Detoxification Flashcards
What are factors for an increased risk in breast cancer
Xenoestrogens Pollutants Xenobiotics Menopause Stress
How is menopause a risk factor for Breast cancer
spikes estrogen relative to progesterone
excessive stimulation through estrogen receptor
How is stress a risk factor for Breast Cancer
Emotions: more cause most damage Physical and surgical- less often Decrease in melatonin Decrease thyroid Cortisol and Dhea out of balance
How does the tumor contribute to breast cancer
tumor becomes like ovary- produces estrogen- and is primarily the source of inflammation
How is the breast tumor a source of inflammation
as its forming need a good source of glucose
over stimulates the insulin receptors leading to insulin resistance
LH/FSH increase-> PCOS-> testosterone-> estradiol
How does estrogen metabolism become a cancer risk
most estrogen hormones in body are estrosulfate
Key Enzymes: CYP1B1- in liver, kidney and other tissue
CYP1A1: both enzymes move estrogen through pathways
4-OH-E1(E2) with COMT-Methylation of 2-A-4-OH-E1(E2) coverts estrogen or estrodial- is bad but not terrible, if patient methylate well will clear them-
If not methylating well, above reaction will down regulate and lead to cancer
How does estrogen metabolism and pollutant lead to cancer
If making too many estrogens with exposure to pollutants-> induce enzymes that will make bad estrogen and cause DNA formation which leads to DNA damage which results in cacner
What factors contribute to DENA formation, damage and ultimately cancer
Trans Fats- more easily oxide estrogen
Heavy metals: mercury, arsenic: oxidize estrogen
What testing is available for Estrogen
Serum and Plasm
Urine( liquid and dry)
Saliva
What is significant about Estrogen vs Estradiol in terms of metabolism and cancer risk
Harmful if metabolized in the wrong way
Progesterone is natural anti-estrogen
Higher levels of estrogen can have higher levels of catechol of estrogen
What is a common Urinary profile in breast cancer patients
- increased estradiol and estrone
- increased 4-OH-E1 and 4-OH-E2
- decreased ratio of 4-MeO-E1/r-OH-E1
- decreased pregnanediol
- Increased ratio of pregnane/pregnene
- Decreased testosterone and dHT
- Increased EPI testosterone
- Decreased DHEA
Increased diurnal cortisol flat
What are lifestyle changes that reduce risk of breast cancer
Lots of organic veggies- crucious veggies- improve estrogen metabolism
avoid pollutants
Exercise
Get adequate sleep
If hormone deficient- take necessary hormones
DIM- indole-3-carbionol or diindolymethane
omega 3 FA
green algae
Whats the pathway for Estrogen metabolism
E1-SO4-> sulfatase->E1->(17B-HSD-Type1)-E2
Conversely: E2-> (17B-HSD2)->(Sulfotransferase)->E1- SO4
What happens when E1-SO4 is converted to E1
depends on the SNP for processing. If CYP1B1 then issues occur, if CYP1A1 more normal and safer outcome
How does CYP1B1 affect estrogen metabolism in the body
E1->( CYp1B1)-becomes 4-OH-E1(E2) which if appropriate methylation will become metabolites: 2 and 4 MeO-E1(E2)
If not methylating well will become 4-Quinone-E1(E2) and if appropriate GST-GSH conjugation of 2 and 4 quinone E1(E2) will become metabolites- if not will produce DNA adduct formation-> DNA damage mutation-> cancer
How does CYP1A1 affect estrogen metabolism
E1 with CYP1A1-> either 2 OH-E1(E2) or 16-OH-E1. Would like to become 16 as it is metabolized appropriately becoming E3 and binds to protein and no affect on the body. If an issue with CYP1A1 and ability to detox- 2-OH-E1(E2) -> 2-Quinonine-E1(E2)- DNA adduct formation and DNA repair
How is cortisol a factor for Breast Cancer patients
Normal profile: cortisol high in am and low at night
Breast cancer patients- flat line diurnal cortisol and high at night
What key hormones make up the matrix for Breast cancer- estrogen matrix
Testosterone Estrogen Progesterone Cortisol DHEA
Where is estrogen found
produced in ovaries and metabolized in liver
What are benefits of estrogen
metabolism functions correctly vessel and skin increase bone formation increase hepatic production of binding protein increase HDL Decrease LDL Increase cortisol: SHBG Increase Cholesterol in bile Promote lung function
What are 2 key estrogen metabolites
2-Hydroyestrone( 2-OHE1)- inhibit cancer growth- implies balanced metabolism: via reasonable intake of veggies and flaxseed
16-a-hydroxyestrone( 16-a-OHE1)- encourages tumor development- bad estrogen- lupus, breast cancer, levels can rise in response to obesity and alcohol, genetics play a role, is modifiable by measuring estrogen
What is important about 2:16 alpha-Hydroxyestrone ratio
Higher ration less risk for estrogen related cancers
Serum great than .4 is considered to be beneficial
What are mechanisms of heavy metal toxicity
metals generate many of deletions effects through the formation of free radicals, resulting in DNA damage, lipid peroxiding depletion of protein sulfydrase
are everywhere- appear mediated through mitochondrial damage from glutathione depletion
why be concerned about heavy metal toxicity
toxic to all living creature everywhere in environment increase in health damage if not removed may take years for sx to appear causes many diseases and blocks healing mercury is usually hidden as the cause
What systems are affected by mercury
nervous, emotions, reproduction, heart, kidneys, hormones, sexual preference, vision, GI, immune, children/fetus
What has WHO stated about mercury?
mercury is toxic to human health, posing a particular threat to development of child
exists in various forms: elemental, inorganic and organic
No threshold below with some adverse affects do not occur( lowest levels produced adverse affects)
Where is mercury stored?
brain, thyroid, liver and adrenals
What are sources of mercury
amalgams-#1 source fish and other food vaccine thermometer flurescant bulb thermostat barometer light up sport shoes cosmetic disinfectant skin cream tattoo-red dye paint blood pressure gauge button cell batteries
1 mcg or mercury is how many atoms of mercury
1 mcg of mercury= 43,000,000,000 atoms of mercury
1 Large amalgram= 1,000,000mcg of Hg
Mercury is double edged sword of attack
Direct: mercury attaches to protein or enzyme with a sulfhydryl group destroying function
Indirect: weaken immune system while depleting body of glutathione and sand selenium
Can mercury be detoxified?
NO!!
must be taken out physical
2 glutathione molecules los for every atom of mercury
How does selenium affect mercury
Binds to it!
mercury binds to selenium forming mercury selenides thus reducing mercury damaging cytotoxicity
selenium availability for many other important enzyme reaction is reduce
How does mercury relate to CVD
patients with amalgam bearing had higher BP and greater amount of chest pain, tachycardia, anemia, fatigue, tiring easily, and being tired in the morning
Atherosclerosis- activates an enzyme called phospholipase D in cells that line arteries causing release of phophatidic acids damaging endothelia cells-
Treatment: chelators
What are some emotions that associated with mercury toxicity
Indecision, low self-esteem, shyness, overwhelm, lack of joy, hopelessness, lack of motivation, depression, fearfulness, anxiety, panic, impeding doom, irritability, aggression, inappropriate anger, rage
How does mercury disrupt the brain
lack of focus brain fog forgetfulness/memory dementia Journal of Neurochemistry- mercury induces cell cytotoxicity and oxidative stress and increase in b-amelyoid secretion and Tau phosphorylation in Neuroblastoma cells; mercury may play a role in pathophysiological mechanism of AD
How does mercury affect the nervous system
frequent chronic headache tremor affects all 5 senses neurodegenerative disease any other neurological disease
How are kids harmed because of mercury
affected in womb and breast feeding irritability and emotional problems ADD and lower IQ autism, vaccines- evidence of arm infertility
What are endocrine disruptors because of mercury
mercury affect hypothalamus, pituitary, thyroid, adrenal gland, and gonad
disruptive effects of mercurial on function of thyroid, adrenal, ovary and testis
: Iodiase is enzyme that helps convert T4-> T3 and is inhibited by mercury
How is thyroid affected by mercury
Hypothyroidism
Damage of Thyroid RNA
autoimmune Thyroiditis
Impaired conversion of T2 to active T3
Hashimoto is mercury- also look at other autoimmune disease
TP -antibodies wind down with removal of mercury
What is hormone havoc because of mercury
fatigue weight gain low sex drive cold extremities insomnia hair/skin issues mood swings
How is immune system affected by mercury
binding to sulfhydryl groups on protein may cause immunosuppression of immunostimulation, autoimmune reactions or hypersenisity 14 days after onset of oral mercury exposure, levels of immunoglobulin E and G( IgE and IgG) increase including autoantibodies to biomolecules Lowered resistance to infection prolonged infection allergies autoimmune disease mutagenic
What are toxins
substances produced during metabolism and growth of microorganism and some plant and animal species- primary factor- pathogenicity
What are examples of toxins
viruses- cytotoxin, lysin bacteria-end and exotoxin fungi-mycotoxin protozoa-endotoxin, phospholipase, protease algae-micrycystins plants-alkaloid higher animals
What are mold and mycotoxin
eukaryotic unicellular organism
include mold, yeast and mushroom
more than 100,000 mold species ID
most fungi grow as tubular filament calle hyphae
reproduce and disperse by formation of spores
play a crucial role in nature by breaking down dead organism and releasing their nutrients for reuse
How are fungi beneficial
decomposition: nutrient and carbon recycling
Biosynthetic factories: to produce drugs, antibiotics, alcohol, acids and foods
model organism for biochemical and genetic studies
How are fungi harmful
destruction of food, lumber, paper and cloth
Animal and human disease- including allergies
What is mold secondary metabolism
not essential to maintaining life cycle of mold
give molds that produce a competitive advantage
Types: mycotoxin, volatile organic amount, extracellular, enzyme, extracellular protein
What are mycotoxins
Low molecular weight produced as secondary metabolites by filamentous fungi
300-400 compounds are recognized as mycotoxin many received attention as human threat
What are mechanism of mycotoxin toxicity
bind to DNA and RNA Alter protein synthesis and function Oxidative stress Depletes antioxidants alters cell membrane function and transport Potent mitochondria
What is Aflatoxin
Mold: aspergillus flavus, aspergillus parasitique,
Mechanism: inhibit protein synthesis
Effect: immune suppression various end point
Liver is primary target organ- also found in lung and brain, : 4 major B1, B2, G1, G2( B1 is natural carcinogen known)
Ochratoxin A what is it
Mold: aspergillus ochraceus, Aspergillus niger, Penicillium verrucosum, penicillium chriysogenum
Mechanism: inhibit phenylalanine’s tRNA synthesis
Effect: suppression of antibody production and globulin synthesis
Found in grains, coffee beans, and some wines
Kidney is primary target
Is nephrotoxic: humans have the longest half-life for its elimination: hepatotoxic, immune suppressant, carcinogen, associated with UTI and bladder cancers
Disturbs cellular physiology: inhibits mitochondrial ATP production, stimulates lipid per oxidation, inhibit synthesis of phenylalanine’s tRNA
What is Trichothecenes
Mold: fusarium spp, Stachybotrys Chararum, Trichoderma viridae
Mechanism: inhibit protein synthesis, inhibit peptide synthesis, causes lymphoid necrosis, causes dysregulation of IgA production
Effect: immunosuppression, cause nausea, vomiting and weight loss
What are Gliotoxins
Mold: aspergilla fumigates, aspergillus versicolor,
Mechanism: inhibit macrophage phagocytosis, induces macrophage apotheosis, blocks T and B cell activation
Effect: immunosuppression, In vivo displays anti-inflammatory activity
Route of exposure: eating food or drink containing toxin, breathing Moldy air in damp indoor areas, Dermal absorption
How do climate changes affect exposure to mycotoxin
Extreme precipitation storms and floods, drought, increased temperatures
What are human health effects related to mycotoxins
Aflatoxicosis Aplastic anemia( bone marrow failure) and bleeding( trichotehecenes) Acute pulmonary hemorrhage Cancer( aflatoxin) Birth defect
What is sick building syndrome
living in moldy environment: common sx include: itchy eyes, nausea, fatigue headache, increased respiratory tract infection
What are some conditions related to chronic exposure of mycotoxin
cancer induction kidney suppression autism neurotoxicity depression
Prevention remedies for mycotoxin
protection from ingesting or inhaling: food, water damaged and moldy homes, folic acid supplement for women
Protect crops- growth and harvest
Education: community leaders and consumer knowledge
What are interventions for mycotoxin
reduce airborne exposure: keep indoor dry, fix all leaks and clean up flooding within 24 hours, do not smoke indoors
Reduce food borne exposure:: protect agricultural crops
Interventions for after a flood
Tetanus booster, food and water safety check, sanitation and hygiene, power outages, carbon monoxide, animal and insect check, clean-up effects, mold and mycotoxins, electrical hazards, reentering flooded buildings
What are some regulatory controls
limit mycotoxin of 20 parts per billion for aflatoxin in all food and feed
using ElISA more for cheaper and better evaluations
How to test for Mycotoxins
ELISA test
What do Mycotoxin do to cells
affect mitochondria
cause cytoprotective responses- KEAP1-> Nrf2 pathway- major regulator of these response caused by reactive oxygen species( ROS) and electrophiles
Nrf2- nuclear factory erythroid 2 related factor
Keap1 Kelch ECH associateing protein 1( a repressor protein that binds to Nrf2 and promote degradation)
Nrf2 constibitue main oxidative stress response drives transcription of genes in glutathione synthesis- if bind to Keap1 will protect, if bind to MAF will cause damage
Evaluating which Genotype will aid in treatment of mycotoxin detoxification
Glutathione S-transferase M1 and T1
These mutations caused y a deletion in the genetic code lead to a reduction or complete loss of capbabliyt - increased risk for lung cancer, bladder cancer, ischemic heart disease, airway disease
What is relationship between NK cells and mycotoxin
Ochratoxin A selectively suppresses NK function in mice- also seen in trichotechecens
Clinically: Low NK function seen in CFS
What are two main tx strategies for mycotoxin
Urine excretion( infarared sauna, glutathione and Nrf2 activators such as green tea, curcumin) Fecal excretion: sauna, glutathione, Nrf2 activators, mycotoxin binder: activated charcoal, bentonite, cholestryamine
What is Pyrrole Disorder
Abnormality in biochemistry resulting in overproduction of pyrrole molecules- by products of hemoglobin synthesis and other processes in the body
When deficiencies are with Pyrrole Disorder?
Vitamin B-6 and zinc
What is pyrrole involved in synthesis of?
Heme- primary constituent of hemoglobin- bind with PLP and zinc
What percent of persons diagnosed with depression or other behavioral disorders have deprived zinc
90%
What vitamin is required for synthesis of Dopamine and GABA in the brain
B-6
How many chemical reactions in the body does B-6 take part of
80
What physical sx associated with low B-6
nervousness, insomnia and muscle weakness
Why is zinc important in the body
required for conversion of dietary B-6 into PLP.
What does a zinc deficiency alter
brain levels of GABA and causes copped overloads that alter brain levels of dopamine and norephinphrine- also associated with delayed growth, temper control, poor immune function, epilepsy, hormone imbalances, neurodegenerative disorders and learning problems
What percent of schizophrenic patients exhibit severe pyroluria
30%
What is relationship between children and Pyrrole disorder
Children showing severe tantrum, bizarre shift in mood, and poor response to small stressor: children treated for pyrrole disorder with nutrients respond quickly
What is Pyrrolic depression
double deficiency in zinc and B-6 with low brain levels of serotonin, dopamine and GABA
females have disturbed periods
prone to delayed puberty after age 16 and runs in family
What other nutrient deficiencies i Pyrrole disorders
Undermethylation: methylation deficiency, eating disorder, perfectionism
Overmethylation: folate deficiency, high anxiety, panic disorder, sensitivities to foods, chemical and environment
Copper overload: lower dopamine and increase norepinephrine
FA imbalances: depression, ADHD, Schizophrenia, Bipolar Disorder, Dementia
What is a powerful tool for assessing toxic effects of heavy metals
Polyphyrin profiling
What is the name of essential pathway needed for proper function of many proteins for O2 transport, energy production and detox
Heme pathway
What is the Heme pathway
8 enzyme driven reactions
reactions begin and end inside the mitrchondria with intervening steps carried out in the cytosol
when porphyriongen build up, easily oxidized to polphryin that appear in urine
toxins bind to one or more enzymes produce specific patterns of urinary porphyrin
oxidized porphyrins accumulate in body become additional toxicant that cause further tissue degradation
is required for oxygen binding, oxygen utilizing and oxidizing systems, hemoglobin and myoglobin, synthesized in human tissue- liver and bone marrow
What are the steps of Heme Biosynthesis
- )Takes place in mitochondrion and involves condensation of 1 glycine and 1 SccinlCoa by the priodoxal phosphatase containing enzyme d-aminolevulinic acid synthase( ALA)
- ) mitochondrial ALA transported to cytosol where ALA dehydratase( also called porphobilinogen synthase) dimerizes 2 molecules of ALA to produce pyrrole ring compound pophobilinogen
- ) involves head to tail condensation of 4 molecules of poprhobilinogen to produce the linear tetrapyrrole intermediate hydroxymethybilane
What is the fate of Hydroxymethlbilane
regulated enzymatic conversion to uroporphyrinogen 2, the next intermediate on path to Heme. step is mediated by holoenzyme comprised of uroporphrinogen synthase plus a protein known as uroporphrinogen iii cosynthase
Where does final reaction in Heme synthesis take place
in mitochondrion and involves the insertion of iron atom in ring system of Heme B- enzyme catalyzing this is ferrochelates- very sensitive to heavy metals
What are sx of porphyrinopathies
acute porphyrins: neurologic presentation due to hepatic accumulation: acute abdominal pain, nausea, vomiting, constipatino and seizures
Others: headache, difficulty concentration, personality changes, weakness in muscles, joint aches, unsteady gait, poor coordination, numbness, tingling of arms and legs, fluid retention, rapid HR, high BP, increased sweating, intermittentlyt fever
What exacerbates a porphyrinopathy
low carb diet
intake of alcohol
medication: sulfa drug, antibiotics, barbiturates, estrogen birth control pill,
exposure to toxic chemicals
Disease associated with Porphrinopathy
Infectious: mono and acute poliomyelitis Liver Malignancies Pregnancy Carbo fasting Hematotologic disease Disturbance of iron metabolism MI, Diabetes and tyrosinemia Bronze baby syndrome Erthrohepatic protoporohia
What is 2- Methylhippurate
specific organic acid product of detox of zylean exposure
Use of gas, paint and paint thinners
What is the organic acid orotate
elevation: failure to remove ammonia
Treatment is arginine- with magnesium
What is organic acid glucarate
exposure to alcohol
Toxins are produced in GI tract
What is organic acid X-hydroxybutyrate( AHB)
marker of hepatic glutathione synthesis rate
Complications seen in Diabetes, COPD, MAC< parkinson, autism
Treat: IV glutathione, NAC, taurine, Alpha-lipoic acid, Whey protein isolate
What is organic acid Pyroglutamate mean
elevated: reveal glutathione at high rates
Treatment: IV glutathione, L-methionine, Alpha-lipoic acid, Why protein, similar to AHB
What is significant about organic acid sulfate
Marker for sulfur metabolism
High is inverse of sulfur in body
Low urinary sulfate is indicator in low demand
Lipoic Acid is used when detox stress on the liver
What is urinary Bile Acid Sulfate
Direct assessment of liver function: hepatic regulates bile acid levels, most converted to sulfate and then excreted
Elevated has high specificity to hepatic biliary diseases
What is significant about cysteine/cystine ration
Cysteine: rate limiting amino acid production of GSH,
Extracellular anti-oxidant and precursor of taurine, inorganic sulfate acetyl-Coenzyme A and protein synthesis
Low levels associated with reduced antioxidant capacity
may be associated with high homocysteine or low B6
Excess free cysteine acts on NMDA glutamate receptors
Low ration associated with higher oxidative stress
What inhibits cysteine deoxygenate( CDO)
Inflammation: TNF alpha and TGF beta, excess cytokines, abnormal FA ratio
Allergies
SNP
Adrenal dysfunction
Low panethenic Acid: B5
to avoid toxicity when CDO not working temporarily avoid sulfur foods
Cysteine/Sulfate ratio
sulfate is produced from cysteine via sulfoxidation- critical part of phase 2 liver metaobilsm
sulfate essential for mucin formation in GI tract and glycosaminoglycans in joint cartilage
Sulfoxidation defects results in increase risk of illness
Molybdenum-B12
People with sulfa drug allergy, tend to have an issue with this pathway
Sulfite->( sulfite oxidase)-> sulfate
What are causes of High cysteine/Sulfate ratio or LOW sulfate?
Leaky gut, environmental disease, food sensitivities
Alzheimer
Sulfoxidation impairment
Low glutathione
Excessive exercise
Chronic RA or IBD
Oxidative stress: MCS, environmental toxicity
What are the functions of sulfation
substrate for many enzymes: lower serotonin, lower dopamine, lower thyroid homrone
How to support sulfation
increase dietary protein and sulfur-rich foods
Molybedenum co-factor( SUOX)
Best way to enhance methylation
Methylfolate: methyl-B12, TMG, SAM2
What stops methylation
Too little glutathione
What is significant about Copper( Cu)
Best dietary source: whole grains, nuts, seeds and shellfish
Most prevalent in SOD -protecting cells
High sources: chlorinated water
Potential for loss of biochemical functions can lead to anemia, neural degernation, lunch and bone problems, CVD and accelerated agin
What is significant about Magnesium( Mg)
Cofactor in over 300 enzyme systems
Many deaths due to nutritional deficiency
Critical factor in phase 1 detox
Most useful in erythrocyte abc test not serum
Plays a vital role in cardiac function, insuffiencency,
Major sources: nuts, beans and dark veggies
Sx: neuromuscular tremor, fascinations and gross muscle spasm
What is significant about Calcium(Ca)
Erythrocyte calcium are indicators if ionic calcium, and not related to dietary
170 biological functions
must be broken down into ionic calcium
associated with etiology of heart disease and stroke playing a role with elevated BP
What is significant about Chromium(Cu)
accumulated primarily in spleen and heart
numerous studies affects sugar metabolism through uptake of insulin and losses in urine
aids in lowering LDL and raising HDL
best sources are liver, yeast, nuts, and whole grains
What is significant about Manganese(Mn)
is involved with a number of enzymes involved with metabolism especially connective tissue maintenance, FA synthesis and Krebs cycle
Absorption is impaired by calcium, phosphate and iron
best source: fruit, whole grain, leafy greens, pecans, peanuts, pineapples, hazelnuts, avocado and seaweed
What is significant about Potassium( K)
Best single measure is erythrocyte potassium
Dietary depletion can lead to hypertension, heart arrhythmia and muscle weakness
Veggie juices, citrus juice, banana, melon and other fruit will increase potassium level
What is significant about Vanadium
is retained by liver and bone transported on blood protein transferring
Lower’s cholesterol and may lower plasma triglycerides
Promotes mineralization of bones, teeth and protect against cavities- play a role in insulin release
Parsley, black pepper, dilll , mushrooms, shellfish good sources
What is significant about Selenium(Se)
primary role of selenium appears in the activation of enzyme glutathione peroxidase- where glutathione reacts with oxygen radicals
Protein containing foods, which selenium is bound to amino acids- meats, grains, brazil nuts and seafood all good sources
Functions: primarily as activator of enzymes necessary for cellular protection from oxidative damage and maintenance of normal redox potential
What is significant about zinc
Growth and repair of tissue is dependent on zinc as activating cofactor for DNA/RNA Polymerase
Zinc is vital for normal wound healing and skin disorders
Required for immune function
will deplete with excessive calcium, copper and iron
good sources: whole grains, nuts, seeds, seafood
Low alkaline phosphatase may be warning of zinc insufficiency
What is significant about toxic metal Aluminum( Al)
best known effects are dialysis encephalopathy and dementia
Sx: impaired memory, dementia, aphasia, ataxia, convulsions and characteristic EEG changes
Urine if major elimination route of aluminum -easily removed with chelate agent
potential sources include: antiperspirants, soda can, baking soda and toothpaste
What is significant about toxic element Arsenic( As)
commonly found on playgrounds, contaminated water, paint smelting, wood preservatives, pesticide, herbicides and fungicide
Increased risk of vascular disease related to athersosclerosis
Ingested arsenic linked to cancers of skin, bladder and lung
unidentified causes of peripheral neuropathy may be reason to rule out arsenic toxicity
What is significant about toxic metal Cadmium
Competes with zinc at all cellular binding sites: result in lost enzyme activity
bound by abundant zinc sequestering protein: metallothionine and protein occurs in high concert in kidney makes it easily removed toxin
Kidney holds major body burden which damage to proximal tubules
Intervention that increases passage of metal chelating agent through kidney will lower burden
Sx: hypertension, femoral pain, osteopenia, vascular disease and emphysema
Sources: drinking water, processed foods, engine exhaust, emissions, soft drinks, canned evaporated milk, cigarette smoke, pain pigment and silver polish
Tx: EDTA suppository, reduce toxin exposure, dietary fiber is helpful along with zinc
What is clinically significant about lead( Pb)
causes paralysis and pain in extremities due to effects on demyelination axonal degernation and presynaptic block
Normocytic siderblastic anemia is consequence of lead inhibiting effect on enzyme in heme biosynthesis pathway
Other clinical signs: kidney damage, epigastric pain, nausea, male and female reproductive organ failure
Common affects sensory, visual, auditory and cerebellar
IV chelation agents such penicellamine and EDTA effective in reducing lead body burden
Sources: house paint, drinking water, newsprint and many others
Ca, zinc and iron deficiency enhances uptake of ingested lead in the body
What is clinically significant about Mercury( Hg)
Can leak into BBB, reduce nerve conduction, decreasing hormones of brain
Sx: metallic taste, increased salivation, paresthesia, with decreased sense of hearing touch and vision, hypertension, headaches, fatigue, insomnia and muscle tremor- poor hand writing
Hall mark sign: Emotional disturbance: sometimes bipolar depression
Sulfur containing agents such as Dimercaptosuccininc acid( DMSA) are more effective for removing mercury rom tissues
Most important protective agent is dietary selenium
Sources: dental amalgams, broken thermometer, costmetics, fresh water fish, contaminated shellfish or seafood, old paint
What is clinically significant about Tin
potentially toxic element and primarily in the erythrocytes but leaves blood rapidly and disturbed to liver, bone and kidney tissue
various organic tin affect enzymes involved in sugar metabolism, oxidative phosphorylation and T-lymphocyte function
Mainly excreted via urine
Effects of organic tin overload: ataxia, headache, blurred vision, vertigo, hyperglycemia, and glycosuria
Sources: tin cans, toothpaste and perfumed soaps, metal alloy, soldered join in can and water systems, PVC, dyes and pigments.
