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Toxicology Final > Metals I > Flashcards

Metals I Flashcards

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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
"dancing cat" disaster in Japan - Minamata
- 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!
25
clinical signs of Hg toxicity
- ataxia - salivation - blindness - tremor/convulsions - GI disturbance (inorganic) - kidney damage (inorganic and elemental)
26
treatment of mercury toxicosis
- 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!
27
Hg poisoning in domestic animals
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
28
Cadmium
- 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
29
how do animals get exposed to cadmium?
- 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
29
cadmium + tobacco
- 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
cadmium PK
- 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
what metal can cause an induced copper deficiency?
cadmium! may replace copper and zinc at binding sites
32
where does cadmium bind?
plasma proteins (thiols) and RBC and is distributed to liver and kidney
33
clinical signs of cadmium toxicity
aggression, anxiety, GI disturbance, mild anemia
34
treatment of cadmium toxicity
- minimize/reduce exposure - EDTA, BAL, DMSA are not effective (chelating agents) - BAL can increase nephrotoxicity!!!
35
arsenic properties
- metalloid, but often classified as a metal - inorganic and organic forms - binds to sulfur in cells - toxicity varies with form
36
what form of arsenic is the most toxic?
Arsenite (As+3) is more toxic than Arsenate (as+5) and inorganic forms are more toxic than organic forms (opposite of mercury!)
37
what is more toxic, arsenate or arsenite?
arsenite: As+3
38
order of toxicity of arsenic from greatest to least
As+3 > As+5 > O As+3 > O As+5
39
sources/uses of As
- insecticides - immiticide (heartworm) - herbicides - treated wood ! - water
40
what does Arsenite (As+3) do?
binds with lipoic acid (cofactor in TCA cycle) thus effecting energy metabolism
41
what does arsenate (As+5) do?
uncouples oxidative phosphorylation because it competes with phosphate during conversion of ADP to ATP
42
target tissues of Arsenic (AS)
those with high oxidative energy use: actively dividing cells: - intestinal epithelium - liver - kidney - spleen - epidermis
43
clinical signs of As toxicity
sudden death, abdominal pain/colic, V+, staggering gait, watery D+, dehydration, resp distress - alot to do with GI!
44
treatment of As toxicity
- minimize exposure - GI decontamination - IVF - Dimercaprol (BAL- British) - Dimercaptosuccinic acid (DMSA, Succiner) get thiols in there to bind to arsenic!
45
how would animals get lead (Pb) toxicosis?
- batteries!! - lead weights, curtains, fishing, paints, shot, pastures near Pb smelters, leaded gas
46
what is the highest frequency metal that causes toxicity in animals?
LEAD!!
47
Pb poisoning in domestic animals is encountered how often
OFTEN! greatest frequency compared to any other metal
48
what is the main source of lead poisoning in american cattle?
lead-acid batteries found on agricultural pasture land! main entry thru GI
49
lead metabolism
- 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
clinical signs of Lead toxicity
neurotoxicity and blindness! - aggression, blindness, head pressing, circling, roaring, anorexia, anemia
51
treatment of Lead (Pb) toxicity
- remove Pb objects from GI tract! - Ca-EDTA: chelating agent! - DMSA, Succimer
52
what abnormalities on a blood smear could make you suspicious of lead poisoning?
pyknotic nuclei, polychromasia, basophilic stippling
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Toxicology Final (4 decks)

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