Other metals 2 Flashcards
Copper interactions, acute tox, chronic tox, factors influencing tox
Mo, Zn, Fe, sulphate;
Acute tox: irritation– cramps, vom, diarrhea
chronic tox– hemolysis of RBCs; liver necrosis, decrease glutathione; methemoglobin formation
factors: ingestion liver disease; mineral imbalance; genetics (Muenke’s disease)
what is wilson’s disease, and what causes it?
Cu; Cu not excreted via biliary route due to autosomal recessive gene mutation; therefore Cu accumulates in liver
what is menkes disease?
opposite of wilson’s disease–inability to store Cu–>bone problems–die at 2 years
describe Mo toxicity
Causes Cu deficiency–>strong interaction b/w Mo and Cu–>decreases abs of Cu and increases excretion of Cu
alters activity of xanthine oxidase and aldehyde oxidase, which are dependent on Cu
wherever Cu is stored, Mo is found–>liver, kidney, blood
how is Mo excreted?
50% in urine
bile
biological effects of Mo?
- Interferes wth Cu storage
- Interferes with Cu enzymes–ceruloplasmin
- interferes with P abs
- Reduces phospholipid synth–>low P, membrane effects
- reduces ATP synth
clinical manifestations of Mo?
anemia, poor growth, diarrhea, joint deformities, depigmentation of wool/hair
treatment of Mo poisoning?
Cu!
what are the forms of Se, and what are the ones which cause major problems?
Selenate– Se 6+
Selenite– 4+
Selenide – 2+
Absorption of Se forms
Selenite (4+) – 90%
Selenide (2+) – 0%
Distribution of Selenite
liver, kidney, blood, brain, muscle
crosses placenta–teratogenic
Se metabolism?
methylation
Se excretion
Urine-- 15-40% Se-Met complex Milk Sweat as a dimethyl selenide (probably 2CH4 + Se4+ --> CH3--Se2+--CH3)--HAS GARLIC SMELL lungs--breath
what is the function of Se in our bodies?
important for GSH peroxidase–>has antioxidant activity again free rad, lipid perox, membrane damage
Acute tox of Se?
severe tissue destruction–lungs, breath problem
dyspnea, cyanosis, diarrhea (destroyed gut cells)
subacute tox of Se?
wandering, weakness, blind, emaciation (gut membrane damage–destroys absorptive epithelial cells); CNS manifestations–>destroys myelin, etc
chronic tox of Se?
hair loss–brittle hair and nails (hair has lots of S, which Se displaces)
skin lesions, blisters
numbness, convulsions, paralysis
simian B monkey virus looks like Se tox in monkeys
Se also reduces fertility, is teratogenic, causes liver tumors but may act as an anticarcinogen
ya
what does Se interact with?
Cd, Hg, As, Th (thorium), Cu, Vit E
factors enhancing Fe tox?
Age
high iron stores
low vit E status–>Fe interacts with vit E heavily; Vit E is needed
low Se status–interacts, Se stabilizes membrane
route of exposure of Fe?
oral, IP, inject (highest)
how is Fe proposed to cause damage
is very redox-active, damages membrane
Iron tox pathogenesis?
- CV collapse–increases perm of mem bc iron damages; fluid loss, and shock
2 liver damage - impaired clotting mechs–hemorrhage
pathgenesis not fully understood
iron tox peracute syndrome?
- anaphylactoid-LIKE rxn
shcok
iron tox subacute syndrome
classic iron tox
CNS–drowsniess, coma, death wthin 4-5 hours
GIT–vomitting, diarrhea, blood in gut
liver– icterus, liver damage,
shock– pale skin, dyspnea, hemorr., acidoses
chronic iron tox syndrome?
poor grwoth, rickets,
Fe interacts with PO34—>soft bones
treatment of iron tox?
milk of magnesia--forms FeOH-->ppts out fluids (for shock) -- something to relieve acidosis --VIT E BIG ONE --chelators okay, NOT CA-EDTA
