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BIO2380: Introductory Toxicology > Chapter 8: Metal Toxicity > Flashcards

Chapter 8: Metal Toxicity Flashcards

1
Q

What are metals and how can they be introduced to humans and the environment?

A

Metals are naturally occurring elements that can be introduced to humans and the environment through industrial, agricultural, and medical activities.

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2
Q

How do metals differ from many toxicants?

A

Metals differ from many toxicants because they are natural and do not quickly break down in the body or environment.

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3
Q

What is an example of a metal that is essential for cell function?

A

Zinc (Zn) is an example of a metal that is essential for cell function.

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4
Q

What kind of dose response curve would metals typically make?

A

Metals typically make a threshold dose-response curve.

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5
Q

How can metals exert toxic effects in the body?

A

Metals can exert toxic effects in the body by inhibiting critical enzyme function, forming highly reactive cations that contribute to oxidative damage, and replacing other metals by binding to molecular targets.

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6
Q

What is the contribution of oxidative damage to the toxicity of metals?

A

The formation of highly reactive cations by metals contributes to oxidative damage, which is a key factor in the toxicity of metals.

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7
Q

How can metals replace other metals in physiological processes?

A

Metals can replace other metals in physiological processes by binding to molecular targets and replacing the original metal.

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8
Q

Which metals can replace Zn in some physiological processes?

A

Cadmium (Cd), Copper (Cu), and Nickel (Ni) can replace Zinc (Zn) in some physiological processes.

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9
Q

What are the different types of metals and their toxicity levels to organisms?

A

The different types of metals and their toxicity levels to organisms depend on the metal. Major toxic metals (e.g., Pb, Cd) can be very toxic, while essential metals (e.g., Zn, Cu) and medicinal metals (e.g., platinum and bismuth) can also be toxic depending on the amount.

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10
Q

What is bismuth subsalicylate used for and what are its side effects?

A

Bismuth subsalicylate is used as an antacid and to kill bacteria that cause diarrhea. Its side effects can include black stool and black tongue, as well as interactions with various drugs.

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11
Q

How are platinum compounds used in pharmacology?

A

Platinum compounds have been effective for cancer chemotherapy, along with gallium and titanium compounds.

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12
Q

What is aluminum hydroxide used for?

A

Aluminum hydroxide is used in antacids.

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13
Q

What is gold salts and how are they used in pharmacology?

A

Gold salts are a form of gold that has been used in treating rheumatoid arthritis.

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14
Q

What is lithium used for?

A

Lithium is used for bipolar disorder.

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15
Q

What factors determine the relative toxicity of metals?

A

The route of exposure, dose, and duration and frequency of exposure are critical factors that determine the relative toxicity of metals.

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16
Q

What are the other important factors that contribute to metal toxicity?

A

Other important factors that contribute to metal toxicity include age, sex, genetics, and protection during any part of the toxicant disposition.

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17
Q

How do different types of proteins influence the disposition of metals in the body?

A

Different types of proteins influence the disposition of metals in the body in various ways. Non-specific binding to proteins (i.e., albumin and hemoglobin) can move metals throughout the body. Metallothioneins are specific metal-binding proteins that protect the cell by binding metals to prevent them from doing oxidative damage. Transferrin binds to Fe in the plasma to help transport it across cell membranes, and ceruloplasmin converts Fe to the right form to bind to transferrin. Ferritin is a primary cellular storage site for Fe and can sequester Fe in the cell if necessary, and it also binds Cd, Zn, beryllium, and Aluminum.

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18
Q

What is the function of metallothioneins?

A

Metallothioneins are specific metal-binding proteins that protect the cell by binding metals to prevent them from doing oxidative damage.

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19
Q

What is the function of transferrin?

A

Transferrin binds to Fe in the plasma to help transport it across cell membranes.

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20
Q

What is the function of ferritin?

A

Ferritin is a primary cellular storage site for Fe and can sequester Fe in the cell if necessary, and it also binds Cd, Zn, beryllium, and Aluminum.

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21
Q

What is mercury used for in dental fillings?

A

Mercury is mixed with silver for dental fillings.

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22
Q

What is the Minamata Convention of Mercury Use?

A

The Minamata Convention of Mercury Use is a UN treaty to limit mercury use.

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23
Q

What are some other uses of mercury?

A

Other uses of mercury include in thermometers and other gauges, mercury (tilt) switches, and Hg gas in fluorescent lightbulbs.

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24
Q

Who still uses mercury to extract gold and silver from ore?

A

‘Artisanal miners’ who produce 25% of global gold still use mercury to extract gold and silver from ore.

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25
Q

How is mercury vapor absorbed?

A

Mercury vapor is absorbed via inhalation, with 80% being inhaled.

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26
Q

How is liquid mercury absorbed in the body?

A

Liquid mercury is absorbed in small amounts in the gastrointestinal tract.

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27
Q

How are mercury salts absorbed in the body?

A

Mercury salts are barely absorbed in the gastrointestinal tract (only 10%).

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28
Q

What happens to organic mercury (methylmercury) once it is absorbed in the body?

A

Organic mercury is rapidly distributed throughout the body and can accumulate in the brain.

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29
Q

Who were the Mad Hatters, and how did they experience chronic mercury toxicity?

A

The Mad Hatters were hat makers who used mercury salts when making beaver-felt hats. They experienced chronic mercury toxicity.

30
Q

What was mercury used for in the past?

A

Mercury was used to treat syphilis.

31
Q

What is the symptom of late-stage syphilis?

A

The symptom of late-stage syphilis is excessive saliva, or “frothing at the mouth crazy.”

32
Q

What are some toxic effects of mercury vapor?

A

High doses of mrcury vapor inhaled can cause acute bronchitis that can be lethal, and it is also neurotoxic and can cause tremors and erethism (memory loss, increased excitability, insomnia, depression, and shyness).

33
Q

What are some toxic effects of mercury salts?

A

Mercury salts (Hg+1 and Hg+2) can cause kidney damage leading to kidney failure in high doses, and can non-specifically bind to –SH groups on proteins, but have limited neurotoxic effects.

34
Q

Who is particularly vulnerable to the neurotoxic effects of organic mercury?

A

Children and fetuses are particularly vulnerable to the neurotoxic effects of organic mercury, such as methylmercury and dimethylmercury, which can cause paresthesia (numbness), ataxia (lack of coordinating muscle movement), and blindness.

35
Q

What are some mechanisms by which MeHg causes neurotoxicity?

A

In cell cultures, MeHg can cause ROS generation, glutathione reduction, high intracellular Ca2+ levels, and mitochondrial damage, which can lead to apoptosis or necrosis in nerve cells. MeHg can also inhibit membrane ion transporters, causing astrocytes to swell and burst.

36
Q

What are astrocytes and how are they affected by MeHg?

A

Astrocytes are a type of glial cell in the brain that surround neurons and hold them in place, supply nutrients and oxygen to neurons, insulate one neuron from another, and destroy pathogens and remove dead neurons. MeHg can cause astrocytes to swell and burst, potentially inhibiting their ability to perform these functions properly.

37
Q

What caused Minamata disease?

A

Minamata disease was caused by a chemical factory in Japan that dumped inorganic mercury salts into the bay, which were converted to MeHg by bacteria and biomagnified in fish.

38
Q

What were the symptoms of Minamata disease?

A

The symptoms of Minamata disease included central and peripheral nervous system degeneration, tingling and numbness of limbs, impaired motor function, impaired vision and speech.

39
Q

What happened in Iraq in 1971 and what were the consequences?

A

In 1971, grain shipped as aid to Iraq was coated in methylmercury to prevent fungal growth and colored with pink dye to show toxicity. However, it was not labeled in the appropriate language and was consumed instead of being planted, resulting in 6,530 patients being admitted to the hospital with poisoning, and 459 deaths were reported.

40
Q

How did the First Nations communities in Ontario, Canada, become impacted by mercury contamination?

A

The First Nations communities in Ontario, Canada, became impacted by mercury contamination by consuming methylmercury contaminated fish in the late 1960s. The mercury contamination was caused by dumping waste from pulping mills, which resulted in over 9000 kg of mercury being dumped from 1962 to 1970.

41
Q

What is kohl and where was it developed?

A

Kohl is a mixture of lead sulfide and other resins used as a mascara. It was developed in Egypt around 3100 BC.

42
Q

What was the purpose of tetraethyl lead (TEL) in gasoline and who patented it?

A

TEL was used as an anti-knocking agent in gasoline, replacing ethanol. It was patented by Thomas Midgley at General Motors.

43
Q

When was TEL phased out of gasoline, and why?

A

The EPA indicated in 1972 that TEL was to be phased out of gasoline due to concerns about lead toxicity. Ethyl corporation sued, but lost. It took until 1982 to completely ban it.

44
Q

What developmental effects can low doses of lead cause in exposed children?

A

Research published in 1979 showed that even low doses of lead can cause developmental effects in exposed children, such as lower IQ ratings.

45
Q

What is the primary use of lead today?

A

88% of lead is now used in batteries.

46
Q

What are some other sources of lead exposure besides old paint and piping?

A

Glass and ceramics, ammunition, solder (electronics), soil and food.

47
Q

How does calcium intake affect lead absorption in the GI tract?

A

Calcium intake can increase the absorption of lead in the GI tract since Pb2+ has similarities to calcium.

48
Q

What percentage of ingested lead is absorbed by growing children?

A

Growing children can absorb 50% of ingested lead.

49
Q

Where is lead primarily stored in the body?

A

Lead is primarily stored in bones and teeth, with a half-life of 20 years.

50
Q

How can teeth be used to estimate childhood lead exposure?

A

Teeth can be tested to estimate childhood lead exposure since lead is stored in them.

51
Q

Does lead readily cross the blood brain barrier?

A

Yes, lead can readily cross the blood brain and placental barriers with a 2-year half-life in the blood.

52
Q

What happens to neuronal cells at high doses of Pb2+?

A

High doses of Pb2+ trigger apoptosis and necrosis in neuronal cells, inhibiting ATP production, superoxide dismutase activity, and exacerbating ROS generation.

53
Q

What is the effect of low doses of Pb2+ on neuronal functions?

A

Low doses of Pb2+ interfere with neuronal functions by inhibiting neurotransmission between neurons and decreasing neuron growth and development in the young.

54
Q

How does internal Pb2+ affect normal neuronal function?

A

Internal Pb2+ dampens the signal in normal neuronal function, causing fewer neurotransmitters to be released into the synaptic cleft and propagating the signal to the next neuron.

55
Q

What is the effect of lead on heme biosynthesis?

A

Lead inhibits many steps in heme biosynthesis, especially ALA dehydrogenase and ferrochelatase, which can result in anemia.

56
Q

What is the effect of lead on neuronal function at high doses?

A

At high doses, lead triggers apoptosis and necrosis in neuronal cells by inhibiting ATP production in the mitochondria, inhibiting superoxide dismutase activity, and exacerbating ROS generation.

57
Q

How does lead affect normal neuronal function?

A

Low doses of lead interfere with normal neuronal function by inhibiting neurotransmission between neurons and decreasing neuron growth and development in young individuals.

58
Q

What is the half-life of lead in bones and teeth?

A

The half-life of lead in bones and teeth is 20 years.

59
Q

What is the primary source of human exposure to As?

A

Drinking water sources.

60
Q

What is the recommended maximum level of As in drinking water according to the WHO?

A

10 ppb.

61
Q

What are some classic dermatitis patterns caused by chronic exposure to As?

A

Dermatitis patterns are most often seen on the feet and hands.

62
Q

What are some uses of arsenic?

A

Arsenic has some industrial chemical synthesis uses, is a component of CCA treated wood, was previously used as a pesticide, and is often used as a poison (arsenic trioxide).

63
Q

How is arsenic metabolized in the liver?

A

Arsenic gets methylated in the liver to methyl-As, which is not as toxic as free As.

64
Q

What are some symptoms of arsenic poisoning?

A

Symptoms of arsenic poisoning resemble food poisoning, dysentery, and cholera.

65
Q

What are the acute toxic effects of arsenic?

A

The acute toxic effects of arsenic include mitochondrial respiration poisoning, interference with ATP synthase, inhibition of pyruvate dehydrogenase, death from cardiovascular failure due to insufficient ATP, replacement of S in thiol groups, inhibition of protein functions, necrosis of GI tract leading to internal bleeding, and skin cancer.

66
Q

What are the chronic toxic effects of arsenic?

A

The chronic toxic effects of arsenic include liver injury, cardiovascular disease, neurological disorders, and impaired cognitive development in children.

67
Q

What are the most common types of cancer caused by arsenic?

A

The most common types of cancer caused by arsenic are fatal skin cancers, as well as cancers of the liver, lung, and bladder.

68
Q

What is the synergistic factor in causing cancer when combined with arsenic?

A

UV radiation is the synergistic factor in causing cancer when combined with arsenic.

69
Q

How can arsenic alter the epigenetic regulation of genes important in carcinogenesis?

A

Methylation of As may deplete the SAM pool, which thus alters the epigenetic regulation of genes that are important in carcinogenesis.

70
Q

How does biotransformation of arsenic damage DNA?

A

The biotransformation of arsenic generates ROS, which can damage DNA in two ways: a) direct strand breakage and b) oxidizing guanine base pairs to form 8-hydroxyguanine.

BIO2380: Introductory Toxicology (16 decks)

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