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toxicology > 9. food toxicology > Flashcards

9. food toxicology Flashcards

1
Q

Food contains nutrients and non-nutrient substances

A

(anything other than carbohydrates, proteins, fats, vitamins/minerals)

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2
Q

Non-nutrients substances are found in

A

‘natural’ foods Also found in heavily processed foods

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3
Q

How is it possible to control what people eat?

A

The Food, Drug and Cosmetics Act (USA) presumes that food is safe if it is free of certain contaminants
• To ban foods, there needs to be clear evidence that death or illness can result from consuming it (this is hard to do…)
• Stuff can be added to food if it falls into a class called ‘Generally Recognized As Safe (GRAS)’
• Food color additives fit within this category
• Certified color additives have the prefix FD&C (e.g., FD&C Blue No. 1)
• Others that are natural in origin, don’t even need certification.

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4
Q

• Many different types of natural toxins that we can react to in our food, the ones we will cover in detail are:

A
  1. Fish and shellfish poisoning 2. Delicious meat
  2. Mycotoxins
  3. Botulism
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5
Q

First, let’s go over how nerve impulse transmission works

A

Step 1. Na+/K+ pumps move Na+ ions out of the nerve cell, and K+ ions in.
Charges of other molecules inside the axon block the +ive charge of the K+ ions.
Thus, a resting state is achieved with a greater +ive charge on the outside of the cell due to the Na+ ions
Outside of nerve axon
Step 2
• When the neuron ‘fires’ it lets the Na + ions back in through sodium channels
• This occurs in a ‘wave’ of depolarization that flows down the nerve axon
• The sodium channels quickly close to allow the neuron to go back to its resting state

So, anything that interferes with this process will interfere with nerve signalling…

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6
Q

Shellfish Poisoning

Toxins are produced by

A

aquatic diatoms and dinoflagellates

Different diatoms & dinoflagellates can produce different toxins.
The type and degree of toxicity depends on the toxin produced.
Humans normally get poisoned by eating shellfish (which are filter feeders) that have eaten these microorganisms and absorb the toxin.

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7
Q
  1. Paralytic Shellfish Poisoning
A

Most common – severe – fatal
∼10 per year – CDC
Dinoflagellates Alexandrium and some cyanobacteria Produce saxitoxin(s)
– Sodium channel inhibitors (keeps them closed) leads to flaccid paralysis
– Heat stable (don’t degrade much from cooking)

Symptoms: tingling, burning, numbness, drowsiness, incoherent speech, respiratory paralysis

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8
Q

Saxitoxin

A

The oral LD50 for humans is 5.7 μg/kg

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9
Q
  1. Neurotoxic Shellfish Poisoning
A

From the dinoflagellate Karenia brevis Makes a number of brevotoxins
Also sodium channel blockers, but not a severe in toxicity
Huge outbreaks and fish die offs from this toxin though

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10
Q
  1. Diarrheic shellfish poisoning
A

The algae (Dinophysis and Prorocentrum spp.) make okadaic acids. Symptoms: mild diarrhea, nausea, vomiting, abdominal pain, chills, headache, fever.

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11
Q
  1. Amnesic shellfish poisoning
A

The diatom Pseudo-nitzschia spp. makes domoic acid.
Symptoms:
– Gastrointestinal: vomiting, diarrhea, vomiting
– Neurological: confusion, memory loss, disorientation, seizure coma
Binds to excitatory amino acid receptors in neurons, causing Ca2+ influx and necrosis/apoptosis in nerve cells
1987 outbreak in PEI:
156 cases, 3 deaths, 12 with permanent short-term memory loss

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12
Q

Blue-Green Algae Poisoning

A

Toxin-producing cyanobacteria in Lake Winnipeg
High inflows of nutrients from agriculture can alter the composition of microorganisms in lakes:
Green algae (plants) uptake N and P
Blue-green algae (bacteria) can fix their own N
Thus… too much P in the water and blue-green algae can out-compete green algae and create algal blooms.

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13
Q

microcystins

A

The blue-green algae Microcystis spp. make a class of 80 different toxins called microcystins that are liver toxins! (This is very toxic to dogs, issue at Lake Winnipeg)

Microcystin levels. Maximum acceptable limits in drinking water is 1.5 μg/L

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14
Q

Microcystin are technically “non- ribosomal peptides”.

A

They inhibit the activity of protein phosphatases that remove phosphate groups from proteins that are necessary for their regulation. In the liver this causes the dis-regulation of glucose metabolism.

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15
Q

Fish Poisoning

Scrombroid poisoning

A

Named for the family Scomberidae (tunas and mackerels)
• Can involve any fish containing high levels of free histidine • Spoilage bacteria break down free histidine into histamine

Onset: immediate to 30 minutes
Initial symptoms: tingling or burning sensation in the mouth, rash on the upper body, drop in blood pressure, headache, itching of the skin Later symptoms: nausea, vomiting, and diarrhea
Duration: 3 hours to several days
Antidote: Antihistamines!

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16
Q

Fish Poisoning

Pufferfish poisoning

A

Pufferfish accumulate tetrodotoxin in (mostly) their liver and gonads.

Some pufferfish also accumulate high saxitoxin concentrations… interactions??

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17
Q

Tetrodotoxin

A

is a potent sodium channel blocker, thus stops neurotransmission.

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18
Q

Terodotoxin is also found in

A

the parrot fish, Taiwanese guppies, arrow poison frogs of the genus Atelopus in Costa Rica, the blue-ringed octopus (Hapalochlaena maculosa) from Australia, certain Japanese mussels, sea snails, and starfish, a few types of Philippine crabs, and a California newt (taricha torosa).

(LD50) for mice as 334 μg per kg

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19
Q

Terodotoxin poisoning might be the basis of zombies

A

In traditional Haitian cultures, zombies are crated by Bokurs (spirit doctors). Wade Davis (a Canadian ethnobotanist) wrote that the Bokurs used tetrodotoxin pufferfish to poison their victims:

  1. They’re paralyzed, appear dead, but are in a comatose state.
  2. They’re then buried (!!!!).
  3. The Bokur then digs up the poor victim at night, gives them a hallucinogenic compound (Datura) and tells them that they’re now his zombie (slave).
  4. Because this was so ingrained in the culture, it actually worked. Brain damage may have played a role.
  5. Also, this all may be nonsense and has not been proven.
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20
Q

Nitrite as an additive creates carcinogenic compounds

A

Nitrite (NO2− ) is used in curing meat and fish products.
• Has antimicrobial activity, sensory attributes, and reacts
with myoglobin and hemoglobin to form red
nitrosylcompounds.
• Nitrite reacts with 2o, 3o amines to form stable
nitrosamines.
• High temperature (i.e. cooking) and acidic conditions
(i.e. digestion) increase the rate of nitrosoamine formation.

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21
Q

Nitrosoamines

A

can alkylate DNA (causing adducts) and can cause mutations and cancer.

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22
Q

In November 2015, the World Health Organization upgraded cured meats to

A

Group 1 carcinogens….

All meat is now considered to be a Group 2A human carcinogen (probably carcinogenic to humans). Higher incidence of stomach and colorectal cancers in heavy meat eaters.

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23
Q

BBQ and Cooking Meat Can Create Carcinogens

A

The high temperature pyrolysis of carbohydrates and proteins when grilling and smoking meats forms polycyclic aromatic hydrocarbons (PAHs) and heterocyclic aromatic amines (PAAs). These can form DNA adducts.

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24
Q

Mycotoxins

A

toxins produced by fungi

Molds can grow on plants, and can contaminate improperly stored food. Mycotoxins can also be passed though food animals to humans.
It’s estimated that 25% of all food produced globally are contaminated to some degree by mycotoxins!
Also… mushroom toxins can be mistakenly consumed.

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25
Q

300 known mycotoxins, 30 are of well-characterized

A
  • A single species of fungi may make several toxins
  • Several species of fungi may make the same toxin
  • Often, only particular strains of a species will make toxins
  • High infection rates on drought-stressed and insect-eaten plants
  • High fungal growth rates when food stored at high humidity
26
Q

Mycotoxins

Aflatoxins

A

A group of toxins produces by Aspergillus species, especially Aspergillus flavus and Aspergillus paraciticus.
• Affects cereals, figs, oilseeds, nuts, tobacco, and a long list of other
commodities
Discovered in England in the 1960s as the causative agent of ‘Turkey X disease’ – which kills young poultry

27
Q

There are four ‘major’ aflatoxins:

A

B1, B2, G1, and G2

These are modified furanocoumarins that are made via fungal polyketide biosynthesis.
Animal bioassays show that it’s in the ‘highly toxic to ’‘extremely toxic’ toxicity class.

28
Q

Acute toxicity data on humans rare. Human acute symptoms include

A

abdominal pain, pulmonary edema (fluid in lungs), and fatty infiltration and necrosis of the liver.

29
Q

Aflatoxin B1

A

metabolically activated in the liver
Aflatoxin B1-8,9-oxide binds to DNA at the guanine base in liver cells. Incorrect repair of these adducts can cause further DNA damage that leads to cancer.

can get really high in some crops!!

30
Q

Aflatoxin carcinogenesis can be additive or synergistic with other liver carcinogens

A
  • Hepatitis viruses (HBV, HCV)
  • Alcohol
  • Oralcontraceptives
  • Iron overload • Vinyl chloride
31
Q

HBsAg

A

HBsAg is an antigen test for Hepatitis B

32
Q

Bt corn

A

has reduced levels of aflatoxin contamination

can reduce mycotoxin contamination in corn compared to non-Bt corn hybrids

33
Q

Bt corn is a GMO that expresses a protein normally made by the soil bacteria Bacillus thuringiensis

A
  • This protein is toxic to some insects
  • Bt corn was developed to increase yields by reducing insect damage
  • An added bonus is that the decrease in insect damage leads to less fungal infestation, resulting in reduced aflatoxin levels
34
Q

Ergotism

A

Produced from eating grains infected by the fungus Claviceps purpurea
Grows in wet and overwintered grains: rye, barley, wheat
The fungus makes sclerotia or “ergots” by consuming a whole seed and replacing it with fungal hyphae.

These float in water… so are easily separated out because rye and barley grains sink!

Ergotism is caused by ergot alkaloids

35
Q

Ergometrine

A
  • potent vasoconstriction drug
  • 5HT1a agonist
    (hallucinogenic)
  • Used to facilitate the delivery
    of the placenta and stop
    bleeding in childbirth
  • WHO ‘essential drug’
36
Q

Ergotamine

A

•Ergotamine

a potent vasoconstriction drug. Used medically to treat migraine headaches

37
Q

Ergotism symptoms and outcomes

A
  1. Gangrene
    • Not enough blood flow to the extremities
    • Ergotamine is used medically for certain migraine headaches
  2. Convulsions
    • From disruption in serotonin levels
  3. Hallucinations
    • From disrupting certain neuro receptors (5HT1a agonist)
  4. Spontaneousabortions
    • Not enough blood flow to the developing child
38
Q

Babylonian tablet (2500 BC)

A

“the women who gather noxious grasses, and who were expelled from the city with the exorcists and mutterers of charms.”

39
Q

Parsees (400 to 300 BC):

A

“…the noxious grasses that cause pregnant women to drop the womb and die in childbirth”

40
Q 
Ergotism is (mostly) a historical disease
Known as “St. Anthony’s Fire” in the middle ages.
A

Whole towns would be afflicted… religious groups would often treat the afflicted.
Only two documented outbreaks world wide in the 20th century.

41
Q

Bacteria toxins

A

Bacterial borne food toxins

42
Q

Exotoxins

A

Soluble toxins that are made and secreted by bacteria but can also released by lysis of the bacterial cell.
• Proteins with enzymatic function
• Partially degraded by cooking
• Sufficient numbers avoid being digested in the gut and make
it into the bloodstream
• Can be made by living bacteria in contaminated food and
persist even after the bacteria is dead

43
Q

Endotoxins

A

Cell-associated substances that are structural lipopolysaccharide components of the outer membrane of Gram-negative bacteria. They’re released from growing bacterial cells, but can also be released from dead bacteria (e.g. after antibiotic treatment). Causes a hyperactive immune response

44
Q

hyperactive immune response

A

“toxic shock syndrome”: fever, blood clots everywhere, hypotension, shock, death

45
Q

Botulism

A

Caused by the exotoxin botulinum produced by the
bacteria Clostridium botulinum • Gram positive
• Obligate anaerobic bacillus
• C. botulinum can form spores
• Ubiquitous in the environment
• Resistant to heat, light, drying and radiation • Specific conditions for germination
• Anaerobic conditions
• Warmth (10-50oC)
• Mild alkalinity

46
Q

C. Botulinum spores

A

contaminates food, and if canned will germinate and make the exotoxin.
Puffy cans = bad!
Avoid even dented cans!

47
Q

• Botulism discovery

A
  • Botulism originally known as “sausage poisoning” in late 18th century and throughout 19th century.
  • Bacterial etiology recognized at end of 19th century
  • Outbreak of botulism in Belgium 1895 revealed the cause as neuroparalytic toxin produced by anaerobic bacterium
  • Outbreak in Germany several years later
  • Bacterium isolated; different from that in Belgium
48
Q

Botulinum toxins are protein exotoxins

A

We have a 3D X-ray crystallography structure of Botulinum Neurotoxin A (BoNT A) and know fairly well its molecular mechanisms of toxicity.
Because it is a protein toxin, we can treat botulism with injection of anti-botulinum toxin antibodies.

49
Q

BoNT A mode of action

A
  1. The binding domain binds to receptors on the outside of the neuron, tricking the cell into up taking the toxin via endocytosis.
  2. Normally, proteins taken up by a cell are transported to the lysosome for destruction. However, the botulinum toxin translocation domain punches a whole through the endocytic vesicle so the protein escapes into the cytoplasm.
  3. In the cytoplasm, the catalytic domain finds its target (another protein involved in secretion of vesicles) and cleaves it (thus destroying it).
50
Q

The catalytic domain cleaves SNARE

A

Normal nerve transmission relies on the release of vesicles containing neurotransmitters to propagate the signal from one neuron to the next (or to a muscle cell, etc.)
To be released, vesicles containing neurotransmitters must first be ‘docked’ by SNARE proteins.
The botulinum toxin catalytic chain specifically cleaves these SNARE proteins, thus no neurotransmitters are released.
This stops neurotransmission between neuronal muscle junctions, causing ‘flaccid paralysis’.

51
Q

Three types of botulism poisoning

A
  1. Food borne botulism
  2. Infant botulism
  3. Wound botulism

All three types of botulism result in symmetric descending flaccid paralysis of motor and autonomic nerves
Symptoms include:
Blurred vision, drooping eyelids, Dry mouth
Difficulty Swallowing, muscle weakness
Death due to respiratory failure
Treatment: Inject anti-toxin antibodies and stick the patient on a ventilator

52
Q
  1. Food borne botulism
A 
• Botulism spores infect food in
anaerobic conditions
• Toxin is produced and released into
food when bacteria die
• Toxin concentration can be reduced
through cooking
53
Q
  1. Infant botulism
A 
• Infants ingest C. botulinum spores
• Spores germinate in gut and bacterial
colony is established
• Bacteria colony releases toxins
• This is why you don’t feed babies food
until their older (especially honey and corn syrup)
54
Q
  1. Wound botulism
A

• Mostly associated with IV drug use

55
Q

Medical uses of botulinum toxin

A

Used to treat conditions when muscles contract when they should not. Botox blocks the nerve transmission that causes the muscle cells to contract.

Used to treat:
• Migraine headaches
• Back pain
• Multiple sclerosis spasms • Excessive sweating

56
Q

Shiga toxin in E. coli

A

Most E. coli strains are non-pathogenic
However… bacteria are really good at swapping DNA bits amongst species (lateral gene transfer)
Some E. coli strains have ‘picked up’ genes that make them pathogenic.

57
Q

E. coli O157:H7

A

is a strain that acquired the genes to make shiga toxin.

O157 asymptomatically grows in cow guts. Infected hamburger meat is the usual exposure route for humans.

58
Q

In 1993, there was a really bad outbreak of O157 poisonings in the USA.

A

• 732 infected (mostly kids)
• 10 died
• 178 with permanent nerve
and kidney damage

59
Q

‘A’ subunit

A

‘A’ subunit
The toxic catalytic bit. Cleaves the 28S ribosomomal RNA, thus destroying ribosomes and halting all protein translation.
So really bad for the cell!

60
Q

Pentacyclic ‘B’ subunit

A

• Interacts with a specific lipid cell membranes (which
cows don’t have!)
• Tricks cells into taking it in by endocytosis.
• Remember receptor mediated endocytosis?

61
Q

allergies to fish muscle contraction and relaxation

A 
1) Membrane depolarization.
Ca2+ released from the sarcoplasmic reticulum.
2) Muscle contraction.
3) Muscle relaxation.
Ca2+ back to the sarcoplasmic reticulum.
Parvalbumin binds free calcium.
Facilitates movement back into the SR.
Parvalbumin correlated with muscle relaxation rate. More parvalbumin = faster relaxation time.
62
Q

Parvalbumin levels in fish

A

can be high in the fast twitch muscles, which makes up the bulk of the fillet that we eat.
The vast majority of allergies to fish in humans is a reaction to parvalbumin.
Parvalbumins can differ between species (mutations! evolution!), this is why somebody may be allergic to eating 1 fish but not another

toxicology (10 decks)

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