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Toxicology > Exam 4 - Metals > Flashcards

Exam 4 - Metals Flashcards

1
Q

What role do metals play in biology?

A

Vital biochemical processes require energy inputs and catalysts

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2
Q

Where are thiols found in biomolecules and why are they important in the mechanism of action of many metals and metalloids?

A

Thiols are present on cysteine, tripeptide glutathione, and cysteine residues of proteins & enzymes

located within the active sites of many enzymes and directly involved in catalysis

they are molecular targets of class B and intermediate elements

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3
Q

What is metallothionein and what role does it play in the mammalian cell?

A

metal binding protein - detoxifies metals

1 molecule can bind 7 Cd & other metals

sequesters heavy metals and prevents oxidation of critical protein or nonprotein thiols

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4
Q

What “form” of mercury is considered the most significant with regards to toxicity and what specifically about the molecular makeup allows it to access the CNS?

A

methyl mercury MeHg

resembles amino acid methionine so amino acid transporter helps cysteine-MeHg cross the BBB through “molecular mimicry”

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5
Q

Mercury toxicity treatment

A

DMSA/succimer

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6
Q

exposure to Cadmium

A

sewer sludge pastures with cattle

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7
Q

what metal toxicities are enhanced by a Calcium deficiency

A

Cadmium
Lead

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8
Q

what does Cadmium replace at binding sites and what can this result in

A

replaces Cu & Zn
Cu deficiency

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9
Q

What effective treatments exist for cadmium toxicosis?

A

minimize/reduce exposure
EDTA

NO BAL - increase nephrotoxicity
NO DMSA/succimer - ineffective

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10
Q

How do the different forms of arsenic differentially target metabolism

A

As3+ binds lipoic acid (in TCA cycle) affecting energy metabolism

As5+ uncouples oxidative phosphorylation

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11
Q

what is the common exposure of arsenic toxicity

A

contaminated ashes or water in cattle

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12
Q

what is the selectivity of target tissues to arsenic toxicosis?

A

targets tissues with high oxidative energy use (actively dividing cells) – intestinal epithelium, liver, kidney, spleen, epidermis

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13
Q

What is the most likely source of lead poisoning in cattle in North America?

A

Lead-acid batteries found on pasture

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14
Q

what metal has the greatest frequency of toxicosis and in what species

A

lead - primarily dogs & cattle

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15
Q

What treatment options are available for acute lead poisoning?

A

Remove lead objects from GI tract
Ca-EDTA
DMA/Succimer

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16
Q

What form of chromium is considered to contribute most to observed toxicosis?

A

Cr6+/CrVI is responsible for toxicity

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17
Q

exposure to Chromium for toxicosis

A

cattle exposed to oil sludge or drip + dermal contamination

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18
Q

What role does copper disposition play in susceptibility to copper toxicity

A

Normally [Cu] in the cell are kept low through Cu-binding proteins, but when too high the “free Cu ions” undergo redox rxn forming ROS

it can also accumulate in the liver = hepatotoxicity

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19
Q

what role does genetics play in Cu toxicity

A

Dogs with inherited/genetic metabolic defects impair biliary Cu excretion

bedlington terriers - COMMD1 gene
doberman pinscher - ATP7A & 7B mutation
Labs ATP7B polymorphism and RETN mutations

20
Q

clinical signs of Mercury toxicity

A

MeHg - neurologic
inorganic - GI & kidney
elemental Hg0 - kidney

21
Q

clinical signs of Cadmium toxicity

A

diffuse signs (aggression, anxiety, GI disturbance, mild anemia)

22
Q

clinical signs of Arsenic toxicity

A

sudden death, diarrhea, ataxia, dehydration, resp distress

23
Q

clinical signs of Lead toxicity

A

sudden blindness, aggression, head pressing, circling, roaring, anorexia, anemia, tonic-clonic epileptic seizures

24
Q

clinical signs of Chromium toxicity

A

inflam/damage to GI, kidney, liver, gastroenteritis, dermatitis

25
Q

clinical signs of Copper toxicity

A

dogs - chronic hepatitis
ruminants - pale mm, icterus/hepatic necrosis, degeneration, dark brown/red urine, abortion, mobilization of Cu from liver to kidneys

26
Q

clinical signs of Molybdenum toxicity

who is more at risk and why

A

ruminants>monogastrics bc rumen delays absorption with thiomolybdates

acute - feed withdrawal, lethargy, weakness, hind limb ataxia
chronic (ass w Cu def) - “teart scours”, weight loss, anemia, alopecia, lameness, poor production and reproduction
renal and hepatic degeneration/necrosis

27
Q

clinical signs of Iron toxicity

A

necrosis of GI, fluid loss, cardiotoxicity

28
Q

clinical signs of Manganese toxicity

A

neurological
high acute dose - liver damage

29
Q

clinical signs of Zinc toxicity

A

hemolytic anemia
renal damage w hematuria
urinary casts and proteinuria
foals - joint enlargements/stiff gait

30
Q

Mercury treatments

A

egg white, charcoal followed by DSMA or Succimer

31
Q

Cadmium treatments

A

minimize/reduce exposure
EDTA effective

NO BAL - increases nephrotoxicity
no DMSA/succimer - not effective

32
Q

Arsenic treatments

A

minimize/reduce exposure
GI detox
IV fluids
BAL
DMA/Succimer
Na thiosulfate

33
Q

Lead treatments

A

remove Pb objects from GI tract
Calcium Sodium-EDTA
DMSA/Succimer

34
Q

Copper treatments in dogs and ruminants

A

dogs - low copper diet, chelating agents (D-penicillamine & Trientine Hydrochloride), Zn supplementation

ruminants - fluids, blood transfusion, ammonium or sodium molybdate & sodium thiosulfate, ammonium tetrathiomolybdate, increased molybdenum in diet, Zn supplementation

35
Q

how does Zn supplementation affect Cu toxicity

A

Zn increases metallothionein which will then decrease Cu

36
Q

Molybdenum treatment

A

Cu supplementation (6:1 optimal Cu:Mo)
<2:1 Mo tox
>15:1 Cu tox

37
Q

Iron treatments

A

GI decontamination
cheating agent (deferoxamine)
symptomatic/supportive care

38
Q

Manganese treatment

A

avoid contamination
GI decontamination
chelation therapy (EDTA)
antioxidant therapy (vitamin E or N-acetylcysteine)
supportive/symptomatic care

39
Q

Zinc treatment

A

antacids
proton pump inhibitors
removal of Zn eluting foreign body
sucralfate
supportive care

chelation therapy controversial - only use after foreign body removed - use Ca-EDTA

40
Q

Zinc bioavailability decreases with what?

A

phosphates and calcium

41
Q

Zinc can be found in what

A

pennies
nuts/bolts
galvanizes steel
diaper cream
sunscreen

42
Q

What is the basis for the interaction of copper, molybdenum and sulfate in ruminants? What role does this play in potential toxicities?

A

Cu toxicity – adding molybdenum + sulfur → thiomolybdate in rumen which decreases Cu availability

43
Q

How does iron “exist” in living systems?

A

Highly regulated and controlled bc very active in redox rxn “Fenton rxn” - free iron will react with hydroxyl radicals (H2O2)

transferrin in blood, lactoferrin in milk, 80% bound to Hb, myoglobin and other heme enzymes, remaining is bound IC to ferritin and hemosiderin

44
Q

Iron exposure

A

supplements, vitamins, molluscides

45
Q

What role does pH play in potential zinc poisoning? How does zinc differ from other metals with regards to chelation therapy?

A

low pH releases Zn rapidly from ingested objects

chelation therapy controversial bc they will facilitate Zn absorption if foreign body is present

chelator of choice - Ca-EDTA

Toxicology (15 decks)

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