plant toxicants to mercury

Question 1

solanine is from _________

Answer 1

greened potatoes and stems/leaves

Question 2

Solanine poisoning is primarily displayed by _________ and _________.

Answer 2

gastrointestinal and neurological disorders

Question 3

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

Answer 3

100

Question 4

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

Answer 4

hydrogen cyanide (HCN)

Question 5

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

Answer 5

cytochrome c oxidase

Question 6

what enzyme in almond seed is toxic?

Answer 6

amygdalin

Question 7

draw metabolic activation of plant toxicants pyrrolizidine alkaloids?!

Answer 7

page 6 of plant toxicants

Question 8

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

Answer 8

22

Question 9

LD50 of ricin
Oral - ______ mg/kg BW

Answer 9

20-30

Question 10

what health effect would ergot alkaloids cause?

Answer 10

ergotism

Question 11

what health effect would alfatoxin cause?

Answer 11

acute toxicity, hepatic cancer, reyes syndrome

Question 12

what health effect would trichothecenes (fungal) cause?

Answer 12

acute toxicity, cancer, alimentary toxic aleukia

Question 13

what health effect would ochartoxin cause?

Answer 13

cancer, kidney disorders, hepatic damage

Question 14

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

Answer 14

inhibitor

Question 15

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

Answer 15

nephrotoxic

Question 16

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

Answer 16

0.80 ug/kg/BW

Question 17

what do insecticides target?

Answer 17

Target on nervous
system (animal specific)

Question 18

what do herbicides target?

Answer 18

• Target on pathways
  essential in plants but not
  mammals

Question 19

why do people argue against pesticides ?

Answer 19

many many are potentially carcinogenic, mutagenic and teratogenic.

Question 20

dioxin TCDD- halogenation is highly electronegative which means….

Answer 20

they want an electron…

Question 21

aflatoxin has no conclusion

Answer 21

true

Question 22

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

Answer 22

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

Question 23

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

Answer 23

fungus

Question 24

which aflatoxin is normally predominant

Answer 24

AFB1

Question 25

what is the toxicity in order of aflatoxins?

Answer 25

: AFB1 > AFG1 > AFB2 > AFG2

Question 26

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

Answer 26

B/G1

Question 27

what is the main target of aflatoxin?

Answer 27

liver but kidneys and lungs are also affected

Question 28

what happens with acute toxicity of afatoxin?

Answer 28

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

Question 29

what happens in chronic toxicity of aflatoxin?

Answer 29

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

Question 30

aflatoxin acute toxicity is the same across species t or f

Answer 30

false! rodents are more resistant to aflatoxin

Question 31

* Distribution of ______ in species and organs determine the metabolic fate of AFB1.

Answer 31

P450s

Question 32

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

Answer 32

M1

Question 33

____ epoxide is the reactive intermediate of aflatoxin toxicity.

Answer 33

AFB1

Question 34

how is aflatoxin excreted?

Answer 34

bile and urine

Question 35

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

Answer 35

p53

Question 36

ADME of aflatoxin

Answer 36

......

Question 37

is methylmercury organic or inorganic?

Answer 37

organic

Question 38

_______ bacteria in the aquatic environment conduct the methylation of mercury

Answer 38

Anaerobic

Question 39

what is the target of mercury?

Answer 39

methylmercury affects CNS

Question 40

effects of mercury?

Answer 40

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

Question 41

exposure of mercury

Answer 41

dietary intake, inhalation

Question 42

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

Answer 42

1‐1.3

Question 43

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

Answer 43

1.0

Question 44

‐‐‐mercury Half‐life: _____days in humans

Answer 44

35‐90

Question 45

disposition of mercury

Answer 45

* 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.

Question 46

Mercurous mercury (Hg+): low solubility → ___________

Answer 46

slowly absorbed

Question 47

methylmercury can be conjugated or _________

Answer 47

demethylated

Question 48

where does demethylization occur with methylmercury?

Answer 48

in the brain

Question 49

disposition of organic mercury (methymerc)

Answer 49

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.

Question 50

mercury poisoning causes shrikage of the _____ and diminution

Answer 50

folia

Question 51

what is nephrotoxicity?

Answer 51

mainly caused by the accumulation of mercury conjugate in the kidney