plant toxicants to mercury Flashcards
solanine is from _________
greened potatoes and stems/leaves
Solanine poisoning is primarily displayed by _________ and _________.
gastrointestinal and neurological disorders
Solanine content in cultivated potato tuber should be below ____ mg/kg.
100
Cyanogenic glycosides can degrade into ______ _______ after the plant tissue is disrupted.
hydrogen cyanide (HCN)
Cyanohydrins (cassva) moiety is the precursor of HCN, an inhibitor of _______________.
cytochrome c oxidase
what enzyme in almond seed is toxic?
amygdalin
draw metabolic activation of plant toxicants pyrrolizidine alkaloids?!
page 6 of plant toxicants
LD50 of ricin
___ ug/kg BW - injection or inhalation
Oral - 20-30 mg/kg BW
1.76 mg for an average adult
22
LD50 of ricin
Oral - ______ mg/kg BW
20-30
what health effect would ergot alkaloids cause?
ergotism
what health effect would alfatoxin cause?
acute toxicity, hepatic cancer, reyes syndrome
what health effect would trichothecenes (fungal) cause?
acute toxicity, cancer, alimentary toxic aleukia
what health effect would ochartoxin cause?
cancer, kidney disorders, hepatic damage
- Trichothecenes, produced by many fungus species, are strong
protein synthesis_______
inhibitor
- Ochratoxins, produced by Aspergillus and Penicillium fungi, are
highly ________
nephrotoxic
What is the most patulin exposure a 1-2 year old can consume?
0.80 ug/kg/BW
what do insecticides target?
Target on nervous
system (animal specific)
what do herbicides target?
- Target on pathways
essential in plants but not
mammals
why do people argue against pesticides ?
many many are potentially carcinogenic, mutagenic and teratogenic.
dioxin TCDD- halogenation is highly electronegative which means….
they want an electron…
aflatoxin has no conclusion
true
what happened to the rat livers in the study of brazilian groundnut meal?
they turned yellow/brownish with red and green cysts. 9/11 had tumors
Aflatoxin was named after the _______ of its
origin (A. flavis).
fungus
which aflatoxin is normally predominant
AFB1
what is the toxicity in order of aflatoxins?
: AFB1 > AFG1 > AFB2 > AFG2
do the B/G 1 have double bonds or B/G2?
B/G1
what is the main target of aflatoxin?
liver but kidneys and lungs are also affected
what happens with acute toxicity of afatoxin?
inhibition of carbohydrate and lipid metabolism and
protein synthesis
‐‐‐disruption of bile secretion (jaundice)
‐‐‐Necrosis of liver cells
what happens in chronic toxicity of aflatoxin?
‐decrease in growth rate
‐‐‐reduced milk or egg production
‐‐‐immune suppression
‐‐‐carcinogenesis
aflatoxin acute toxicity is the same across species t or f
false! rodents are more resistant to aflatoxin
- Distribution of ______ in species and organs determine the
metabolic fate of AFB1.
P450s
Aflatoxins ___ is secreted through the milk of lactating animals.
It is a reliable indicator of aflatoxin exposure in food and feed
M1
____ epoxide is the reactive intermediate of aflatoxin toxicity.
AFB1
how is aflatoxin excreted?
bile and urine
- _____ tumor suppressor gene is attacked by aflatoxin. The
inactivation of ____- potentially allows for uncontrolled cell
proliferation.
p53
ADME of aflatoxin
……
is methylmercury organic or inorganic?
organic
_______ bacteria in the
aquatic environment conduct
the methylation of mercury
Anaerobic
what is the target of mercury?
methylmercury affects CNS
effects of mercury?
kidney damage, coronary heart disease, sprem damage, birth defects
exposure of mercury
dietary intake, inhalation
Blood methylmecury concentration in the US population is _________ng/mL (ranging from 0.1 to 24.6 ng/mL)
1‐1.3
methylmercury‐‐FDA action level:___ ppm in the edible portion of fish
1.0
‐‐‐mercury Half‐life: _____days in humans
35‐90
disposition of mercury
- 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.
Mercurous mercury (Hg+): low solubility → ___________
slowly absorbed
methylmercury can be conjugated or _________
demethylated
where does demethylization occur with methylmercury?
in the brain
disposition of organic mercury (methymerc)
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.
mercury poisoning causes shrikage of the _____ and diminution
folia
what is nephrotoxicity?
mainly caused by the accumulation of
mercury conjugate in the kidney
