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55 Cards in this Set
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Natural toxins |
animal and plant products *evolved as protection from predators *many more poisonous plants than those safe for consumption use of fire enabled removal/inactivation of plant toxins |
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bacteria |
soil, fresh water, ocean, plants, animals, human gut *co-exist with humans (gut micro biome) *pathogenic and non-pathogenic *natural state of food--covered w/ bacteria food-borne illness (FBI)improper food handling, preparation, storage caused by bacteria (infection) or toxins produced by bacteria (intoxication) |
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bacteria pathogenicity |
non-pathogens: harmless and can provide benefit: like intestinal bacteria they digest unused energy substances like fibre *train the immune sys, prevent growth of pathogens and produce vitamins (biotin and Vit.K) and SCFA |
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bacteria pathogenicity |
pathogens: cause infection/disease opportunistic: part of normal flora and can cause infection /disease in right circumstances |
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bacteria: Gram Stain |
identification and characterization of bacteria based on cell wall characteristics-->detects peptidoglycans Gram-positve: thick peptidoglycan layer, exposed, stains purple Gram-negative: thin layer btw other membranes stains pink |
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bacteria: Gram stain process |
1.application of crystal violet (purple dye) and add water 2. application of iodine--interacts with CV within inner and outer layers 3. alcohol wash (decolorization)--reacts with lipids of cell membrane *gram-negative will lose outermost layers and expose peptidoglycan layer 4. application of safranin (counteractive stain) plus water to get gram-+ve or gram -ve |
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morphology of bacteria |
variety of shapes/sizes 0.5-5micrometer single cells diploid (pairs) chains (Streptococcus) clusters (eg: Staphylococcus) bioflims (aggregate on surfaces) |
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motility of bacteria |
flagellum: whip-like extension, propeller-like motion cilia: hair-like extensions, beat in waves mvmt on food surface |
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spores of bacteria |
dormant stage for some bacteria *survival of extreme conditions (heat, drought) resistant to desciccation, low nutrient conditions, radiation, high temp germinate and reproduce when conditions become favourable |
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gastroenteritis: gastric flu or stomach flu (not caused by influenza) |
clinical syndrome caused by FBI inflammation of GI tract (stomach and SI) acute diarrhea vomiting, abdominal pain primary treatment: rehydration |
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Clostridia: gram positive, rod-shaped, flagellate, endospore producing ,naturally inhabit soil
C.botulinum |
C.botulinum produces potent neurotoxins-->stop nerve pulses from crossing the synapse and presents muscle contraction *botulism: flaccid paralysis (affects muscles involved in chewing, facial expression, eye mvmt, swallowing, breathing) *estimated >100ng/kg fatal to humans heat stable, tolerates low acid and low NaCl concentrations (improper home canned veggies, cured meats) |
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Escherichia: gram negative, rod-shaped, flagellate, non-spore forming, naturally inhabit mammalian gut
E.coli 0157:H7 |
E.coli: intestines in cattle: contamination from slaughter. If meat is cooked thoroughly, bacteria will be killed grows in host gut and forms shiga-like toxin (SLT-pathogenic) in situ SLT inhibits protein sun by interfering with ribosome fxn FBI: bloody diarrhea, severe abdominal pain/tenderness, no fever, lasts 1-10 days |
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Salmonella: gram negative, rod shaped, flagellate, non-spore forming inhabits intestines of cattle and poultry S.enterica |
s.enterica: not heat stable not killed by freezing (frozen raw meat and uncooked egg-based foods are potential sources) salmonellosis: diarrhea, vomiting, fever for 4-7 days 8-72hrs after infection chicken highest risk meat (some meats are more susceptible to contamination than others) |
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Listeria: gram positive, rodshaped, flagellate, non-spore forming found in soil and waterways, some animal intestines (meat, dairy, seafood, veggies, fruit) |
only L.monocytogenes causes FBI in humans (listeriosis) can grow over a broad temp (4-37 degrees C) host cells internalize the bacterium by phagocytosis and it becomes an intracellular parasite that grows and reproduces in host cytoplasm |
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Listeria: Listeriosis (FBI in humans caused by L.monocytogenes) |
non-invasive: fever, muscle achnes, vomiting (diarrhea less common) invasive: infect tissues-->CNS infection often fatal (meningitis) |
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Listeriosis symptoms occurs more often in very young or very elderly (>70) or those with immune sys disorders (30% of cases are preg women) evidence of increasing incidence |
symptoms, 3-70 days after exposure (average 21) bacteria must enter the gut, infiltrate gut epithelial cells and reproduce before there is enough present in certain location to cause symptoms
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Marine toxins |
tetrodotoxin, saxitoxin, scromboid poisoning |
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Marine toxin: tetrodotoxin |
tetrodotoxin: Fugu (Japanese puffer fish) TTX in organs (liver, ovaries, eyes also in bile), skin non-poisonous potent neurotoxin, Na+ channel blocker flaccid paralysis: paralyzes muscles, doesn't cross BBB, death from asphyxiation not affected by cooking LD50 (oral)= 334microg/kg body weight (mouse) 25mg lethal to 50% of ppl |
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marine toxin: tetrodotoxin |
origin: farmed fugu puffer fish don't produce TTX until fed tissues from a toxin producing fish Blue-ringed octopus (Pacific &Indian oceans) accumulates TTX in special salivary glands-->transfers when attacks prey Xanthid crabs collected from the same waters contain TTX and saxitoxin |
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marine toxin: saxitoxin |
potent neurotoxin, Na+ channel blocker produced by dinoflagellates (marine protozoa present in algae) that are eaten by shellfish (mussels, clams, scallops) not destroyed by heat paralytic shellfish poisoning (flaccid--paralysis-->asphyxiation)
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marine toxin: saxitoxin |
LD50 (oral)= 5.7ug/kg (human estimate) LD50 (dermal)= 0.05mg/kg (human estimate) environment monitoring (algal bloom) |
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marine toxin: scromboid poisoning |
mackerel, tuna, mahi mahi, sardines, anchovies fish spoilage: bacteria (scrombotoxin) convert histidine to histamine heat resistant can concentrate up to 100mg/kg in fish (20-50mg/kg toxicity threshold in humans)
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scromboid poisoning |
acute allergic response: burning/swelling of mouth, body rashses pseudo allergic fish poisoning (treated with antihistamines)
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Plant toxins: most commonly encountered natural toxins in food broad array of molecular structures &mechanisms of toxicty many are phytoelexins (produced by plant in response to stress, i.e.: natural pesticides) |
Glycoalkaloids, Cyanogenic glycosides, mycotoxins, aflatoxin, patulin, trichothecenes, ochratoxin |
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plant toxin reading: Nature's chemical and synthetic chemicals: comparative toxicology b/c synthetic chemicals are recent, mechanism animals possess to copy with natural vs. synthetic chemicals are different |
false!!! many natural toxins are carcinogens and general defense mechanisms include: shedding of cells, biotrans and DNA repair concerns over syn pesticides: many organic farmers breed plants that are naturally insect-resistant, but high conc of natural toxins (natural pesticides) natural pesticides are far less evaluated for safety |
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plant toxin: glycoalkaloids LD50= 590mg/kg in rats |
nightshade family: potatoes, tomatoes, peppers, egg plants protect against pathogens (bacteria, fungi, viruses, insects & animals) heat stable solanine and chaconine potates (low levels provide flavour)-->increase in bitterness, increase in solanine) |
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adverse effects of glycoalkaloids signs of physical change or damage (sprouting, greening, bruising) |
symptoms: bitter or burning sensation in the mouth and flu-like symptoms (nausea, vomiting, stomach and abdominal cramps and diarrhea) very few deaths more severe cases can have neurological effects ( i.e.: drowsiness, apathy, restlessness, shaking, confusion, weakness and disturbed vision) |
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distribution in potatoes |
glycoalkaloid content increases in response to stress: potato blight infection, defoliation by insects, selection for potato leafhopper resistance, bruising, exposure to light |
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Cyanogenic glycosides: natural herbicide precursors for hydrogen cyanide |
cyanide halts cellular respiration (mental confusion, muscle paralysis, respiratory failure) amygdalin ( bitter almonds, kernels of cherries, apricots and peach seeds) linamarin (cassava, lima beans) |
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mycotoxins:secondary metabolites produced by mild (filamentous fungi) |
cereals, nuts, fruit and dried fruit, coffee, cocoa, spices, oilseeds and milk mutagenic, carcinogenic, teratogenic in mammals Aspergillus, penicilium & Fusarium proudce most of toxic syndromes in mammals many heat stable (even when mold is killed) & insoluble in water
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Mycotoxin--Aflatoxin: produced by Aspergillus flavus grows ons tored grains (maize) & nuts 14+ varieties-->aflatoxin B1 most toxic very potent: LD50--0.5mg/kg (human estimate) |
acute toxicity: liver damage, hemorrhaging in GI tract very low MRL--(15microg/kg) for peanuts direct relation with liver cancer: requires bioactivation, binds to N7-Gua, causes a mutation in p53, hepatitis B infection increases risk |
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Mycotoxin--Patulin: produced by penicillium grows on apples, and pears, causes them to rot |
LD50= 15-35mg/kg (human estimate) partially rotted fruit sometimes used for juice (has been found in apple juice >1 000microg/kg (infants and babies risk group) suspected carcinogen (cross-link, micronucleus formation) MRL= 10microg/kg for baby foods 50microg/L for apple juice |
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Trichothecenes: produced by Fusarium Wheat, barley, maize, oats, rye, rice |
LD50= 60mg/kg (human estimate) binds to ribosomes -->inhibits all steps of protein alimentary toxic aleukia: atrophy of bone marrow (extreme reduction in WBC-->death in extreme cases) MRL 0.025-0.1mg/kg |
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Ochratoxin: MRL: 3-5ug/kg in cereals, 10ug/kg in dried fruit |
produced by Aspergillus ochraceus cereals, coffee, dried fruit, red wine LD50= 20-50mg/kg (human estimate) nephrotoxicity in birds and fish (impairment of proximal tubular fxn) teratogenic in rats and chickens (target CNS) |
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Reduction:Traditional vs. emerging Traditional |
Tradition: limit bird and insect damage, harvest grain ASAP , adequate drying and storage of grain, annual crop rotation, avoid planting susceptible crops in adjacent fields |
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Reduction: Emerging |
pre-harvest host plant resistance genetic engineering/selection of naturally resistant hybrids
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Aflatoxin: A global health crisis? |
aflatoxin responsible for 28% of the total worldwide cases of heptocellular carcinoma (most common form of liver cancer) |
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Toxicities |
acute: FBI, allergic rxn, physiological disruption/irritation chronic: neurological , behavioral, teratogenic, carcinogenic |
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genotoxicty and carcinogenicity |
genotoxin: affects DNA (genetic material) significant damage to an essential gene-->cell death/severe malfxn mutation-->generates permanently changes mutation occur: naturally/spontaenously at a very slow rate (shortcomings in syn and handling of DNA), external agents: environmental toxicants not necessarily carcinogenic |
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DNA damage |
chromosomal aberrations DNA adduct Mutations: base-pair substitutions : SNPS frameshift mutations: ins/Del |
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Initiators and promoters |
Initiators: bind to and damage DNA promoters: promote expansion of initiated cell |
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carcinogen bioactivation procarcinogen, proximate carcinogen, ultimate carcinogen |
procarcinogen: requires metabolic activation proximate carcinogen: reactive intermediary ultimate carcinogen: electrophilic compound that binds to DNA |
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Carcinogen pathway |
look at diagram in slides |
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classification of agents Group 1: carcinogenic to humans Group 2A: probably carcinogenic to humans Group 2B: possibly carcinogenic to humans Group 3: not classifiable as to its carcinogenicity to humans Group 4: probably not carcinogenic to humans |
Group 1: aflatoxins, alcoholic beverages, abestoes Group 2A: frying (emissions from high temp), shift work that disrupts circadian rhythms Group 2B: coffee (urinary bladder), engine exhaust (gasoline) group 3: caffeine, chlorinated drinking water group 4: caprolactam |
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DNA repair |
cells developed protein/enzymatic sys to detect and repair damage to DNA highly evolutionarily conserved |
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Direct repair O6-methylguanine-DNA methyltransferase (MGMT) |
damage caused by alkylating agents or UV light no significant NT modification, backbone breakage or DNA sun |
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Base-excision repair |
single base/non bulky adducts (1-5NTs) AP site-->apurinic: A, G; or apyrimidnic: T, C AP endonuclease cleaves back bone at AP site resynthesis |
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NT-exicsion repair |
bulky adducts (removes 12-24 NTs) ex: pyrimidine dimer: thymine dimer upstream & downstream excision resynthesis |
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mismatch repair: post-replicative process to correct DNA pol errors that have escaped proof-reading daughter strand specific MSH-2, MLH-1: germinate mutations associated with CRC |
1. identify incorrect base on daughter strand 2. nicking by endonuclease 3. digestion by exonuclease 4. resynthesis by DNA pol 5. ligation by DNA ligase |
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Failure or absence of repair |
depurination/depyrimidation: formation of AP site strand breakage: single strand or DS breakage cross-linking: blocks DNA replication DNA syn on alkylated template |
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Consequences of failure or absence of repair |
erros in DNA (apoptosis) mutations (Detrimental or beneficial) |
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Thought experiment and process of carcinogenic xenobiotic to cancer |
look at diagram in slides |
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Variations in cancer risk among tissues can be explained by the # of stem cell divisions : article |
lifetime risk of cancers strongly correlated (0.81) with total # of divisions of normal self-renewing cells maintaining that tissue's homeostasis |
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potential dietary modifiers |
caloric restriction: 10-40% reduction in total caloric requirement decreases serum IGF-1, cell proliferation, oxidative stress increases DNA repair, genomic stability, immunosurveillance |
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potential dietary modifiers |
Phytochemicals: cruciferous vegetables (broccoli, cabbage, brussels sprouts, kalet), onions, garlic, induce phase II enzymes Red meat: increase risk of CRC (inflammation from glycans) |
