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Toxicology Final > Metal Toxicity II > Flashcards

Metal Toxicity II Flashcards

1
Q

Does metal in general metabolize?

A

No the have a long half life in the body.

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2
Q

What occurs when As is absorbed as soluble As salts?

A

80-90% Oral bioavailability.

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3
Q

As has good dermal what?

A

absorption

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4
Q

As inhalation is mainly in what?

A

As2O3, it is size dependent.

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5
Q

As distribution for skin is what?

A

predilection for skin, excreted in sweat (cancer).

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6
Q

As is found accumulated where for forensic uses?

A

concentrated in nails and hair.

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7
Q

Elimination of As in blood t1/2?

A

10-30hr

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8
Q

What is the main route of elimination for As?

A

urine (50-80% excreted in about 3 days)

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9
Q

Which As is recovered in urine?

A

High recovery as As (V) in urine.

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10
Q

DMA as a major form is what?

A

excreted in urine.

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11
Q

What does elemental Hg do to the renal system?

A

Kidney dysfunction

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12
Q

What are the symptoms for elemental Hg?

A

Asthenic vegetative syndrome: severe salvation, increased tremor, depression.

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13
Q

What does inorganic Hg salts do to renal?

A

predominant glomerular injury (model toxicant)

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14
Q

What is pink disease?

A

acrodynia

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15
Q

What is Acrodynia?

A

Erythema of extremities, chest, and face with photophobia.

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16
Q

What element causes pink disease?

A

Inorganic Hg salts.

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17
Q

What are the neurological implications of Organic Hg(MeHg)?

A

Visual disturbance, hearing loss, mental deterioration, muscle tremors, movement disorder (cerebral cortex), microcephaly.

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18
Q

6% of woman of childbearing age have what?

A

blood mercury levels in excess of the EPA reference dose.

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19
Q

uncharged Hg is what?

A

very lipophilic

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20
Q

inhaled mercury vapor produces what?

A

selective damage to brain function.

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21
Q

Mercury vapor readily crosses pulmonary membranes and enters what?

A

the bloodstream where is dissolves in plasma.

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22
Q

Once passing the blood-brain barrier what occurs to Hg0?

A

is oxidized to a highly reactive metabolite, Hg++ by catalase.

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23
Q

Demethylation increases what?

A

Mercury toxicity.

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24
Q

What occurs in demethylation of methymercury?

A

Lipid peroxidation and it binds to soft tissue ligands.

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25
Q

Cysteine complex of MeHg enters what?

A

brain using amino acid carrier.

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26
Q

The hemolytic cleavage of the carbon-Hg bond produces what?

A

methyl free radicals that initiate the lipid peroxidation.

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27
Q

MeHg-Cysteine complex mimics what?

A

Methionine

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28
Q

What does MeHg-Cysteine complex inhibits?

A

Protein synthesis in neuronal cells.

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29
Q

MeHg initiates what?

A

Free radical reactions

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30
Q

What does Fe-catalyzed what?

A

Free radical reactions.

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31
Q

Lipid peroxidation causes what?

A

membrane damage

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32
Q

What does DNA oxidation cause?

A

strand breaks, mutations.

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33
Q

What does protein oxidation cause?

A

loss of enzyme activity, transport system.

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34
Q

What does the Fenton reaction portray?

A

Fe-Catalyzed Free radical reactions.

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35
Q

Transcriptional alteration of DNA is an example of what?

A

Alteration of gene expression

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36
Q

Translational alteration at mRNA level is an example of what?

A

Alteration of gene expression.

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37
Q

Post-Translational alteration at proteins expression level is an example of what?

A

Alteration of gene expression.

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38
Q

What can take over Sp1 and will bind to DNA?

A

Lead

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39
Q

Lead may alter brain development through modulation of what?

A

The zinc finger protein SP1 It will take the place of zinc easily.

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40
Q

Sp1 is a component of what?

A

Transcriptional complex for gene regulation.

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41
Q

Target genes encode what?

A

MBP, PLP, and other proteins.

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42
Q

What is MBP?

A

Myelin basic protien

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43
Q

What is PLP?

A

proteolipid protein

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44
Q

What kind of cancer does Cr cause?

A

Respiratory cancer in chrome worker

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45
Q

What kind of cancer does Cd cause?

A

Cancer in lung, prostate, testes, and kidney.

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46
Q

What kind of cancer does Ni cause?

A

Lung and Nasal cancers via air.

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47
Q

What kind of cancer does As cause?

A

Lung cancers via air, Skin cancer via drinking water.

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48
Q

What kind of cancer does Si cause?

A

Lung cancer via air.

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49
Q

What is known as asbestos main reactant?

A

Si.

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50
Q

Who is sensitive to cadmium via inhalation?

A

Humans and rats

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51
Q

Who is NOT sensitive to cadmium via inhalation?

A

Mice and hamster

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52
Q

Who is sensitive to Arsenic via all routes?

A

Human

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53
Q

Who is not sensitive to arsenic via any route?

A

Rats and Mice

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54
Q

What is direct genotoxicity of metal induced carcinogenesis?

A

DNA damage, altered infidelity of DNA synthesis, altered gene expression due to DNA binding.

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55
Q

What is indirect genotoxicity of metal induced carcinogenesis?

A

Inhibition of DNA repair, generation of free radicals.

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56
Q

What are the interactions with regulatory proteins in the metal induced carcinogenesis?

A

Finger loop proteins.

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57
Q

What is the immunotoxicity of metal induced carcinogenesis?

A

Immunosuppression.

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58
Q

What type of damage to DNA does metal induced carcinogenesis cause?

A

Single strand damage, Double strand damage, DNA-DNA crosslink damage, DNA protein crosslink damage, and Free radical damage.

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59
Q

All metal carcinogens act by the same what?

A

Mechanism

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60
Q

What is the mechanism for all metal carcinogens.

A

The same mechanism

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61
Q

An individual metal has what?

A

The same mechanism in all target tissue.

62
Q

An individual metal has exclusive what?

A

Genotoxic or non-genotoxic mechanisms.

63
Q

Ionic form of the metal is what?

A

The carcinogenic species.

64
Q

Slenium has what so special about it?

A

Anti- Carcinogenic property.

65
Q

What metal is associated with Alzheimers etiology?

A

Lead exposure.

66
Q

What metal is associated with Parkinson’s etiology?

A

Manganese exposure.

67
Q

What are there neurodegenerative symptoms that lead cause?

A

Learning deficiency causes of Alzheimer disease presumed.

68
Q

What are the the neurodegenerative symptons that manganese cause?

A

High concentration in striatum in Manganism patients and implication in mad cow.

69
Q

What does Cu overload cause?

A

ATP7B genetic defect leading to Wilson’s Disease.

70
Q

What causes Wilson’s disease?

A

an overload of copper due to the defective ATP7B gene.

71
Q

What causes Menkes disease?

A

A copper deficiency due to the defective ATP7A gene.

72
Q

What does a copper deficiency due to the defective ATP7A gene cause?

A

Menke’s disease.

73
Q

Iron is found in the implication of what disease?

A

Parkinson’s

74
Q

Mercury causes what type of neurodegenerative symptoms?

A

Developmental learning deficit.

75
Q

Al will cause what type of neurodegenerative symptoms?

A

Dialysis encephalopathy, motor neuron degeneration.

76
Q

What can be seen at high concentrations of Zn and Cu in the brain in imaging?

A

Most distinct distribution pattern in the hippocampus up to 15ug/g

77
Q

Lead shows what type of distribution in brain imaging?

A

A more homogenous distribution throughout all regions and at a low concentration in ng/g range.

78
Q

What is bone made up of?

A

5-10% of water, 50-70% apatite, 20-40%organics aka collagen, 10% non collagen proteins (osteocalcin and etc)

79
Q

What has 80% of compact bone?

A

Cortical bone

80
Q

What has 20% of spongy bone?

A

Trabecular bone

81
Q

Explain bone remodeling?

A

Life time, cycles of resporption and accretion

82
Q

What is the bone toxicity in Cd exposure?

A

Causes Itai-Itai disease

83
Q

What is Itai-Itai disease?

A

Osteoporotic bone loss and increased fragility.

84
Q

What is the bone toxicity in Pb exposure?

A

Lead line in long bones occurs. It inhibits osteoblasts and slows bone formation.

85
Q

What is the bone toxicity in Al exposure?

A

Osteitis, osteodystrophy; altered bone metabolism.

86
Q

Borne is a major storage site for which metals?

A

Ca, Mg, Zn, and Cu.

87
Q

What is lead in bone linked to?

A

Children with Pb toxicity and Alzheimer’s risk.

88
Q

Why do metals store in bones?

A

A defense mechanism for body protection.

89
Q

Give an example of Bone as an internal source of exposure?

A

Slow release Pb form bone is a known source of chronic Pb exposure.

90
Q

What are industrial sources of Al exposure?

A

Modern industrial uses of Al: occupation environmental exposure.

91
Q

What are medical sources of Al exposure?

A

Dialysis dementia: renal failure.

92
Q

What are prenatal sources of Al exposure?

A

Parental nutrition to preterm infants.

93
Q

What bone diseases that Al cause?

A

Osteodystrophy, osteomalacia, and adynamic bone disease.

94
Q

What causes hematopoietic toxicity?

A

Aluminum in the bone

95
Q

What is the t1/2 of Al in bone?

A

7.2 years

96
Q

Al is known to have a large volume of distribution (T/F)

A

True

97
Q

34% of total body Al is where?

A

In bone.

98
Q

Al inhibits what?

A

Bone remodeling

99
Q

Al hinders both what?

A

Osteoblast and osteoclast activities.

100
Q

Al disrupts what?

A

Parathyroid hormone levels

101
Q

Al forms a physical barrier to for what reason?

A

to interfere bone calcification.

102
Q

Infants having parenteral nutrition have significantly less what?

A

Less lumbar spine bone mineral contents and smaller bone area at age 13-15y/o

103
Q

Subjects with neonatal Al exposure have what type of bone issues?

A

Significantly lower hip bone mass, independent of their bone or body size.

104
Q

Parenteral nutrition in preterm infants can lead to what?

A

cognitive deficiency.

105
Q

Al modifies the response of what?

A

Bone cells to external stimuli such as subsequent loading from physical activity or nutritional exposure.

106
Q

Manifestation of Al neurotoxicity mechanism is what?

A

Al toxicity on hypothalamus affects the secretion of neuropeptides that controls bone remodeling.

107
Q

t 1/2 of Mn in rat bone is what?

A

143 days

108
Q

for the t 1/2 life of Mn in rat bones being 143 days, how does that translate to human bone half life?

A

8.6 years for Mn.

109
Q

What is the MOST important thing you can do in treatment f metal poisoning and NEEDS to be done first!?

A

Remove the person from the environment in which metal exposure occurs.

110
Q

What is the number 2 thing that needs to be done in order to treat metal poisoning?

A

Treat symptoms that may threat individual’s life.

111
Q

What is the last thing done in metal poisoning treatment.

A

Treat with metal mobilizing drug: chelator or chelating agent to reduce body burden.

112
Q

Chelate comes from what root?

A

Greek word chele meaning crab’s claw.

113
Q

Chelating agents provide what?

A

An electron rich group to form covalent bonds with metals in a coordinate ring structure.

114
Q

Chelates form stable complexes between what?

A

Chelator and metals.

115
Q

What do the stable complexes that chelator and metal form do?

A

Prevent or reverse the binding of metals to cellular ligands.

116
Q

The formed complexes are soluble in what?

A

Water soluble and more readily excreted from the body.

117
Q

What is the chelating regimen?

A

four days and then pause for 3 days.

118
Q

Why does the chelating regimen pause?

A

to give the body time to recooperate and release more metal from the bones.

119
Q

Why is EDTA an issue with kids for administration?

A

It is IV injection and not oral dose.

120
Q

What is provacative or challenge test for Pb burden?

A

EDTA

121
Q

EDTA causes what type of toxicity?

A

Renal tox.

122
Q

DMSA has what type of toxicity?

A

Low tox and doesn’t interfere with essential metals.

123
Q

DMSA is administered how for lead eposure?

A

Orally and has no CNS redistribution.

124
Q

D-PEN is commonly used for what?

A

Hg poisoning

125
Q

What will facilitate Hg absorption?

A

D-PEN

126
Q

DMSA is beneficial effects are similar to what for Hg?

A

those of DMPS

127
Q

What may limit the intracellular distribution of DMSA in Hg exposure?

A

Two carboxyl groups

128
Q

DMPS was created for what?

A

Increase urinary excretion of Hg.

129
Q

DMPS administration and side effects for Hg exposure?

A

low side effects and available in IV and orally

130
Q

For As what was the firs chelating agent to treat organic arsenical war gas?

A

British Antilewisite aka BAL

131
Q

What is BAL primarily used for?

A

Severe As poisoning, deep intramuscular injection, and CNS redistribution.

132
Q

DMPS for As increases what?

A

Urinary excretion of arsenic

133
Q

DMPS formed water soluble complex that is what?

A

Less penetrable to CNS

134
Q

DMPS clinically is what for As?

A

Improves significantly the symptoms.

135
Q

DMSA for As has similar benefits to what?

A

the effects of DMPS

136
Q

DMSA Chelates As where?

A

Extracellular As

137
Q

What is Cd therapy?

A

No therapeutic agent.

138
Q

Cd tightly binds to what?

A

Metallothionein.

139
Q

What do chelators potentiate in Cd?

A

nephrotoxicity

140
Q

What does EDTA reduce in Mn exposure?

A

Serum Mn concentration

141
Q

What does EDTA increase in Mn exposure?

A

Urinary Mn elimination

142
Q

What does EDTA improve in Mn exposure?

A

Symptoms improve and varies widely.

143
Q

What does DMSA neglect in Mn exposure?

A

It has a negligible effect

144
Q

What does DMSA possible unable to do in Mn exposure?

A

Unable to access intracellularly distributed Mn ions.

145
Q

What does PAS do in Mn exposure?

A

Alleviate signs and symptoms

146
Q

What is PAS?

A

An antibacterial drug for treatment for tuberculosis.

147
Q

What is the chelator for Uranium?

A

No proven chelator available.

148
Q

What is an effective treatment in Wilson’s diseases in regards to copper?

A

D-Penicillamine

149
Q

What is a general chelator for copper?

A

DMPS and Mercaptodextran

150
Q

What are chelation agents for Zinc?

A

N-Acetylcystein and Clinoquinol

151
Q

Metals are known to participate in the what of human disease?

A

Etiology

152
Q

What should therapeutic intervention consist of?

A

removal of patient from exposure, followed by symptomatic relief, then chelation Tx.

Toxicology Final (7 decks)

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