620 Cu, Zn, Se + cancer
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1. What type of minerals are Se, Cu, Zn?
2. Where is Cu absorbed? Zn, Se?
- 1. Trace minerals
- 2. Upper GI (stomach/duodenum; Se = duodenum; Zn = jejunum)
1. Can Zn undergo redox changes under physiological conditions?
2. What does it do in cysteine rich proteins?
3. Good sources? (2)
4. Why would men need more Zn?
5. Main excretion?
6. important organs in balancing Zn?
- 1. No
- 2. Forms ZnII thiolate clusters in cysteine rich proteins b/c it has high affinity for thiols
- 3. Oysters & meats
- 4. Because it's found in muscle.
- 5. Feces
- 6. Intestine and pancreas
1. What is major regulator of Zn metabolism homeostasis?
2. What dec bioavailability of Zn in diet? (2)
3. What are the 3 types of Zn transporters?
- 1. Zn dietary intake
- 2. Phytates and iron
- 3. Zip (into cell or efflux from IC vesicles), ZnT (lowers [Zn] in cytoplasm through efflux out of cell or influx into IC vesicles) DVMT1
1. What is largest Zn reserve in body? In blood? In what form? What else can it be bound to?
2. What is transport b/t blood and tissues regulated by? 3
3. What else acts as a sink for Zn? What is it inducible by? What is it mediated by? How many Zn can it bind to? What does it provide Zn for?
1. Muscle; RBCs/WBCs in form of Zn-enzymes and proteins; albumin
2. Zip, ZnT, DVMT transporters
3. Metallothioein (MT) is inducible by zinc, is mediated by metal-binding transcription factor (MTF-1) and metal response element.
MT can bind to 7 Zn2+ and is IC source of Zn for proteins/enzymes that may need Zn for structural reasons.
1. What does MRE control for Zn?
2. How is pancreas in charge of excreting Zn?
3. Describe the two turnover phases (what is this regulated by?
- 1. Zip/ZnT and metallthioein
- 2. Pancreas secretes enzymes & lipases into the gut along with Zn to regulate Zn loss.
- 3. Rapid phase (~12.5 days) involving liver, kidney, pancreas, spleen. SLOW phase (~3,000 days) CNS & bone
Excretion of Zn through feces
What are its 5 main functions?
- 1. Catalytic
- 2. Structural (SOD/Zn-finger motifs)
- 3. Regulatory ((metalresponsive transcription factor)MTF-1 is essential for life regulates lots of different things).
- 4. Antioxidant defense - Cu/Zn SOD is the major superoxide radical scavenger; Zn-thiolate clusters of MT can act as reductants forming disulfide bridges.
5. Supplementation of Zn inhibits apoptosis.
1. Who requires more Zn?
2. What does mild deficiency lead to? (3)
3. Severe Zn deficiency?
- Caused by? (3)
- Main consequence of severe Zn def?
- 1. Vegetarians
- 2. Anosmia, increased susceptibility to infection diseases in children, impaired physical/neurphysiological development.
1. Zn as treatment for? (2)
2. What is major consequence of chronic Zn toxicity? How? What else? (1)
3. What else is Zn used for? (3)
- 1. Cold & HIV (but may be needed for HIV's progression too)
- 2. Cu deficiency (b/c it induces intestinal MT that binds preferentially to Cu leading to loss through feces. Also leads to neuronal death
- 3. Dandruff shampoo, breakfast cereal, diaper rash
1. Majority of body's copper is in what form?
2. Why is it important in scavenging free radicals?
3. What is a great source?
4. How much of Cu is normally absorbed?
5. Transporter? (2)
6. What must it bind to in enterocytes (4)
- 1. Cu2+
- 2. B/c its ability to easily accept and donate electrons (redox rnxs too)
- 3. Nuts
- 4. 25-50%
- 5. Ctr1 (CU2+--> CU+) to be takne up by DVMT
- 7. CCS --> SOD1 in cytoplasmic and intermitochondrial membrane.
- COX17 --> CCO
- Atox1 --> Cu translocating ATPases (ATP7A or ATP7B) Menkes Syndrome
or to MT
1. How is Cu delivered to proteins in cytoplasm/membranes of organelles? 3
2. What is needed to translocate Cu into cytoplasmic vesicles for exocytosis OR into Golgi to incorporate Cu into proteins? 1
3. What are good sources of intake of cu?
1. Through Cu-chaperon proteins. (CCS--> SOD1 in cytoplasm and inner mit membrane) and Atox1 --> ATPases (ATP7A or ATP7B); COX 17--> CCO.
2. ATP7A and ATP7B (ATPases)
1. What is the major Cu protein produced in liver and secreted in blood? What is it important for?
2. How much of metabolized Cu is excreted in bile?
1. Ceruloplasmin - is the major Cu-protein produced in liver and secreted in blood. It's responsible for transporting/carrying Cu
Broadly, what are the 7 functions of Cu?
- 1. Energy production (CCO)
- 2. Connective tissue formation (LO) - req for cross-linking collagen and elastin (why Cu is put in face creams)
- 3. Iron metabolism/hemopoiesis (Cp = feroroxidase 1 and oxidizes Fe2+ --> Fe3+).
- 4. CNS (makes NE, monoamine oxidase)
- 5. Melanin formation (tyrosinase - needed to form melanin)
- 6. Antioxidant defense (SOD1&3, catalase tx, Cp prevents Cu from catalyzing oxidative damage)
- 7. Gene transcription regulation (Cu-dep tx factors for genes that encode SOD1&3, catalase, Cu-chaperones, MT via MTF-1 and MRE). Ex. ATOX1
1. How does Cu def affect Fe mobilization?
1. Cu is major in ceruloplasmin which is a ferroxidase i which is important for mobilizing Fe from storage sites.
1. What are symptoms of Cu def or toxicity? 7
- 1. Anemia (can only be fixed with copper supp, not Fe!)
- 2. Osteoporosis b/c of def in lysyl oxidase (esp in Cu def low BW infants and children)
- 3. Disorders of immune system (less pro inflammatory cytokines)
- 4. Disorders of CV system (cardiac hypertrophy, arrythmia)
- 5. Disorders of nervous system -> myelopathy and ataxis
6. Menkes syndrome - loss of ATP7A b/c of genetics. Results in severe Cu deficiency and severe infections in infants.
7. Wilson's disease = toxicity due to impaired excretion of Cu into bile. Can use zinc acetate to prevent Cu uptake, but may need liver transplant.
1. What causes Cu acute toxicity? Symptoms?
2. What are symptoms of chronic toxicity? Why are infants susceptible? Who else?
3. Why are crabs/lobster blue?
1. Cu-containing containers; GI symptoms, severe liver damage, kidney failure, coma, death
- 2. B/c they cannot excrete Cu efficiently in bile, same with those with wilson's
- 3. B/c O2 binds to hemocyanin (we bind to hemoglobin)
1. Who does selenium react avidly with? Like whom else?
2. How does Se create new AAs?
3. What are good sources? (3)
4. Bioavailability %? What inhibits d bioavailability?
6. How is homeostasis regulated? (2) NOT? (1)
1. Thiol groups, like Zn.
2. By replacing sulfur in common AAs.
3. Meats, BRAZIL NUTS, seafoods
4. 50-100%, buti nhibietd by things like mercury
5. None identified for either inorganic form or amino acid form.
6. By excretion through urine (@ high levels respiration through lung - garlic odor), NOT BY INTAKE. Same with copper.
1. What mediates Se metabolism from one form to another? (3)
2. What are the two most important Se-amino acids?
3. What is the substrate for SEc synthesis? It's also the product of breakdown of Sec and Se-Met?
4. What happens to this substrate later? (1)
5. Can humans maek Se-Met?
1. Thioredoxin reductase, GSH or GSH reductase
2. Sec = selenocysteine and Se-Met - selenomethionine.
4. reincorporated into selenoproteins
5. No, but it can be randomly incorporated into our proteins
1. What is the 21st amino acid?
2. How is Sec made?
3. What ist he important struture?
4. What is needed to actually make the protein? (5)
- 1. Selenocysteine
- 2. Sec is encdoed by TGA/UGA (DNA/mRNA respsectively) that usually functions as STOP CODON but if it has SECIS (selenocysteine insertion sequence) it will code for Sec.
3. SECIS element consensus structure - stem-lop.
4. ATP, 4 enzymes and tRNA^sec (takes tRNA that usually binds for serine)!!!!
1. Which body parts contain the most selenium? 4
2. Which enzymes require selenium? 9
1. Muscle, liver kidney blood
- 1. GPx (require selenium)
- 2. Thoredoxin reductase - maintains thioredoxin in reduced form
- 3. Selenoprotein R - antioxidant
- 4. Selenoprotein P - contains up to 10 sec stores/transports 40% of plasma Se; antioxidant
- 5. Selenoprotein W - Se Def --> decrease in selenoprotein W --> white muscle disease from Ca2+ deposits
6. Selenoprotein N --> multiminicore disease (congenital muscular dystrophy)
7. Selenophosphate synthetase 2 - makes precursor of sec for all selenoproteins
8. Iodothyronine deiodinases (T4-->T3)
1. What is Keshan disease? Who? where? Why?
2. Why not men?
3. how can Se supp help?
4. What infectious agent is involved? (2)
5. What is toxicity called?
1. Cardiomyopathy affecting young women and children in regions of low SE content in soil, esp in CHINA!
2. B/c men go to cities to work so have enough Se.
3. Protection from developing disease, but cannot reverse it.
- 4. Coxsackievirus (linked to Keshan disease and causes myocarditis). Oxidative stress induced by Se deficiency results in change sin viral genome capable of converting harmless viral strain to myocarditis strain. Also contributes to flu via mutation.
- 5. Selenosis (ponies, manufactuerer's error, garlicky odor = first clue).
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