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Toxicology Final > Metals I > Flashcards

Metals I Flashcards

1
Q

Class A metals

A

Hard- highly stable and preferentially bind anions with O2 as electron donors

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2
Q

Class B metals

A

Soft metals- pronounced preference for S and N. certain soft acids bind strongly with Se

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3
Q

intermediate metals

A

ligand-binding characteristics that are intermediate to soft and hard, but still readily bind with S

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4
Q

Class B important metals

A

Mercury (Hg)
Cadmium (Cd)

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5
Q

Intermediate important metals

A

Arsenic (As)
Lead (Pb)

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6
Q

what do the relevant class B and intermediate metals all have in common (for this class purposes)

A

all of these elements bind with sulfur (thiols) in biological systems

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7
Q

thiol groups

A
  • present in residues of proteins and enzymes
  • important for structure and function: located within the active sites of enzymes, and directly involved in catalysis
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8
Q

molecular targets of Class B and Intermediate elements

A

thiols

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9
Q

metal ligand interactions

A

animal cells are heterogenous that have many sites for metal binding
also have metal binding proteins: metallothionein: which can detoxify metals to some extent
- if too prevalent, metals overwhelm antioxidant defenses and result in oxidative stress

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10
Q

metallothionein (MT)

A
  • low molecular weight protein
  • 30% of amino acid residues are cysteine (therefore MT has a large # of thiols)
  • 1 molecule of MT can bind 7 atoms of Cd and other metals
  • certain metals are strong inducers of MT
  • MT can sequester heavy metals and prevent oxidation of critical protein
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11
Q

what is special about MT binding?

A

1 molecule of MT can bind 7 atoms of Cd and other metals

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12
Q

what is the purpose of binding “prevalences”?

A
  • help determine how metals are distributed in animal cells
  • used when treating patients in a clinical setting
  • detoxification involves preventing inappropriate binding of non-essential metals with sensitive sites
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13
Q

adverse outcome pathway

A

framework for understanding toxic effects at various levels of biological organization
- effects to individuals and populations are anchored to toxicant/molecular interactions

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14
Q

Mercury (Hg) as a global contaminant

A
  • emission sources include mining, coal combustion, volcanic eruptions
  • elemental mercury vapor can travel for up to a year or more in the atmosphere!!
  • deposits where it rains most!
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15
Q

various forms of Mercury (Hg)

A
  1. Metallic: Hg0
  2. Inorganic: Hg II, HgS, HgCl2
  3. Organic: MeHg
    toxicity of these various forms differ (MeHg is most toxic)
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16
Q

what form of mercury is most toxic?

A

Methyl Mercury: MeHg: is bound to carbon

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17
Q

metallic mercury (Hg0)

A
  • lipid soluble
  • not well absorbed in Gi
  • readily absorbed as vapor in lungs
  • neurotoxicant!!
  • oxidized to HgII in blood, then accumulates in kidneys
  • toxicities rare because it is the “visible” form (liquid metal)
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17
Q

organic mercury

A
  • highly bioavailable- cross the BBB!!!
  • 90-95% absorbed in the GI
  • potent neurotoxicant especially for the developing fetus
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18
Q

inorganic mercury

A
  • damage to kidneys! filters and accumulates
  • more readily absorbed in GI than metallic
  • oral route damages GI and kidneys
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19
Q

what form of mercury crosses the BBB and is neurotoxic esp for the developing fetus?

A

organic: MeHg

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20
Q

what form of mercury is found highest in the kidneys?

A

inorganic

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21
Q

methylmercury uniqueness

A
  • the structure resembles the essential amino acid methionine
  • amino acid transporter helps cysteine-MeHg cross the BBB through “molecular mimicry”
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22
Q

methylmercury properties

A
  • elemental Hg oxidized to inorganic Hg in atmosphere
  • inorganic Hg is removed from atmosphere during dry or wet deposition
  • inorganic Hg is converted by bacteria to MeHg (mainly in aquatic environments)
  • MeHg bioaccumulates in organisms and biomagnifies in food webs
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23
Q

where does MeHg bioaccumulate?

A

in organisms and biomagnifies in food webs

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24
Q

“dancing cat” disaster in Japan - Minamata

A
  • cats were eating fish and died of mercury poisoning because a factory had been contaminating water
  • excessive salivation, convulsions, collapsed dead, jumped into sea to drown
    Minamata - alerted world to MeHg toxicosis!
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25
Q

clinical signs of Hg toxicity

A
  • ataxia
  • salivation
  • blindness
  • tremor/convulsions
  • GI disturbance (inorganic)
  • kidney damage (inorganic and elemental)
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26
Q

treatment of mercury toxicosis

A
  • acute exposure, inorganic Hg: egg white, charcoal followed by DMSA or Succimer: lots of thiols
  • MeHg often futile by time of clinical signs: too much in brain
    bind up and get it away!
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27
Q

Hg poisoning in domestic animals

A

uncommon, but related to obsolete products
- ex dog broke into a barometer: necrosis in liver and kidney
- sled dogs in Yukon exposed to MeHg thru consumpion of fish! MeHg is more bioavailable than inorganic or elemental Hg

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28
Q

Cadmium

A
  • soft, silver-white metal
  • cadmium oxide, cadmium chloride, cadmium sulfate
  • used in batteries, semiconductors, solar cells, plastics
  • enters environment from coal combustion, mining activities, zinc smelting, sewage sludge as fertilizers
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29
Q

how do animals get exposed to cadmium?

A
  • Cd containing mineral supplements in feed and application of phosphate fertilizers and sewage sludge on pastures/fields increases Cd in soils
  • cattle grazing on sewage sludge-treated pastures
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29
Q

cadmium + tobacco

A
  • some plants concentrate Cd from soils (clover, willow, tobacco)
  • cadmium exposure and accumulation in cats play a role in feline hypertension
  • cigarette burning! generates high levels of calcium oxide
30
Q

cadmium PK

A
  • GI absorption low: 5-8%
  • dietary deficiency of calcium can increase uptake
  • cadmium may replace copper and zinc at binding sites, causing an induced copper deficiency?
31
Q

what metal can cause an induced copper deficiency?

A

cadmium! may replace copper and zinc at binding sites

32
Q

where does cadmium bind?

A

plasma proteins (thiols) and RBC and is distributed to liver and kidney

33
Q

clinical signs of cadmium toxicity

A

aggression, anxiety, GI disturbance, mild anemia

34
Q

treatment of cadmium toxicity

A
  • minimize/reduce exposure
  • EDTA, BAL, DMSA are not effective (chelating agents)
  • BAL can increase nephrotoxicity!!!
35
Q

arsenic properties

A
  • metalloid, but often classified as a metal
  • inorganic and organic forms
  • binds to sulfur in cells
  • toxicity varies with form
36
Q

what form of arsenic is the most toxic?

A

Arsenite (As+3) is more toxic than Arsenate (as+5) and inorganic forms are more toxic than organic forms (opposite of mercury!)

37
Q

what is more toxic, arsenate or arsenite?

A

arsenite: As+3

38
Q

order of toxicity of arsenic from greatest to least

A

As+3 > As+5 > O As+3 > O As+5

39
Q

sources/uses of As

A
  • insecticides
  • immiticide (heartworm)
  • herbicides
  • treated wood !
  • water
40
Q

what does Arsenite (As+3) do?

A

binds with lipoic acid (cofactor in TCA cycle) thus effecting energy metabolism

41
Q

what does arsenate (As+5) do?

A

uncouples oxidative phosphorylation because it competes with phosphate during conversion of ADP to ATP

42
Q

target tissues of Arsenic (AS)

A

those with high oxidative energy use: actively dividing cells:
- intestinal epithelium
- liver
- kidney
- spleen
- epidermis

43
Q

clinical signs of As toxicity

A

sudden death, abdominal pain/colic, V+, staggering gait, watery D+, dehydration, resp distress
- alot to do with GI!

44
Q

treatment of As toxicity

A
  • minimize exposure
  • GI decontamination
  • IVF
  • Dimercaprol (BAL- British)
  • Dimercaptosuccinic acid (DMSA, Succiner)
    get thiols in there to bind to arsenic!
45
Q

how would animals get lead (Pb) toxicosis?

A
  • batteries!!
  • lead weights, curtains, fishing, paints, shot, pastures near Pb smelters, leaded gas
46
Q

what is the highest frequency metal that causes toxicity in animals?

A

LEAD!!

47
Q

Pb poisoning in domestic animals is encountered how often

A

OFTEN! greatest frequency compared to any other metal

48
Q

what is the main source of lead poisoning in american cattle?

A

lead-acid batteries found on agricultural pasture land!
main entry thru GI

49
Q

lead metabolism

A
  • organic lead compounds are more bioavailable than inorganic or metallic
  • calcium deficiency leads to increased absorption
  • cattle and dogs are most commonly reported with Pb intoxication
50
Q

clinical signs of Lead toxicity

A

neurotoxicity and blindness!
- aggression, blindness, head pressing, circling, roaring, anorexia, anemia

51
Q

treatment of Lead (Pb) toxicity

A
  • remove Pb objects from GI tract!
  • Ca-EDTA: chelating agent!
  • DMSA, Succimer
52
Q

what abnormalities on a blood smear could make you suspicious of lead poisoning?

A

pyknotic nuclei, polychromasia, basophilic stippling

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Toxicology Final (4 decks)

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