficiency anemia
- Fe2+ must be converted into Fe3+ by a copper containing enzyme before it can be used
51
how does zinc affect copper levels in the body?
- high supplemental zinc intake of 50mg/day can lead to a copper deficiency
- zinc stimulates the synthesis of thionine which has higher binding affinity for copper than zinc so causes copper to be trapped in the enterocyte and will cause it to be sloughed off with old intestinal cells so additional copper must be taken when supplementing high doses of zinc for extended periods
52
how does copper interact with molybdenum?
copper forms an insoluble complex with molybdenum in the digestive tract preventing the absorption of either mineral
53
distribution of zinc in the body
zinc is widely distributed - found in all tissues and fluids
54
sources of zinc
shellfish
beef and other red meats
nuts and legumes are relatively good plant sources of zinc
55
bioavailability of zinc in meat vs plant sources
- zinc is more bioavailable in meat, eggs, and seafood because the compounds that inhibit zinc absorption are not present and these are sulfur-containing AAs that improve zinc absorption
- zinc is less bioavailable in plant products because of the high content of phytic acid which inhibits zinc absorption
56
how do maillard reaction products affect zinc absorption?
they decrease zinc absorption
57
digestion of zinc
first needs to be hydrolyzed from AAs and nucleic acids in the stomach and SI by HCl, proteases and nucleases before it can be asbrobed
58
absorption of zinc in the body
how many pathways?
what are they pathways?
3 pathways:
carrier mediated processes are more efficient with low zinc intake:
-1. ZRT and IRT-like proteins 4 (ZIP4)
-2. divalent mineral transporter 1 (DMT1) plays a minor role
when zinc intake is high:
-3. passive paracellular diffusion
59
factors that enhance zinc absorption
organic acids (citric acid, picolinic acid)
low pH
amino acids, glutathione
low zinc status
60
factors that inhibit zinc absorption
phytates
oxalates
polyphenols
folate and other minerals (iron, calcium, magnesium)
61
transport of zinc in the body
- CRIP (cystiene rich intestinal protein) transport zinc within the cytoplasm of a cell
- ZnT1 (zinc transporter 1) transports zinc across the basolateral membrane of the enterocyte
- bound to proteins in the blood like albumin
62
storage of zinc in the body
- what organs?
- storage form?
all organs of the body
- especially the liver, kidneys, muscles, bones, skin
- is usually stored bound to thionein as metothionein which also binds copper
63
main functional roles of zinc in the body?
- catalytic role - zinc used as a cofactor for enzymes
- structural role in the proteins of cell membranes
- regulatory role (gene expression, spermatogenesis in men, immune system function)
64
what is a zinc finger motif?
a finger like structure that stabilizes the structure of several proteins in the body and also regulate gene expression by acting as transcription factors
65
which viruses does zinc possess direct antiviral activity against?
- rhinovirus
| - herpes simplex virus (HSV)
66
symptoms of severe zinc deficiency
- growth retardation and skeletal anomalies
- delayed sexual maturation
- dermatitis, especially around orifices, impaired wound healing
- diarrhea
- impaired immune function
- dysgeusia - impaired sense of taste
- night blindness
- hair loss
- white spots on finger nails
67
who is at risk for severe zinc deficiency?
severe burns
prolonged diarrhea
chronic alcohol abuse
genetic disorder affecting zinc metabolism
68
who is at risk for MILD zinc deficiencies?
premature or low birth weight infants and older breast fed infants and toddlers with inadequate intake of zinc-rich foods
adolescents
pregnant and lactating women
elderly people
inflammatory bowel disease or severe prolonged diarrhea
strict vegetarians
69
clinical indications of zinc supplementation
the common cold
- reducing duration
- free ionized zinc may directly interfere with viral replication processes
70
of the different forms of zinc, which ones are: less bioavailable; not well tolerated; better absorbed; preferred for lozenges/colds
zinc acetate, zinc gluconate, zinc sulfate, zinc oxide, zinc picolinate
less bioavailable: zinc sulfate, zinc oxide
not well tolerated: zinc sulfate
more bioavailable: zinc picolinate - debated
lozenges: zinc acetate and zinc gluconate
71
what is the main consequence of zinc toxicity?
copper deficiency
72
signs and symptoms of acute zinc toxicity
```
metallic taste
headache
N&V
abdominal cramps
bloody diarrhea
```
73
nutrient interactions of zinc
- copper - high zinc intake can lead to copper deficiency
- vitamin A - zinc is required for conversion of retinol to retinal AND deficiency of zinc could result in decrease in mobilization of retinol from liver stores
- calcium, magnesium and iron may decrease zinc absorption and vice versa
74
sources of selenium
meats - especially organ meats and seafood
| selenium content of plants is extremely variable but brazil nuts, whole grains, legumes are good sources
75
bioavailability of selenium
fish contains substantial amounts of selenium but can have low bioavailability due to the mercury content which forms an insoluble complex with selenium
76
location of absorption of selenium
small intestine - mainly duodenum
77
what inhibits selenium absorption
phytates
| heavy metals - especially mercury
78
what are the main forms of selenium that are absorbed in the body?
why?
selenimethionine
selinocystiene
due to its structural similarity to sulfur
79
transport of selenium in the body
bound to proteins to travel in the blood like:
- VLDL
- LDL
- selenoprotein P
80
what organs store selenium in the body?
```
thyroid gland
kidney
liver
heart
pancreas
muscle
```
81
functions of selenium in the body
a cofactor in selenium-dependent enzymes
enhances immune function
may have direct antiviral activity
82
selenium and iodothyronine deiodinases (IDI)
the IDI enzyme converts T4 -> T3 which selenium is required for
ie. selenium maintains normal growth, metabolism, and development because of its role in regulating thyroid hormones
83
selenium and glutathione peroxidase (GPX)
GPX is an important antioxidant enzyme that reduces potentially damaging ROS (like hydrogen peroxide and lipid hydrogen peroxides) to harmless produces like water and alcohols
84
what is the function of selenoprotein P (SEL P)
SEL P functions primarily as a transport protein for selenium
it also acts as an antioxidant that protects endothelial damage by reactive nitrogen species
85
excretion of selenium
- primary
- what regulates homeostasis
- how is it excreted as dimethylselenide?
primarily via urine and feces
homeostasis is maintained by the kidneys
can also be excreted by the lungs as dimethylselenide with high intakes
86
results of selenium deficiency?
- decreased activity of glutathione peroxidases and thyroid deiodinases
- if severe: muscle weakness, muscle wasting, cardiomyopathy
87
selenium deficiency related diseases?
Keshan disease
| Kashin-Beck disease
88
what is Keshan disease?
| what causes it?
a cardiomyopathy that affects young women and children in a selenium-deficient region of China
thought to be caused by oxidative stress (due to selenium deficiency) that causes malignant changes to the Coxackie virus that invades and damages the heart
89
does selenium supplementation help Keshan disease?
prevents/protects people from developing Keshan dsiease but CANNOT reverse heart damage once it occurs
90
what is Kashin-Beck disease?
| what causes it?
degeneration of articular cartilage between joints
| associated with poor selenium status in areas of northern Chia, North Korea, eastern Siberia
91
who is affected by Kashin-Beck diasese?
affects children ages 5-13
| mostly in northern Chia, North Korea, eastern Siberia
92
clinical indications of selenium supplementation
Hashimoto's thyroiditis
| HIV/AIDS
93
is the organic or inorganic form of selenium better absorbed and metabolized by the body?
neither seems to be consistently shown as better than the other
94
what is the difference in absorption between:
selenate
selenite
selenomethionine
- selenate - almost completely absorbed but most of it is excreted before being used
- selenite - about 50% is absorbed but is better retained
- selenomethionine - is 90% absorbed, occurs naturally in foods
95
what is selenosis?
| what are the early warning signs?
selenium toxicity
early warning signs: brittle nails, hair loss, dermatitis
96
symptoms of chronic selenosis
```
hair and nail brittleness and loss
diarrhea, N&V
skin rashes
a garlic breath odor
fatigue, irritability
nervous system abnormalities
```
97
nutrient interactions of selenium
iodine - selenium deficiency can trigger or worsen hypothyroidism in those with severe iodine deficiency
98
sources of chromium
brewer's yeast contains GTF - a biologically active, organically complexed form of chromium
meats, whole grains, green beans, slices like cinnamon, cloves, bay leaves, turmeric
99
absorption of chromium
- location
- mechanism
in small intestine
| through diffusion or a carrier mediated transporter
100
factors that enhance chromium absorption
picolinate
| vitamin C
101
factors that inhibit chromium absorption
phytates
| antacids
102
transport of chromium in the body
bound to transferrin but if transferrin sites are unavailable chromium will bind to albumin for transport in the blood
103
storage sites of chromium in the body
```
kidneys
liver
muscle
spleen
heart
pancreas
bone
```
is thought to be stored along with iron
104
function of chromium in the body and mechanism
potentiates the action of insulin via
- glucose tolerance factor (GTF) which enhances insulin activity
- acts as part of the protein chromodulin which attaches to insulin receptors to enhance their activity
105
symptoms of chromium deficiency
weight loss
impaired glucose tolerance and insulin resistance
peripheral neuropathy
106
who has increased risk of chromium deficiency
regular exercise at high intensity
| insulin resistance, metabolic syndrome, diabetes mellitus
107
clinical indications of chromium supplementation
type 2 diabetes
108
symptoms of chromium toxicity
enhanced dreaming and psychomotor agitation due to high-dose chromium supplementation
109
food sources of iodine
- fish, seafood, kelp, other seaweeds
- dairy products
- meat, eggs, beans
- iodized salt
110
what forms of iodine are absorbed?
free iodine and iodate are absorbed as they are
iodine bound to AAs must first be hydrolyzed to release free iodine (except for thyroid hormones which are absorbed unchanged)
111
what percentage of dietary iodine is absorbed?
100%
112
where is iodine absorbed in the body
stomach and SI
113
transport of iodine in the body
transport freely as iodide in the blood
114
where is iodine stored in the body?
| does it require any special transport system?
70-80% in thyroid gland which requires a Na-dependent active transport system with a Na/I symporter
115
functions of iodine
- essential in the formation of thyroid hormones and thyroid function
- has direct antimicrobial activity
116
iodine excretion
| is there a mechanism to conserve iodide?
excreted freely through the kidneys
| there is NO mechanism in kidneys to conserve idodide
117
who has increased risk of iodine deficiency?
- vegans, vegetarians but not if they regularly consume seaweeds
- infants of mothers who smoke
- exposure to high amounts of goiterogens
118
what are goiterogens?
substances that interfere with iodine metabolism and inhibit thyroid hormone production
119
examples of goiterogens
- halide ions (bromide), thiocyanate, perchlorates
- edible plants have some amounts of thiocyanates ang goiterin (brassica vegetables, soy, millet, cassava)
- perchlorates interfere with organification of iodide required for thyroid hormone synthesis
- polycyclic hydrocarbonds and some phenol compounds interfere with iodine metabolism in the body also
120
how is goiter related to iodine deficiency
thyroid enlargement (goiter) is one of the earliest signs of an iodine deficiency
121
who is most negatively affected by iodine deficiency? why?
it is most damaging to the developing brain
- can cause cretenism: a condition caused by severe congenital hypothyroidism and results in irreversible mental retardation
122
what are the 2 forms of cretenism?
neurological cretenism
| myxedematous cretenism
123
clinical indications of iodine supplementaiton
prevent radiation induced thyroid cancer
| fibrocystic breast changes
124
what are the preparations of iodine available?
- potassium iodide
- Lugol's solution - a combination of molecular iodine and potassium iodide
- kelp and other seaweed extracts - are much less concentrated
125
signs and symptoms of acute iodine toxicity
```
burning of the mouth, throat and stomach
increased salivation and swelling of thyroid glands
metallic taste
N&V, diarrhea
severe headache
```
126
signs and symptoms of chronic iodine toxicity
- in iodine deficiency: can see iodine induced hyperthryoidism in iodine supplementation
- in iodine sufficiency: see hypothyroidism, goiter
127
nutrient interactions of iodine
- selenium deficiency can exacerbate the effects of iodine deficiency
- high doses of vitamin A have been associated with decreased iodine uptake by the thyroid gland
128
sources of manganese
whole grains, legumes, nuts and seeds
leafy green vegetables
tea
