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toxicology > plant toxicants to mercury > Flashcards

plant toxicants to mercury Flashcards

1
Q

solanine is from _________

A

greened potatoes and stems/leaves

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2
Q

Solanine poisoning is primarily displayed by _________ and _________.

A

gastrointestinal and neurological disorders

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3
Q

Solanine content in cultivated potato tuber should be below ____ mg/kg.

A

100

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4
Q

Cyanogenic glycosides can degrade into ______ _______ after the plant tissue is disrupted.

A

hydrogen cyanide (HCN)

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5
Q

Cyanohydrins (cassva) moiety is the precursor of HCN, an inhibitor of _______________.

A

cytochrome c oxidase

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6
Q

what enzyme in almond seed is toxic?

A

amygdalin

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7
Q

draw metabolic activation of plant toxicants pyrrolizidine alkaloids?!

A

page 6 of plant toxicants

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8
Q

LD50 of ricin
___ ug/kg BW - injection or inhalation
Oral - 20-30 mg/kg BW
1.76 mg for an average adult

A

22

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9
Q

LD50 of ricin
Oral - ______ mg/kg BW

A

20-30

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10
Q

what health effect would ergot alkaloids cause?

A

ergotism

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11
Q

what health effect would alfatoxin cause?

A

acute toxicity, hepatic cancer, reyes syndrome

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12
Q

what health effect would trichothecenes (fungal) cause?

A

acute toxicity, cancer, alimentary toxic aleukia

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13
Q

what health effect would ochartoxin cause?

A

cancer, kidney disorders, hepatic damage

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14
Q
  • Trichothecenes, produced by many fungus species, are strong
    protein synthesis_______
A

inhibitor

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15
Q
  • Ochratoxins, produced by Aspergillus and Penicillium fungi, are
    highly ________
A

nephrotoxic

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16
Q

What is the most patulin exposure a 1-2 year old can consume?

A

0.80 ug/kg/BW

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17
Q

what do insecticides target?

A

Target on nervous
system (animal specific)

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18
Q

what do herbicides target?

A
  • Target on pathways
    essential in plants but not
    mammals
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19
Q

why do people argue against pesticides ?

A

many many are potentially carcinogenic, mutagenic and teratogenic.

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20
Q

dioxin TCDD- halogenation is highly electronegative which means….

A

they want an electron…

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21
Q

aflatoxin has no conclusion

A

true

22
Q

what happened to the rat livers in the study of brazilian groundnut meal?

A

they turned yellow/brownish with red and green cysts. 9/11 had tumors

23
Q

Aflatoxin was named after the _______ of its
origin (A. flavis).

A

fungus

24
Q

which aflatoxin is normally predominant

A

AFB1

25
Q

what is the toxicity in order of aflatoxins?

A

: AFB1 > AFG1 > AFB2 > AFG2

26
Q

do the B/G 1 have double bonds or B/G2?

A

B/G1

27
Q

what is the main target of aflatoxin?

A

liver but kidneys and lungs are also affected

28
Q

what happens with acute toxicity of afatoxin?

A

inhibition of carbohydrate and lipid metabolism and
protein synthesis
‐‐‐disruption of bile secretion (jaundice)
‐‐‐Necrosis of liver cells

29
Q

what happens in chronic toxicity of aflatoxin?

A

‐decrease in growth rate
‐‐‐reduced milk or egg production
‐‐‐immune suppression
‐‐‐carcinogenesis

30
Q

aflatoxin acute toxicity is the same across species t or f

A

false! rodents are more resistant to aflatoxin

31
Q
  • Distribution of ______ in species and organs determine the
    metabolic fate of AFB1.
A

P450s

32
Q

Aflatoxins ___ is secreted through the milk of lactating animals.
It is a reliable indicator of aflatoxin exposure in food and feed

A

M1

33
Q

____ epoxide is the reactive intermediate of aflatoxin toxicity.

A

AFB1

34
Q

how is aflatoxin excreted?

A

bile and urine

35
Q
  • _____ tumor suppressor gene is attacked by aflatoxin. The
    inactivation of ____- potentially allows for uncontrolled cell
    proliferation.
A

p53

36
Q

ADME of aflatoxin

A

……

37
Q

is methylmercury organic or inorganic?

A

organic

38
Q

_______ bacteria in the
aquatic environment conduct
the methylation of mercury

A

Anaerobic

39
Q

what is the target of mercury?

A

methylmercury affects CNS

40
Q

effects of mercury?

A

kidney damage, coronary heart disease, sprem damage, birth defects

41
Q

exposure of mercury

A

dietary intake, inhalation

42
Q

Blood methylmecury concentration in the US population is _________ng/mL (ranging from 0.1 to 24.6 ng/mL)

A

1‐1.3

43
Q

methylmercury‐‐FDA action level:___ ppm in the edible portion of fish

A

1.0

44
Q

‐‐‐mercury Half‐life: _____days in humans

A

35‐90

45
Q

disposition of mercury

A
  • Inhalation of mercury vapor: Mercury gas is highly diffusible
    and lipid soluble.
    ‐‐‐Absorption and distribution: Inhalation of vapor → Readily
    absorbed and dissolve in tissue fluids → Distribute throughout
    the body and cross the blood–brain and placental barriers
    ‐‐‐Metabolism: Hg is oxidized to Hg++ in vivo
    ‐‐‐Excretion: Fecal excretion is dominant in the first week of
    exposure and urinary excretion is more dominant later.
46
Q

Mercurous mercury (Hg+): low solubility → ___________

A

slowly absorbed

47
Q

methylmercury can be conjugated or _________

A

demethylated

48
Q

where does demethylization occur with methylmercury?

A

in the brain

49
Q

disposition of organic mercury (methymerc)

A

Absorption : Methylmercury is highly lipophilic. 95% of
methylmercury ingested in fish is absorbed.
5
* Distribution: Distribution of methylmercury to all the body
tissues is completed. The concentration in brain is about 5
times and in scalp hair about 250 times the corresponding
concentration in blood.
‐‐‐Metallothionein, a small cysteine‐rich protein, is protective
against methylmercury toxicity through capturing mercury.
* Excretion: The main route is via the feces (>90%).
‐‐‐Enterohepatic circulation occur after glutathione conjugate
in the bile is broken down, releasing methylmercury.

50
Q

mercury poisoning causes shrikage of the _____ and diminution

A

folia

51
Q

what is nephrotoxicity?

A

mainly caused by the accumulation of
mercury conjugate in the kidney

toxicology (3 decks)

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