1 TERM

BIOCHEMISTRY NU
LECTURE \ MR. GALVEZ 03 01
TRANS UNIT 7.2: REGULATORY PROTEINS

OUTLINE
ACID-BASE BALANCE
I) Acid-Base Balance • Acid – a substance that can donate hydrogen ions
A) Types of Acid o Lower pH = below 7
B) How the Body Proceeds to Acidic Condition • Base – substance that can accept hydrogen ions
i) CO2 Excretion and Production • Higher pH
ii) Kidneys Excretory Function
C) Fixed Acids
D) Clinical pH Range TYPES OF ACID
II) Plasma Bicarbonate Concentration • Mostly dictate the pH level in our body
A) Bicarbonate Buffer System • Carbonic Acid
B) Determining pH o Volatile Acid - readily change composition
i) pH vs. [H+] o Carbon Dioxide - released to make body less acidic
ii) Normal Values
III) Metabolic Disorders
o Note: Carbonic acids has 15000 mmol/d and is
IV) Respiratory Disorders eliminated by the lungs
V) Buffering • Non-carbonic acids
A) Effects of Buffers on pH o Nonvolatile acids such as phosphoric and sulfuric
VI) Purpose of Acid-Base Balance acids, 50-100 meq/d).
A) Compensatory Mechanisms o Present to the body but in minimal accounts only
B) Summary o Byproducts of processes in the body
C) Simple Acid-Base Disorders
VII) Disorders
• Combine with buffers and subsequently excreted by the
A) Metabolic Acidosis kidneys
i) Causes o Buffers – prevent drastic changes in pH
B) Respiratory Acidosis o Cushion changes in pH
C) Respiratory Alkalosis
D) Metabolic Alkalosis HOW THE BODY PROCEEDS TO ACIDIC CONDITION
i) Causes
E) Expected Changes for Respiratory Disorders
• CO2 production
VIII) Renal Acid Excretion o 13,000-20,000 Millimoles/day
IX) Titratable Acidity o If not released from the body, can cause acidosis
X) Ammonium Excretion (acidic blood = ph 6.5)
XI) Sodium-Chloride Relationship
XII) Mixed Acid-Base Disorder
XIII) Mineral Balance
A) Fluid and Electrolyte Balance
B) Regulation of Fluid and Electrolyte Balance
C) Regulation of Blood Pressure
XIV) Electrolytes
A) Sodium
B) Chloride
C) Potassium
D) Calcium
i) Blood Calcium Regulation
ii) Effects of Chronically Low Calcium Intake
iii) Factors That Enhance Calcium Absorption
E) Phosphorus • Kidneys Excretory Function
F) Magnesium o If not excreted by the lungs or liver, it will be excreted
G) Sulfur
XV) Trace Minerals
by the kidneys
A) Iron o Other acids will be excreted in kidneys
i) Iron Toxicity
B) Zinc
C) Iodine
D) Selenium
E) Copper
F) Manganese
G) Chromium
H) Molybdenum

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 TRANS UNIT 7.2: REGULATORY PROTEINS

FIXED ACIDS pH vs. [H+]

• H2SO4 [H+] = 80-decimal digit of pH
o Helps with degradation of proteins
• H3PO4
o Helps with degradation of phospholipids

CLINICAL PH RANGE
• pH between 7.80 and 6.80 (H+ concentrations between 16
-160 meq/l) are the extremes of pH compatible with life
• Clinical laboratories measured pH, carbon dioxide, and
oxygen in arterial samples.
• Bicarbonate concentration can be calculated from the
Henderson equation.
• Laboratories measure total CO2 concentration (dissolved
CO2 plus bicarbonate concentration, ~25-26 meq/l) in
venous samples
• Note: remember the equation namely Henderson–
Hasselbalch equation (no need to memorize)

PLASMA BICARBONATE CONCENTRATION

• Measured by the amount of carbon dioxide present, partial
pressure of CO2
• Laboratories measure total CO2 concentration (dissolved
carbon dioxide plus bicarbonate concentration, ~25-26
meq/l)
• As a result, total CO2 concentration exceeds plasma NORMAL VALUES
bicarbonate concentration by 1.0 to 1.5 meq/l Normal pH – 7.35-7.45 (7.40)
• Normal plasma bicarbonate concentration is approximately – pH = -log[H+]
24 mEq/l – [H+] = 24 x pCO2/[HCO3-]
Normal pCO2 36-44 mm Hg (40 mmHg)
CONDITIONS/PROCESS Normal HCO3- 22-26 meq/L (24 meq/L)
Acidemia Reduced pH (elevated hydrogen ion
concentration) METABOLIC DISORDERS
• Processes that modify bicarbonate concentration directly
Alkalemia Increased pH (reduced hydrogen ions o Bicarbonate deficiency is a symptom of metabolic
concentration) acidosis.
Acidosis The process that lowers pH o Metabolic alkalosis: increased bicarbonate
Alkalosis The process that increases pH
RESPIRATORY DISORDERS
BICARBONATE BUFFER SYSTEM • Processes that directly alter CO2
CO2 + H20 H2CO3 → H+ + HCO3 - • Respiratory acidosis – increased CO2
• If a closed system, pKa = 6.1 (normal pH= 7.40) o Asthma, COPD, Fibrosis, muscle disorders, medicines
• We are an open system, with CO2 being excreted through that suppressed breathing
the lungs, making this a highly efficient buffer. o Bronchodilator – vasoconstrictor
o Narcotics and alcohol
DETERMINING PH o Severe obesity
• The concentration of the hydronium ion in moles per liter is • Respiratory alkalosis – decreased CO2
required to calculate the pH of an aqueous solution o Asthma, hyperventilation (respiratory rate is high),
(molarity). COPD
o After that, using the expression, the pH is computed. • Buffer Effect – slightly increased HCO3 with respiratory
alkalosis
o Prevent from going into alkalosis or acidosis

BUFFERING
• Prevent wide changes in pH in response to the addition of
base or acid
• Bicarbonate is the major extracellular buffer (can be easily
measured)
• There are also intracellular buffers (electrolytes)

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 TRANS UNIT 7.2: REGULATORY PROTEINS

EFFECTS OF BUFFERS ON PH SUMMARY

• The presence of buffers attenuates changes in pH in Disorder pH HCO3 - pCO2 Comment
response to acid-base disorders. Metabolic ↓ ↓ primary ↓ All 3
acidosis Compensatory markers
• Immediate onset
• Isohydric principle (all buffers change in the same direction) go in
same
PURPOSE OF ACID-BASE BALANCE direction
• Because enzyme action is pH dependent, maintaining an Metabolic  ↑ primary ↑ All 3
alkalosis ↑ Compensatory markers
acid–base balance is critical for the regular functioning of
biological systems. go in
• This page discusses acid–base balance definitions as well same
as the normal physiology of acid–base metabolism in the direction
extracellular fluid and blood. Resp. ↓ ↑  ↑ primary pH goes
acidosis Compensatory opp. Other
2 markers
BUFFER PAIR BUFFER PAIR H+ DONOR Resp.  ↓ ↓ primary pH goes
alkalosis ↑ Compensatory opp. Other
Bicarbonate HCO₃- H₂CO₃ 2 markers
(ECFV)
GOLDEN RULES: SIMPLE-ACID BASE DISORDERS
Phosphate (Urine) H₂PO₄²- H₂PO₄ 1 • PCO2 and HCO3 always change in the same
direction.
Ammonia (Urine) NH₃ NH₄+ o They are related to one another
2 • The secondary physiologic compensatory
Protein Protein Protein mechanisms must be present.
o When you say secondary physiologic
COMPENSATORY MECHANISMS compensatory mechanism this is the other
homeostatic balance or checkpoints within
• In addition to buffering mechanisms, additional secondary
your body for example the blood, food, and
(compensatory) physiologic responses occur in response to
nutrients.
changes in pH.
3 • The compensatory mechanisms never fully
• Invariably present in simple acid-base disorders (if not
present, it is a mixed disorder) correct pH.
o It's always your body which will be correcting it
• The respiratory system compensates for metabolic
naturally.
disorders by altering CO2 (via the lungs, rapid onset,
o Your compensatory mechanism will only be for
minutes)
us for initial responses, it is more like a first aid
o The respiratory system compensates for metabolic
but it is not a total cure.
disorders by altering the carbon dioxide or its either by
o Your body will always go in its natural state
hyperventilation.
because that is homeostasis that will make
o So if you need a lot of carbs you need an exchange of
your body balanced.
the gases within your body it will be signaling your body
so that it could increase the amount of the exchange of
carbon dioxide or if ever hyperventilation is not possible DISORDERS
what happens is that you could deep breaths
• Compensation for respiratory disorders occurs by METABOLIC ACIDOSIS
alterations in bicarbonate concentration (via the kidney, • Process the reduces plasma bicarbonate concentration
slower onset 1-2days) • Etiology:
Buffer systems Extracellular Immediate
o Decreased renal acid excretion
(primarily fluid (HCO - + H+ ↔ H₂CO
3
o Direct bicarbonate losses (GI tract or urine)
bicarbonate) ↔CO + H₂O )
2
o Increased acid generation (exogenous or endogenous)
Increased rate Lungs Minutes to hours
and depth of CAUSES OF METABOLIC ACIDOSIS
breathing to 1 • Increased Acid Generation
decrease CO o Lactic acidosis
Buffer systems Intracellular 2-4 hours o Ketoacidosis
(phosphate, fluid o Ingestion of acids (aspirin, ethylene glycol,
bicarbonate, methanol)
protein) o Dietary protein intake (animal source)
Hydrogen ion Kidneys Hours to days 2 • Loss of Bicarbonate
excretion, bicarb o Gastrointestinal (diarrhea, intestinal fistulas)
reabsorption, & o Renal: type 2 proximal renal tubular acidosis
bicarb 3 • Decreased acid excretion (impaired NH4+
generation excretion)

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 TRANS UNIT 7.2: REGULATORY PROTEINS

o Renal failure (reduced GFR) EXPECTED PH CHANGES IN RESPIRATORY

o Decreased ammonium excretion DISORDERS
o Type I (distal) renal tubular acidosis
o Type 4 renal tubular acidosis Acute • A condition in which carbon dioxide
(hypoaldosteronism) respiratory builds up very quickly, before the kidneys
acidosis can return the body to a state of balance.
RESPIRATORY ACIDOSIS o HCO3- increases 1 meq for each 10
• Induced by hypercapnia (decreased alveolar ventilation). mm increase in pCO2
o Buildup of CO2 in the bloodstream Chronic • The PaCO2 is elevated above the upper
• Buffering mechanisms raise plasma bicarbonate Respiratory limit of the reference range, with a normal
concentration. Acidosis or near-normal pH secondary to renal
• Kidney minimizes the change in extracellular pH by compensation and an elevated serum
increasing acid excretion generating new bicarbonate bicarbonate levels (i.e., >30 mEq/L).
ions. o HCO3 increases 4 mEq for each 10
mm increases in PCO2
RESPIRATORY ALKALOSIS Acute • The PaCO2 is below the lower limit of
• Reduced carbon dioxide due to increased alveolar Respiratory normal and the serum pH is alkemic.
ventilation. Alkalosis o HCO3 decreases 2 mEq for each 10
• Buffering processes lower plasma bicarbonate mm decrease in PCO2
concentration. Chronic • A common acid base disturbance
• Kidney response is to reduce net acid excretion (eliminate Respiratory characterized by a primary and sustained
bicarbonate into the urine or decrease ammonium Alkalosis decrease in arterial carbon dioxide
excretion). tension (PaCO2).
• The PaCO2 is below the lower limit of
NOTE: RESPIRATORY DISORDERS normal, but the pH level is relatively
• Acute respiratory acid-base disorders always have a normal or near normal due to
greater change in pH than chronic disorders compensatory mechanisms.
• Plasma Cl changes equally and inversely with plasma o HCO3 decreases 5 mEq for each 10
HCO3. mm decrease in PCO2
• The plasma anion gap does not change with respiratory •
disorders.
• Plasma sodium is not directly altered by acid-base RENAL ACID EXCRETION
disorders. • All of the filter of bicarbonate must be reabsorbed (primarily
in the proximal tubule and loop of Henle)
METABOLIC ALKALOSIS • Final excretion of the daily acid load occurs primarily in the
• Raise plasma bicarbonate concentration. collecting duct (approximately 50-100 meq/d)
• ORIGIN/CAUSES: Vomiting and Diuretic Therapy
• Excessive urinary net acid excretion (primary TITRABLE ACIDITY
hyperaldosteronism). • Phosphate homeostasis is maintained by urinary excretion
of dietary phosphate
CAUSES OF METABOLIC ALKALOSIS • Monobasic phosphate is an effective urinary buffer,
HYDROGEN LOSS especially at lower urinary pH
1 • Gastrointestinal loss • Accounts for excretion of 10 to 40 mEq of hydrogen ion daily
o Removal of gastric secretions • Cannot be increased beyond this due to the fixed amount
o Due to vomiting or nasogastric suction of phosphate in urine
2 • Urinary loss
o Loop or thiazide-type diuretics AMMONIUM EXCRETION
o Hyperaldosteronism • Contributes the major adaptive response to an acid load
o Posthypercapnic alkalosis • Can be increased in response to physiologic needs
3 • Movement into the cells • Normally 30-40 mEq/d and maximal excretion is
o Hypokalemia approximately 300 mEq/d
• Administration of bicarbonate or an organic ion that can • NH4+ is lipid soluble and therefore trapped in the urinary
be metabolized to bicarbonate, such as citrate in blood lumen
transfusions. • An indirect estimate of Urinary NH4+ excretion
CONTRACTION ALKALOSIS • Urine Na+ K+ minus urine Cl
1 • Loop or thiazide-type diuretics in edematous • Normally ~ 10 meq/ and becomes less positive and even
patients. become negative with increase urinary NH4 excretion (Cl-
must accompany NH4+)
• URINE CHLORIDE CONCENTRATION:
o Cl responsive: urine Cl <20 meq/l (usually <10 meq/l)
o Cl resistant: urine Cl > 20 meq/l (usually >50 meq/l)

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 TRANS UNIT 7.2: REGULATORY PROTEINS
SODIUM CHLORIDE RELATIONSHIP
• Law of Electroneutrality:
o Sodium concentration is not directly altered by acid
base disorders
o Plasma Cl is altered in all acid base disorders (except
increased plasma anion gap metabolic acidosis)
• Conclusion: If sodium concentration stays constant but
chloride concentration changes, an acid base disorder is
present
MIXED-ACID DISORDER
• Defined as the presence of just one of the foregoing
derangements.
• More than one disorder may be present at the same time in
a mixed disorder.
• A mixed disorder may include an acidosis and alkalosis that
partly counterbalance each other, or two separate
conditions impacting the pH in the same direction.
Respiratory • Occurs when the lungs are unable to
acidosis eliminate all of the carbon dioxide
produced by the body.
• the bodily fluids, particularly the blood,
become overly acidic as a result of this.
Metabolic • Is a condition in which the body's fluids
acidosis contain too much acid.
Respiratory • Characterized by a primary reduction in
alkalosis carbon dioxide partial pressure (PCO2),
which may or may not be accompanied
by a compensatory decrease in
bicarbonate (HCO3)
o pH may be high or near normal.
• An increase in respiratory rate or volume
(hyperventilation) or both may be the
cause.
• Acute or chronic respiratory alkalosis
may occur.
Metabolic • A condition in which the blood becomes
alkalosis too alkaline.
• The polar opposite of alkaline is acidic.
• When the acid-alkaline balance in our
blood is slightly tilted toward the alkaline,
our bodies function optimally.
MINERAL BALANCE
DISSOCIATION OF SALT IN WATER
• Positively or negatively charged ions that help your body
regulate fluid balance.
• Three important electrolytes that carry out this function
are:
o Sodium
o Potassium
o Chloride
BONE GROWTH AND MAINTENANCE
• Normal bone development requires vitamins D, C, and
A, as well as minerals like calcium, phosphorus, and
magnesium.
• Hormones such as parathyroid hormone, growth
hormone, and calcitonin are also important for bone
growth and maintenance.
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TRACE MINERALS
• Iron, zinc, iodine, selenium, copper, chromium,
manganese, fluoride, chromium, and molybdenum.
FLUID AND ELECTROLYTE BALANCE
• Dissociation of salt in water results to the electrolyte
solution.
o This is because as salt dissolves, the dissociated ions
in the solution are free to move around, allowing a
charge to flow freely.
o The resulting solution will conduct electricity since it
contains ions.
• Ions – any atom or group of atoms that has one or more
positive or negative electrical charges
o Cations – ions with positive charge
o Anions – ions with negative charge
• Positive & negative charges balance inside and outside
of the cell
o A neuron is negatively charged while it is at rest: the
inside of the cell is about 70 millivolts more negative
than the outside
o It has a positive charge because it is missing one
electron.
• Count charges in milliequivalents
o The expression mEq represents the amount of solute
in mg equal to 1/1000 the gram of the equivalent weight
of the substance.
o Equivalent weight = 147/2 = 73.5 grams and 73.5
grams/1000 = 0.0735 grams or 73.5 mgs.
• Dissociation of water
o At 25 °C, water molecules break into equal amounts of
H3O+ and OH, resulting in concentrations of 1.00107
mol dm3.
o A neutral solution is defined as one in which the
concentrations of H3O+ and OH are equal.
o The pH of the neutral point is usually calculated to be
12pKw.
• Electrolytes attract water
o Your body maintains its fluid balance through the action
of substances called electrolytes, which are mineral
compounds that, when dissolved in water, become
electrically charged particles called ions.
• Water follows electrolytes
o In this case, electrolytes come into play. The cell (or,
more precisely, the numerous sodium-potassium
pumps in its membrane) continually pumps sodium
ions out to form a chemical gradient.
o The sodium-potassium pump restores equilibrium by
reintroducing sodium into the extracellular fluid,
followed by water.
• Osmosis is when water moves across a membrane
toward more concentrated solutes (proteins regulate
flow)
o When a semipermeable membrane divides two fluid
spaces, water will flow from one with a lower solute
concentration to the other with a greater solute
concentration to reach equilibrium and balance the
osmotic pressures.
 TRANS UNIT 7.2: REGULATORY PROTEINS

REGULATION OF FLUID AND ELECTROLYTE o Creates much of the osmotic pressure of ECF; the
BALANCE most abundant cation in ECF
• Mineral concentrations and variations in the body must be o Essential for electrical activity of neurons and muscle
consistent cells.
• Regulation occurs in the GI tract and kidneys • Salt in diet
• Liver recycles 8 liters of fluids/minerals per day o 2400 mg per day
• The adrenal glands are responsible for regulating the o High sodium intake lead to high blood pressure
kidneys, potassium, and sodium o Will adapt to a low-sodium diet

REGULATION OF BLOOD PRESSURE CHLORIDE

• 750mg/day
MECHANISMS • Functions
1 Blood pressure drops = renin is excreted o Major anion of extracellular
• The renin-angiotensin-aldosterone system is a o Part of HCI in gastric juice
fundamental regulator of arterial blood pressure, with o Most abundant anion in ECF, diffuses easily into and
activation of the cascade boosting blood pressure out of cells, helps regulate osmotic pressure.
and suppression reducing it. • Toxicity
2 Blood pressure drops = kidney reabsorbs sodium o Vomiting – acts on goblet cells
• Aldosterone helps the kidney to reabsorb more salt
and water into the bloodstream, increasing blood POTASSIUM (K+)
volume and restoring salt levels and blood pressure. • 2000mg/day
3 Angiotensin excreted = vasoconstrictor • Functions
• Angiotensin also promotes salt retention by the o Intracellular cation
kidneys by stimulating the production of aldosterone o Creates much of the osmotic pressure in ICF; the most
from the adrenal cortex. abundant cations in ICF
• It's a part of the blood pressure-controlling renin- o Essential for electrical activity of neurons and muscle
angiotensin system. cells
4 Aldosterone and sodium retention = retain more • Deficiency
sodium and water o Paralysis, muscular weakness
• Aldosterone helps the kidney to reabsorb more salt • Toxicity
and water into the bloodstream, increasing blood o Vomiting, heart, muscular weakness
volume and restoring salt levels and blood pressure.
5 High sodium diets aggravate hypertension through CALCIUM (Ca2+)
water retention (interstitial space) • 1000-1200 mg /day
• When you consume too much sodium-containing • Functions
salt, your body stores more water to "flush" the salt o Most (98%) is found in bones and teeth
out of your system. This may cause blood pressure o Maintains normal excitability of neurons and muscle
to rise in certain persons. The extra water puts your cells
heart and blood arteries under strain. o Essential for blood clotting
o Nerve function
ELECTROLYTES • Food source
• Cations (positively charged ions) o Fish w/ bones, dark green vegetables, fortified foods
o Calcium (Ca2+)
o Extracellular BLOOD CALCIUM REGULATION
§ Sodium (Na+) • Calcitonin
o Intracellular • Lower Blood Calcium
§ Potassium (K+) and Magnesium (Mg2+) o Decrease calcitriol and parathyroid hormone
• Anions (negatively charged ions) • Parathyroid Hormone
o Extracellular o Increase calcium absorption via increased calcitriol
§ Chloride (Cl− ) o Increase calcium release from bone
o Intracellular o Increase blood calcium
§ Phosphate (HPO42−) o Retain calcium from excretion
o Bicarbonate (HCO3−) EFFECTS OF CHRONICALLY LOW CALCIUM INTAKE
o Sulfate (SO42−) • Deficiency
o Stunted growth, osteoporosis
SODIUM (Na+) • Increase in Blood Parathyroid Hormone
• Minimum requirement: 500mg/day Concentration
• Rare deficiency o Persistent
o Muscle cramps, mental apathy o Increase in Bone Resorption, hence bone turnover
• Toxicity • Reduction in Bone Mineral Content (BMC) and
o Acute hypertension, edema Density (BMD)
• Chief functions = extracellular cations

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 TRANS UNIT 7.2: REGULATORY PROTEINS

• Increased Risk of Fracture of Trabecular and Cortical • Carrier proteins

Bone Tissue in Bones o Mucosal transferrin
• Increased Risk of Osteoporotic Fractures o Blood transferrin
FACTORS THAT ENHANCE CALCIUM ABSORPTION § Delivers iron to bone marrow & cells
• Stomach acid • Storage – protects from free radical action
• Vitamin D o GI mucosal ferritin
• Lactose § Receives iron & stores it in intestinal cells
• Growth hormone o Ferritin
o High levels store as hemosiderin
PHOSPHORUS
IRON TOXICITY
• Recommended Daily Allowance = 700mg/day
• Iron Overload = tissue damage (tissue damage = iron
• Function
overload)
o Mineralization of bones & teeth, part of every cell, part
o Hemochromatosis
of phospholipids, used in energy transfer & in buffering
system o Hemosiderosis
o Worsened by ETOH, Vitamin C
• Deficiency
• Iron & Heart Disease - inconclusive
o Weakness & bone pain
• Toxicity • Iron & Cancer
o Low blood calcium levels • Iron Poisoning - 200 mg Fe has led to death of young
children (5 tablets)
o This is why iron supplements needs to be
MAGNESIUM maintained
• RDA = 310 - 400 mg/day • Constipation with supplements
• Function
o Bone mineralization, building of protein, enzyme
action, muscle contraction ZINC
o Protects against hypertension and heart disease • Functions
• Deficiency o Cofactor for over 100 enzymes - this is why you can
o Weakness, confusion, convulsions, growth failure see zinc in multivitamins even vitamin C
• Toxicity - not known o Helps make DNA/RNA
o Helps manufacture heme
o Helps release Vitamin A for storage
SULFUR
o Helps metabolize CHO (carbohydrates)
• Function o Synthesize proteins
o Part of proteins, biotin, thiamin and insulin
o Metabolize ETOH (Ethanol)
• Deficiency – none known • Absorption & Metabolism
• Toxicity o Cell storage binding protein = metallothionein (also
o Depresses growth binds copper)
• Sources – all protein foods o Transport protein = albumin
o Transferrin also binds zinc
TRACE MINERALS • Excretion via feces

IRON
• Reduced iron (Fe2+) = ferrous iron
• Oxidized Iron (Fe3+) = Ferric Iron
• Allows Fe to participate in oxidation reduction reactions in
every cell, such as
o ETC protein
• Accepts carries & releases oxygen
o Myoglobin – muscle
o Hemoglobin – red blood cells
• Iron Sources to meet RDA 10 – 15 mg/day
o Heme iron (meat sources)
§ Absorption >20%
§ Meat fish protein factor (MFP)
• Nonheme iron (veg & meat sources)
o Absorption 2-20%
o Enhance absorption: vitamin C (keeps non-heme
iron reduced), as does citric acid, lactic acid, HCl from
the stomach, sugars
o Iron deficiency
o Inhibit absorption: phytates & fiber, calcium &
phosphorus, EDTA, tannic acid - bind iron
IODINE
• Function
o Part of the hormone thyroxine (T3 & T4 - thyroid gland
hormones)
o Regulates body temperature, metabolic rate,
reproduction, growth, blood cell production, nerve and
muscle functions
• Example:
o Females have thyroid diseases = usually they have a
hard time conceiving a child
o Affects muscle functions and calcium concentration
within the body
NOTE:
• Females are more sensitive to deficiencies and
concentration of minerals in the body.
• This is why they should be vigilant in taking vitamins
and always eat a balanced amount of food because
they are prone to a lot of disorders, especially mineral
disorders.

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 TRANS UNIT 7.2: REGULATORY PROTEINS

• RDA = 150 micrograms/day MOLYBDENUM

o Iodized salt, seafood, plant & animals from soil • Function
• Deficiency o Facilitator of many enzymes
o Goiter leading to sluggishness & weight gain • Al = 75 = 260 microgram/day
o During pregnancy leads to cretinism (MR) - a disorder • Deficiency = rare
for the unborn child • Toxicity rare
o Iodized salt is developed to fight off deficiency in iodine. o Gout like symptoms with exposure
• Toxicity > 2000 micrograms o “With exposure” – meaning one have other conditions
o Goiter that could lead to the increase of the viability of having
toxicity with molybdenum
SELENIUM
• Function NOTE:
o Antioxidant working with vitamin E • Most of the traced elements mentioned, they are
• RDA = 55 to 70 micrograms/day usually related to being cofactors and coenzymes.
o Seafood, meat, grains (where you can get selenium) • That is why even in small amounts they are important
• Deficiency because it triggers a lot of cellular functions and
o Heart disease from viruses and cancer like symptoms metabolic functions.
o Cancer – lacking evidence, needs more research • If not for these, there are metabolic functions that will
• Toxicity (rare & minimal) not continue or ensue.
o Vomiting, diarrhea, loss of hair & nails, skin lesions, •
and NS problems

COPPER
• Function
o Many reactions - like iron in metabolic reactions related
to release of energy
o Related to enzymatic functions and cofactors
• RDA = 1.5 - 3.0 mg/day
• Deficiency rare
o Genetic disorder
o Only happens in Menkes disorder
o Menkes disorder – releases copper into the
bloodstream and it could be life threatening because it
could poison the blood
• Toxicity
o Genetic disorder = Wilson’s disease copper
accumulates in liver and brain (give chelating agents
such as zinc)
o Usually doesn’t happen unless we have Wilson’s
disease

MANGANESE
• Function
o Cofactor of many enzymes
• RDA = 2-5 mg/day in most foods
• Deficiency rare
o Phytates, iron & calcium inhibit absorption
• Toxicity
o Brain disease

CHROMIUM
• Function
o Facilitates CHO (carbohydrate) & Lipid metabolism
• AI = 50 - 200 microgram/day
• Deficiency
o Diabetes like syndrome
• Toxicity
o Damage skin & kidneys
o Supplements for chromium picolinate
• Others
o Nickel, Silicon, Vanadium, Cobalt

BENIG | BERNARDINO | COLLAMAR | CALOMOT | DANCEL | GO | GONZALVO | LACAO | MANGOBA | ROALES |

ROSALES | SORIANO | PARULI | PORLAS | VILLEGAS | VILLAFLOR | VILLAMAYOR