exam open Q:/// Flashcards
What are mycotoxins? Give two examples of mycotoxins. Describe the conditions that favour
mycotoxin formation in agricultural commodities and the challenges associated with their
prevention and control.
They are toxic compounds, which are produced by molds, which are growing on grains/fruits (can be growing while storing or in the field)
Examples of mycotoxins:
1) Aflatoxin B1 (from genus Aspergilus)
2) Ergot alkaloids (from C. purpurea)
Conditions that favour mycotoxin formation in agricultural comodities:
1) moisture: High relative humidity and high moisture content promote fungal growth and mycotoxin production
2) drought, pests weaken plants making them more affected by fungal infections
3) storge conditions: Improper storage in warm conditions or sudden temperature changes can lead to condensation, encouraging fungal growth.
Poor airflow in storage facilities can trap moisture and heat, creating favorable conditions for mold.
4) Contamination during handling:
dirty storage equipment or mixing infected grains with healthy ones spreads fungi.
Challenges associated with mycotoxin
prevention and control:
1) unpredictable weather: unexpected rainfall or prolonged drought create favorable conditions for mycotoxin production.
2) Its also hard to control pests, who can damage grains and spread fungal
3) Mycotoxins are chemically stable and can survive food processing.
4) In some countries, regulations on mycotoxin limits in food and feed are poorly enforced or non-existent.
Why are countries near the equator generally more likely to have aflatoxin contamination of
foods? How do aflatoxins get into poultry, cattle, and milk?
Warm temperatures- The optimal temperature for aflatoxin production is between 25°C and 30°C
High Humidity: Persistent humidity above 70% provides an ideal environment for fungal growth.
Monocropping: repeated planting of susceptible crops (e.g. peanuts, corns) allows fungal spores to persist in the soil.
Aflatoxins get into poultry (chicken, turkey):
through the feed, like seeds
milk: feed is metabolised and excreted in milk.
cattle: by ingesting grains contaminated with fungi.
What is the mechanism of action of botulinum toxin? Additionally, discuss the different forms
of botulism, considering the variations in their presentations, causes, and potential outcomes.
Botulinum toxin- neurotoxin.
Mechanism of action -Block nerve functions and can lead to respiratory and muscular paralysis.
Different forms of botulism: foodborne, infant, wound botulism
Foodborne botulism:(preform toxin is ingested)
Found in: improperly preserved food, like in canned vegetables. Anaerobic environment created (a cause)
Outcomes: muscle weakness, paralysis; respiratory failure
Infant botulism (mostly affecting newborns)
These spores
can germinate in a baby’s immature intestinal tract, producing botulinum toxin
Found in: honey, soil, dust, containing C. botulinum spores
Outcomes: Constipation,
respiratory failure
Caused by: ingestion of spore, then toxin is produced in gut.
Wound botulism:
Found in: Wounds contaminated with soil or dirt containing C. botulinum spores
Caused by: C. Botulinum spores, that produce toxin in the wound.
Outcomes (same as in foodborne botulism) muscle weakness, paralysis; respiratory failure.
Provide specific examples of diseases where bacterial toxins play a crucial role and discuss
potential strategies for therapeutic interventions targeting bacterial toxins.
Bacterial toxin like tetanospasmin (caused by Clostridium tetani bacteria, which enters body through wound) causes Tetanus disease. Therapeutic intervention:
1) using TIG (Tetanus Immunoglobulin), that contains antibodies that bind to and neutralize tetanospasmin, preventing it from entering nerve endings.
2) antibiotics: used to eliminate Clostridium tetani bacteria at the wound state
Diphtheria (caused by Diphtheria toxin, which is produced by bacteria C. diphtheriae )
1) Antitoxin: Early administration of diphtheria antitoxin to neutralize the toxin.
2) Antibiotics: Penicillin to kill C. diphtheriae.
Discuss the mechanism of action of the tetanus toxin, its impact on the nervous system, and
the role of immunization in preventing this potentially life-threatening disease.
Mechanism of action: Tetanus toxin is produced by Clostridium tetani at the site of infection, typically a wound.
Tetanospasmin:
Toxin binds in central nervous system
* Interferes with neurotransmitters releasing signals to block inhibitor impulses;
* Leads to unopposed muscle contraction and spasm
the role of immunization in preventing this potentially life-threatening disease:
1) vaccine: it contains toxoid (inactive form of tetanospasmin) which stimulates an immune response.
Examine the causes, symptoms, and potential sources of algae-related food poisoning.
Causes: ingestion of toxins produced by certain species of algae.
Symptoms:
Paralytic Shellfish Poisoning (PSP) headache
Ciguatera Fish Poisoning (CFP)
Nausea, vomiting, diarrhea
Amnesic Shellfish Poisoning (ASP)
Neurological: Confusion, memory loss, seizures, coma
Neurotoxic Shellfish Poisoning (NSP):
Gastrointestinal: Nausea, diarrhea, vomiting.
Potential sources:
Seafood: oysters, clams.
Examine the mechanisms of action of atropine, emphasizing its role as a competitive antagonist
to acetylcholine and its impact on muscarinic receptors. Discuss how atropine interferes with
acetylcholine
Atropine-natural toxin that comes from Atropa belladonna (plant).
Competitive Antagonism of Acetylcholine (a neurotransmitter)
Atropine binds to muscarinic receptors (M1, M2, M3, M4, and M5) (they are part of parasympathetic nervous system) competing with acetylcholine (prevents acetylcholine from binding)
Symptoms of poisoning: dryness in the throat, increased pulse and temperature, skin-dry and flushed.
Impact on Muscarinic Receptors:
Affect on neural receptors (M1) (in CNS):
Reduced cognitive function
Affect on cardiac receptors (M2)(located in the heart)
Increases heart rate
Affect on salivary and sweat glands glands (liaukos) (M3)( found in bladder, bronchi): decreased secretion (dry mouth, reduced sweating)
how atropine interferes with
acetylcholine:
Atropine blocks acetylcholine signaling by
1) Binding to Muscarinic Receptors (inhibition)
this way interrupting Normal Parasympathetic Functions: Inhibits processes like salivation, heart rate regulation, and normal cognitive functioning.
Discuss the roles of key species, the flow of energy through trophic levels, and the dynamics of
biotic and abiotic factors.
PRODUCERS- autotrophs: to capture energy from sunlight/chemicals and convert into food source for others.
CONSUMERS (heterotrophs):
acquire energy from other organisms by ingesting
them:
Herbivores – eat plants
* Carnivores – kill and eat other animals
* Omnivores – diets include both plant and animal matter
* Detritivores – feed on detritus (small pieces of decaying
matter)
DECOMPOSTERS (Saprotrophs) – chemically break down
organic matter (bacteria and fungi)
Energy flow:
energy flows through an ecosystem
in one direction, from primary producers to
consumers
On average, only 10 percent of energy available in
one trophic level is transferred to the next level!
The rest is given off as heat!
Dynamics of biotic and abiotic factors:
Temperature extremes can limit the survival and reproduction of species.
Drought or flooding can drastically alter the distribution of plant and animal species.
Rising sea temperatures (abiotic) lead to coral bleaching, affecting marine life (biotic).
Describe the intricate metabolic pathways involved in the metabolism of methanol in humans,
include chemical names, structure and enzymes converting methanol.
Methanol (CH₃OH) is rapidly absorbed into the bloodstream from the gastrointestinal tract after ingestion, and it is widely distributed to various tissues, including the liver, brain.
Methanol is metabolized to formaldehyde (highly reactive and toxic substance) by alcohol dehydrogenase (ADH)
Formaldehyde is rapidly converted to formic acid (HCOOH)( inhibits mitochondrial enzymes) .This conversion is catalyzed by formaldehyde dehydrogenase (FDH).
Formic acid → CO₂ (The enzyme formate dehydrogenase (FDH))
CO2 then can be exhaled—for reducing the toxic effects of formic acid
Explore the multifaceted aspects of benzene toxicity, considering its impact on human health
and the environment
Benzene can be absorbed through inhalation, skin contact, ingestion.
Acute toxicity:
1) short term exposure to high concentrations of benzene can lead to headaches, dizziness, sometimes can cause unconsciousness.
2) respiratory effects: inhalation of benzene vapors can cause shortness of breath
3) skin and eye irritation
Chronic toxicity:
1) Chronic exposure has been strongly linked to an increased risk of leukemia
2) Benzene can suppress the production of blood cells, leading to conditions like anemia
3) Prolonged exposure to benzene has been associated with weakened immune function
Benzene is also harmful to the environment, particularly to air, water, and soil.
Air: because its a volatile organic compound, it contributes to formation of ground-level ozone and smog.
Water: Benzene is highly soluble in water, which means it can easily contaminate groundwater and surface water bodies when improperly disposed of or when there is a spill.
Soil contaminant: Benzene can leach into the soil from industrial spills, waste disposal, or leaks from underground storage tanks.
Examine the mechanisms through which benzene is metabolized in the body and the potential formation of reactive intermediates.
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Discuss the health effects associated with chronic exposure to benzene, including its link to hematological disorders and carcinogenesis.
Chronic exposure can cause a decrease in white blood cells, compromising the immune system and increasing posibility of infections.
Chronic benzene exposure can lead to bone marrow failure characterized by the inability to produce sufficient blood cells, finaly resulting anemia
CARCINOGENESIS: process by which normal cells transform into cancerous cells.
The key mechanisms of benzene-induced carcinogenesis involve DNA damage, chromosomal aberrations, and mutations
Leukemia: Benzene exposure is most strongly linked to leukemia;
Name at least four sources, including industrial processes and natural occurrences, that
contribute to dioxin release into the environment. Discuss the mechanisms of dioxin toxicity in
living organisms, considering its long-term effects on human health and wildlife.
DIOXINS are persistent organic pollutants. They are chlorinated aromatic hydrocarbons.
Industrial Processes:
By burning waste: when chlorine-containing materials are burned, dioxins are formed as byproducts.
Chemical Manufacturing: The production of certain chemicals, such as herbicides and pesticides, can produce dioxins.
Natural Occurrences:
Dioxins can also be released during volcanic eruptions as a result of the combustion of organic materials and the presence of chlorine compounds in volcanic gases.
Certain types of fungal activity can contribute to the release of dioxins into the environment in small quantities,
Mechanisms of Dioxin Toxicity in Living Organisms:
Interaction with the Aryl Hydrocarbon Receptor (AhR): triggers the expression of several genes.
Immune System Suppression: Dioxins can weaken the immune system,
Chronic Diseases: Chronic exposure to low levels of dioxins can lead to long-term health problems such as diabetes, cardiovascular diseases, and liver damage.
Toxic Effects on Wildlife:
Bioaccumulation: Dioxins are lipophilic (fat-soluble) and can accumulate in the tissues of animals over time, leading to biomagnification (refers to an increase in the
concentration of a substance as you
move up the food chain) in the food chain.
Dioxins weaken the imune system of wildlife.
In which ways people are exposed to flame retardants and what can be done to reduce this
exposure.
Retardants: Chemicals added to materials to to slow the spread of fire.
Like brominated flame retardants.
Household Dust: as they are released from furniture, carpets, electronics
Soft Furnishings: Many furniture items, such as sofas, chairs, and mattresses, contain flame retardants in their foam padding, fabric, or other materials to meet fire safety standards. Over time, these chemicals can migrate out of the furniture and into the surrounding environment. (skin exposure)
Contaminated Packaging: Certain food packaging materials, such as microwave popcorn bags, pizza boxes, and fast food wrappers, may contain flame retardants that can leach into food.
To minimize: use air filtration
Avoid Flame Retardant-Containing Electronics and Materials:
Be Cautious with Food Packaging (such as microwave popcorn bags or fast food wrappers)
Explain the multifaced aspects of PFAS, a group of synthetic chemicals known for their
widespread use and environmental persistence and consider the effectiveness of such frameworks in managing the global impact of these substances on ecosystems and public
health
PFAS: per- and Polyfluoroalkyl substances.
Examples: Perfluorooctanic Acid (PFOA), Perfluorooctane Sulfonic Acid (PFOS) and Perfluorohexane Sulfonic Acid (PFHxS).
Its fluorinated substances that contain at least one fully fluorinated methyl or methylene carbon atom.
Its suspected to cause cancer in gastrointestinal system, liver and kidneys.
PFAS sources: shampoo, fast food packaging, paint, non-stick cookware, pesticides.
Since its called a forever chemical (components break down very slowly over time) Stockholm convention restricted PFAS production.
Drinking water limits were set by EU for all PFAS;
Environmental Protection Agency (EPA) set limits also for PFAS;
European Food Safety Authority (EFSA) set limitations of tolerably weekly intake of 4.4 nanograms/kg of body weight per week for certain PFAS group compounds.
By setting these frameworks, government and institutions are protecting ecosystems from getting affected by POPs (Persistent Organic Pollutants) and also people from getting suspected health problems like cancer in livers, gastrointestinal and in kidneys.
