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BIOCHEM B

Minerals MINERAL BIOAVAILABILITY


Dra Alcantara Physiologic need for a particular mineral at the
time of consumption
Definition: Amount of substance that reaches the
4% of total body weight circulation readily available for metabolic
Plays a vital role in the different metabolic processes
processes in the body Bioavailability of the body will depend on the
Inorganic compounds physiologic need of the individual
No carbon structure (need absorption of specific mineral)
No caloric value
Remain as ash when completely burnt Bioavailability will be affected by:
Divided into two:
o Macrominerals Mineral-Mineral Interaction
o Microminerals E.g. VERY HIGH IRON LEVEL

MACROMINERALS/BULK ELEMENTS Transport mechanism of iron: TRANSFERRIN


RDA: 100mg or more ZINC also uses Tranferrin.
IRON: primary mineral that uses transferrin
Cations (+)
Calcium High Fe level Less transferrin that will carry
Magnesium ZINC to other parts of body
Sodium
Potassium Both of these minerals (Fe and Zn) compete with
the same transport system (TRANSFERRIN).
Anions (-)
Chloride Fiber - Mineral Interaction
Sulfate Calcium can be affected by the level of fibers in
Phosphorus the body coming from cereals and plants
E.g.
MICROMINERALS/TRACE ELEMENTS PHYTIC ACID
RDA: <100mg o From plants
o Tries to bind with calcium
Essential Trace Elements
Capable of homeostatic control Phytic acid + Ca = Non-absorption of Calcium
Can be controlled by means of their level in the
body Vitamin-mineral interaction
Whenever it is already of toxicity, the body has Fe can be enhanced in terms of reduction
something to do about all those minerals so that FERROUS STATE: absorbable form of Fe
you will not attain toxicity until a certain level only
Cations (+): Before Ferric can be reduced to Ferrous state, the
o Iron conversion will be enhanced by the presence of
o Zinc VITAMIN C.
o Manganese There will be more IRON absorption in the presence
o Copper of vitamin C.
o Cobalt
o Nickel The specific vitamin that affects calcium is
o Vanadium VITAMIN D.
o Tin
o Molybdenum
o Selenium GENERAL FUNCTIONS
o Chromium Structural
o Silicon o Calcium, Phosphorus: main components
Anions (-): of skeletal system
o Iodine
o Fluoride Acid - base balance
o Cl, P, PO4, K
Non-Essential Trace Elements
Presence of it in the body would already indicate Neuromuscular irritability (excitability)
toxicity o Ca = irritability, excitability
o Lead o Ca = irritability, excitability
o Mercury
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As constituents of hormones
o Iodine: used in the synthesis of T3 & t4 IRON
o Chromium: potentiates activity of insulin
2 IONIC STATES OF IRON:
Co-factor for catalytic activity Ferrous iron (reduced) Fe++
o Chloride: used by Amylase o Absorbable form of Fe
o Zinc: used by Carbonic anhydrase Ferric iron (oxidized) Fe +++
o Copper & Iron: used by Cytochrome o Used for storage and transport
o Binds with Ferritin for storage

CHROMIUM 2 FORMS OF DIETARY IRON


Important component of stainless steels and Heme iron
metal alloys o derived from flesh of animals (MFP)
Cr(III) is an essential dietary nutrient M Meat
F Fish
FUNCTIONS: P Poultry
Carbohydrate metabolism Non-heme
o constituent of the glucose tolerance o iron derived from plants
factor (GTF)

GTF Facilitates reaction of insulin


Will try to potentiate/facilitate the
action of insulin

Thereby, if insulin causes blood sugar to


decrease, Chromium then is also capable of
decreasing the sugar level by means of GTF
(increasing/ potentiating the action of insulin)

That is the reason why chromium is used as an


alternative agent to treat diabetes (together with
zinc). But insulin is still better because you are
already giving the hormone so the effect is
already direct.

If there is no insulin, chromium will have no effect.


You have your heme and non-heme component.
Cholesterol metabolism
o stimulation of synthesis of fatty acids
( LDL and HDL)
o beneficial to those with atherosclerosis
and diabetes
Entering the Cytoplasmic Area:

MOLYBDENUM Heme could readily enter or be absorbed in the brush


can be used as co-factor for different oxidase border or cytoplasmic area by means of HCP1 (Heme
enzymes Carrier Protein 1).
constituent of specific enzymes: (Molybdenum
cofactors) Non-heme has a Ferric iron (Fe3+). The non-heme will give
you the oxidized form of iron (Fe2+). For it to be absorbed,
XANTHINE OXIDASE Ferric needs to be reduced to Ferrous iron.
oxidation of purines and pyrimidines and the
production of uric acid Enzyme responsible: FERRIC REDUCTASE (also
Conversion of: known as Duodenal Cytochrome B or Dcytb).
Hypoxanthine Xanthine Uric acid
ALDEHYDE OXIDASE Ferrous can now be readily absorbed but it needs a
oxidation of aldehydes carrier called Divalent Metal Transporter 1 (DMT 1).
SULFITE OXIDASE
involved in the metabolism of sulfur amino acids
oxidation of amino acids containing the sulphur Heme Carrier: HCP1
group (Cysteine, Methionine) Non-heme Carrier: DMT1

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Inside intestinal mucosa:

You have now here your ferrous and heme.

HO-1 (Heme Oxygenase 1): Enzyme responsible to


release the ferrous component of heme.

Ferrous needs to be oxidized again to Ferric because it is


ferric that binds with FERRITIN for storage.

Those that remained to be ferrous will go to the


circulation.

Into the circulation:

These (ferrous) will be carried from the intestinal mucosa


to the circulation by FPN (Ferroportin). Q: If there is too much Fe in the blood, do I still need
transferrin to function (distribute the other Fe to
If ever Fe is not needed in the circulation because there is the different parts of the body)?
adequate amount already, FPN will be down-regulated
by HEPCIDIN. A: NOT ANYMORE.
Fe level Transferrin activity
Ferroportin: carrier
Hepcidin: down regulator of FPN Too much Fe level, there will be stimulation of hepcidin
Hepcidin down regulates Ferroportin (-) Ferroportin (-
) Fe will go into the blood because Ferroportin is the
carrier.
Circulation:
Hepcidin Ferroportin Fe level
There is now ferrous in the circulation. Ferrous needs to be
oxidized again into Ferric because it is Ferric that binds
with TRANSFERRIN. Q: During inflammatory conditions, you have seen a
patient looking pale. There are no bleeding
HEPHAESTIN (Hp) tendencies or trauma but the Hgb is low. Why?
Enhances the conversion of Ferrous to Ferric A: Fe is needed for heme synthesis
Contains the enzyme FERROUS OXIDASE There is pallor because there is inflammation
Could only function in the presence of Copper within the body. Inflammation stimulates
Is copper dependent Hepcidin High hepcidin decreased
ferroportin decreased iron
Summary of the CHONs working in the transport of Fe:
1. HCP1 Q: What if there is increased RBC synthesis?
2. DMT1 A: RBC synthesis inhibit Hepcidin Ferroportin
3. Ferric Reductase/Dcytb (enhanced by Vit C) availabilty of Fe
4. Heme Oxygenase (HO-1)
5. Ferritin
6. Ferroportin (FPN) FACTORS THAT ENHANCE NON-HEME ABSORPTION
7. Hepcidin Conversion of Fe3+ Fe2+
8. Hephaestin Activity of Ferric Reductase
9. Transferrin (transports Fe into the circulation)
1. MFP factor
HEPCIDIN o factor that promotes the absorption of
master regulator of iron homeostasis non-heme iron from other foods eaten at
Down-regulates ferroportin same meal
Encoded by HAMP gene 2. Ascorbic acid
Composed of 25 amino acids 3. Citric acid and lactic acid from foods
hemojuvelin 4. Hydrochloric acid in the stomach
o This is the reason why Fe should be taken
on an EMPTY STOMACH so that
hydrochloric acid will be high then there
will be better absorption of Fe.
5. Sugars

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FACTORS THAT INHIBIT IRON ABSORPTION 2 ways to regulate:
Inhibit conversion of Fe3+ Fe2+ 1. Regulate its entry into the plasma membrane
2. Regulate its entry and exit into Zincosomes
1. Phytates and fibers (grains and vegetables)
2. Oxalates (spinach) 2 Zinc Transporters:
3. Calcium and phosphorus (milk) 1. ZnT (Zinc Transporter)
4. EDTA (food additives) 2. ZIP (Zinc Protein)
5. Tannic acid (in tea and coffee)
PLASMA MEMBRANE
ZIP carries Zn IN to plasma membrane
ZINC ZnT carries Zn OUT of the plasma membrane

FUNCTIONS ZINCOSOMES
It is absolutely required for normal ZnT going IN to the zincosomes
spermatogenenesis, fetal growth, and embryonic ZIP going OUT of the zincosomes
development (Zn Dwarfism)
Prevents prostatic CA (males) METALLOTHIONEIN
Boost immune system (stimulates leukocytes) Binding CHON for ZN and Cu
Boost brain activity (adds a little intelligence; a special binding protein that regulates the
because intelligence is more of genetics) amount of zinc that is released in the blood
Synthesis and action of insulin (like Chromium)
Stabilizes membrane structure by preventing lipid
peroxidation and reducing free radical formation If body does NOT
If body NEEDS zinc
(ANTIOXIDANT) need zinc
Component of GUSTIN, a salivary protein that has
an ability to increase appetite
Zinc and PMS (Zn PMS)
Involved in the synthesis and stabilization of Zinc is incorporated Zinc is incorporated
into intestinal into intestinal
proteins, DNA and RNA and plays a structural role metallothionein metallothionein
in ribosomes and membranes.
Necessary for the binding of steroid hormone
receptors and several other transcription factors
to DNA (steroid synthesis) Zinc SLOUGHED OFF Zinc is transported
As Co-factors of enzymes: with intestinal cells into BLOOD STREAM
o PT
Peptidases
Thymidine Kinase PROSTATE GLAND:
o CLAS
Carbonic Anhydrase
Lactate DH
Alkaline Phosphate
Superoxide Dismutase

ZINC HOMEOSTASIS

Zn will apoptosis in 2 weeks by 2 ways.


Zn will try to stimulate BAX GENE as well as
activate CYTOCHROME C (stars in the photo above)
Release of Cytochrome C will stimulate CASPACE
CASCADE.
Caspace cascade promotes APOPTOSIS
Zn could enter into the plasma membrane or into the
Apoptosis death of cell no chance for that
zinncosomes.
cell to proliferate

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Thereby, if you have prostate CA and a Zn that will
promote apoptosis, then there will be aa lesser chance 6. Blood clotting
for this prostate to increase in size. o Especially Factor VII
7. ANS function
ZINC DEFICIENCY o TYROSINE HYDROXYLASE
Severe growth retardation - Dwarfism
Arrested sexual maturation TRANSPORT
Hinders digestion and absorption leading to
diarrhea because (-) regeneration of mucosa

Q: Can Zn be given to patients with diarrhea?


A: YES, because this will treat the mucosa to
regenerate faster.

Impaired immune system


Poor motor development and cognitive
performance
Impaired sense of taste (GUSTIN)

ZINC INTERACTION WITH IRON


Zn level will be dependent on the Fe level
because Zn and Fe competes with transferrin
Some plasma zinc binds to transferrin
If there is too high zinc intake, there is no more
transferrin to bind with iron, hence, impairs its
absorption.
hCTR1 (Human Copper Transporter 1)
ZINC INTERACTION WITH COPPER carrier of Cu into cell membrane
Zn will also be dependent on the level of Cu
Copper and zinc compete for binding with From the plasma membrane, Cu will then be taken in by:
metallothionein COX17 to the mitochondria
Metallothionein binds strongly with copper ATOX1 to trans-Golgi network
CCS to Copper-Zinc-Super Oxide Dismutase
2 MINERALS THAT AFFECTS THE LEVEL OF ZINC: (CuZnSOD)
o Iron As part of Glutathione component to be linked to
o Copper the transporter Metallothionein

COPPER In the trans-Golgi network, the ATP-7B GENE has 2


functions:
Antioxidant
1. Could give again the Cu and transport it out into
highest concentrations are in the liver, brain,
the biliary circulation (excretion)
kidneys, heart and skeletal muscle
2. Bind the Cu to become Holo-ceruloplasmin so
90% bound as CERULOPLASMIN
that Cu can go outside the membrane and be
transported to other tissues mainly by ALBUMIN
part of the circulation
found in enzymes (co-factor)
COPPER DEFICIENCY
FUNCTIONS [COPPER-DEPENDENT ENZYMES]
Copper is widely distributed in foods so a
1. Iron utilization
deficiency is not common but may occur in
o oxidation of iron
premature infants or in malnourished patients
o FERROUS OXIDASE
repleted with low copper diet
2. Antioxidant
MENKES DISEASE
o removal of superoxide radicals
o kinky or steely hair syndrome
o SUPEROXIDE DISMUTASE
o Copper binding P- type ATPase(Efflux)
3. Development of bone and connective tissues
o X- linked, male infants
o synthesis of collagen and elastin
o Nervous system, vessels, connective
o LYSYL OXIDASE
tissue
4. Melanin production
o MR, DEC Cu, dec CP
o converts tyrosine to melanin
o TYROSINASE
COPPER TOXICITY
5. Energy metabolism
Defective ATP78 gene
o ETC/formation of ATP
Acute Toxicity
o CYTOCHROME ENZYME
o ingestion of >15 mg elemental Cu
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o Causes 7. SECRETION OF T3 AND T3
N&V o Recycled; or
Diarrhea o T3 and T4 will be released into the
Abdominal cramps circulation
Chronic Toxicity (WILSONS DISEASE)
o Rare inherited disease SUMMARY OF EFFECTS OF IODINE
o Free tissue copper & total liver copper Iodine Heat production O2
are increased consumption metabolic rate
o Excess Cu is stored in the liver, brain & Thyroid Hormone Food Utilization
cornea of the eye Appetite, but HIGH BMR Thin figure
o PENICILLAMINE BMR needed ATP (to provide energy to
such metabolic processes)
ANTIOXIDANTS In order to produce HIGHER ATP size and
number of mitochondria Higher ATP
Enzymatic Antioxidants
SUPEROXIDE DISMUTASE CHO: Glycolysis (due to need for ATP)
o metalloCHON containing Cu, Zn, Se, Mn Rapid uptake of glucose by cells
CHON: CHON synthesis
Types of superoxide dismutases in humans: FATS: Lipogenesis < Lipolysis
Copper, Zinc VIT: Convert Carotene Vit. A
o Cytosol
o Mitochondrial intermembrane space HYPERTHYROIDISM Lahat mabilis
o Extracellular space HYPOTHYROIDISM mabagal
Manganese
o Mitochondrial matrix IODINE DEFICIENCY OR GOITROGENIC FOODS
Selenium Cassava, corn, bamboo-shoots, sweet potatoes,
o Part of glutathione component Turnips, cabbage, garlic and onions
o Higher tendency of IODINE deficiency
because all of these will try to inhibit
IODINE iodide trapping (1st step); therefore, T3
and T4 are not produced
T3-T4 METABOLISM
1. IODIDE TRAPPING
o Is Na-K ATPase dependent CALCIUM
o Without Na, Iodide cannot enter Most abundant mineral in the body
cytoplasmic area 1.5 to 2% of body weight
Main structural component of bones and teeth
2. OXIDATION 99%: OH apatite [Ca10(PO4)6(OH2)]form
o Hydrogen peroxide (oxidizing agent 1% - in extracellular fluids (ionized form)
used) is produced by a NADPH-
dependent enzyme 3 ORGANS INVOLVED IN CALCIUM HOMEOSTASIS
o PEROXIDASE: Enzyme used for oxidation
of iodine

IODIDE PEROXIDASE IODINE

3. ORGANIFICATION
o Iodine will bind to tyrosine
o Aka IODINIFICATION

TYROSINE + IODINE IODOTYROSINE


Enzyme: IODINASE

4. COUPLING MECHANISM
o MIT (MONOiodotyrosine) 1
o DIT (DIiodotyrosine) - 2

MIT + DIT T3
DIT + DIT T4

5. PROTEOLYSIS
6. DEIODINATION

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Zinc absorption can be decreased by which of the following:
A. Iron content of the body
Ca DEPOSITION(bones) B. Magnesium
Ca uptake (intestines) DECREASE C. Both A and B
CALCITONIN
Ca reabsorption from overall Ca D. None of these
urine
True of Iron
A. Increase iron level increases Transferrin
B. DCYTB has a ferrous reductase activity
C. Increase hepcidin level increases iron absorption
D. A and C
Ca RELEASE (bones) INCREASE E. A and B
PTH Ca uptake (intestines) overall
Ca reabsorption from urine Ca Minerals serve as co-factor in different enzymes. Which of the
following is correctly paired?
A. Molybdenum Xanthine Oxidase
B. Copper Carbonic Anhydrase
ABSORPTION OF CALCIUM C. Zinc Amylase
INCREASE DECREASE D. Chloride Superoxide Dismutase
Body need Binders:
Oxalic acid in beets, rhubarb, Zinc level in the prostate gland is said to be preventive of
Healthy adults: 10-40% dietary spinach prostate cancer. Which of the statements below describe/s such
calcium principle:
Phytates in seeds, nuts A. Zinc stimulates expression of BAX gene that increases
Growing children, pregnant caspase cascade activity
and lactating mothers >40% B. Zinc decreases cytochrome C release to increase
Lactose Excess PO4 apoptosis
C. A/B
Vitamin D Induces the synthesis Vitamin D deficiency
D. None of the above
of calbindin
Gastric acidity Lack of gastric acid
Copper can be distributed in its subcellular location in the body
PTH Calcitonin
thru copper chaperons. Which of the following then is/are
Amino acids: Lack of exercise correctly paired?
Lysine/Arginine/Serine Dietary fat A. COX 17 Mitochondria
High fiber intake and laxatives B. ATOX 1 ZnCuSOD
C. CCS trans golgi apparatus
SELENIUM D. A/B
E. All of the above

FUNCTIONS Calcium level can be controlled by hormonal regulation. Which


Selenium is an essential component of the bodys of the following is/are true then regarding this/these hormones?
antioxidant defense system. A. Vitamin D increases intestinal and renal absorption of
Part of the enzyme Glutathione peroxidase, calcium
B. Calcitonin increases delivery of calcium in the bones
which catalyzes the breakdown of toxic
C. A/B
hydroperoxides. D. None of the above
Component of the enzyme that converts T4 to T3
(Iodothyronine Deiodinase) Ca could directly activate which of the following enzymes:
A. Lipase
Vitamins that Convert T3 T4: Selenium & Iodine B. Adenosine triphosphatase
4 ANTIOXIDANT Minerals: Cu, ZN, Mn, Se C. Glycogen synthase
D. A and B

Absorption of iron is regulated by:


SAMPLE QUESTIONS: A. Ferroportin
B. Hepcidin
Copper plays as an integral part of which of the following C. Level of Transferrin
enzymes: D. A and C
A. Cytochrome-C oxidase E. All
B. Ferrous oxidase
C. A and B This is the function of chromium
D. None of the above A. Forms bone and teeth
B. Bone metabolism and enzyme reaction
Calcium absorption is increased by: C. Utilization of glucose
A. Phytic acid
B. Gastric acid
C. Oxalic
D. ALL

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