L11 : Life in High Toxicity Flashcards

1
Q

Name earth, space and anthropogenic sources of ionising radiation?

A

Earth:
- Radioactive decay of mantle/crust, minerals
- high altitude
Space:
- Solar radiation
- Cosmic radiation
Anthropogenic:
- Healthcare applications
- Nuclear power and waste, accidents

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2
Q

Explain why radioresistant lineages are unclear?

A

Scattered distribution of radioresistant species
- Ability lost gradually from lineages through natural selection/genetic drift
- Ability evolved independently through horizontal gene/convergent evolution

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3
Q

What is the link between radiation and origin or life?

A

Much higher background radiation when life emerged
Early life must have had considerable radiation resistance and used energy from ionising radiation

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4
Q

How does direct dionising radiation damage the cell (DNA, protein, lipid)?

A

DNA:
- Mutations
- Direct breaks
- Loss of nitrogenous bases
- Cell cycle arrest
Proteins:
- Denaturation
- Misfolding
- Carbonylation
Lipids:
- Oxidation
- Membrane disruption
- Ion leakage

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5
Q

How does indirect ionising radiation damage the cell?

A
  • Organelle damage
  • Mitochondrial dysfunction (ATP depletion)
  • Dehydration (H2O becomes ROS)
  • Inflammation (cytokines, chemokines released
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6
Q

What is the consequences of ionising radiation on cells?

A

Apoptis or necrosis

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7
Q

What are 3 examples of reactive oxygen species (ROS)?

A

Superoxide (O2-)
Hydrogen peroxide (H2O2)
Hydroxyl free radicals (OH-)

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8
Q

What are 6 DNA adaptations for high radiation?

A
  1. Robust DNA repair mechanisms
  2. Gene redundancy
  3. Formation of highly compact, stable genome
  4. Use of pigmentation
  5. DNA dimer prevention
  6. Robust cell cycle checkpoint
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9
Q

What are proteins and components involved in the cellular stress response to high radiation?

A
  1. Extracellular polymeric substances (EPSs)
    - Retain H2O, form biofilms
  2. Outer membrane/LPSs
    - Extra protection, retain H2O
  3. Aquaporins
    - Allow H2O into cell
  4. Thick membrane, modified lipids (unsaturated)
  5. High levels antioxidants (carotenoids, CAT, SOD)
  6. Osmolytes
    - Protect from osmotic stress, dehydration
  7. High levels of dark pigments
    - Protect cell, antioxidants
  8. Mn(II)-phosphate complexes
    - Protect from ROS, enhance recovery
  9. Hydrolases, ATP-dependent proteases]
    - Removal of damaged DNA, proteins, organelles
  10. Chaperones (HSPs)
    - Protect from denaturation/aggregation
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10
Q

Example of radioresistant archaea?

A

Euryarchaeota
(Hyperthermophilic - thermococcus gammatolerans)

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11
Q

Example of radioresistant bacteria?

A

Deinococcus
(Deinococcus radiodurans)

Bacteroidetes
(Hymenobacter xinjiangensis)

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12
Q

Example of radioresistant eukaryotes?

A

Fungi
(Cryptococcus neoformans, cladosporium)
Algae
(Hematococcus)
Tardigrades

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13
Q

Deinococcus radiodurans

A

C

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14
Q

Chernobyl fungi variety

A
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15
Q

Cross contamination concerns

A
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16
Q

What are xenobiotics?

A

Substances that are foreign to an organisms normal chemistry

17
Q

How can xenobiotics cause damage?

A

Dose dependent
Heavy metals compete with normal components
- Bind to and damage lipids, proteins, DNA

18
Q

What are metalophiles?

A

Organisms that have an affinity for or thrive in the presence of xenobiotics and metals

19
Q

Examples of toxic environments for metalophiles?

A
  • Mining sites
  • Metal processing plants
  • Industrial sewage
  • Earth crust
  • Hydrothermal vent systems
  • Volcanic areas
  • Healthcare and cosmetics
20
Q

Why do cell membrane adaptations help with high toxicity?

A
  • Increased permeability
  • Maintain osmotic gradient
  • Expel heavy metals
21
Q

What are cell membrane adaptations to high toxicity?

A
  1. More unsaturated phospholipids - increase permeability
  2. FAs with either bonds and isopropenoid chains - aid nutrient transport
  3. More phosphate lipid head groups - bind +ve HM ions
  4. More free -COOH groups - bind +ve HM ions
  5. Metal specific ion channels (eg. ArsB/C)
  6. Non specific ion channels (porins, voltage, pH etc.)
  7. Efflux pumps (eg. ABC transporters)
  8. Proton pumps - power transporters
22
Q

Why do cell environment stress responses help with high toxicity?

A
  • Remove excess metals
  • Neutralise toxicity
  • Prevent cellular damage
23
Q

What are cell environment stress responses to high toxicity?

A
  1. Extracellular sequestration/ chelation in periplasm
  2. Precipitation/ mineralisation - transform HM into solid mineral forms and neutralise toxicity
  3. Antioxidant production (eg. Glutathione, SOD, thioredoxins)
  4. Intracellular chelation (citrate, histidine)
  5. Metal redistribution through compartmentalisation - minimise HM interference
  6. Chaperones (HSPs) - regulate adaptation to HM stress
  7. Sequestration - HM binding with metallothioneins, phytochelatins etc.
  8. Vacuolar sequestration - HM storage
24
Q

What are adaptations against protein misfolding in high toxicity?

A
  1. Cys and His - strong affinity for HMs
  2. Asp and Glu acid - COOH bind +ve metal ions
  3. Zinc finger motifs - stabilised by Zn+, allow cellular interaction under metal stress conditions
  4. Alpha helices to tolerate mild unfolding
  5. Chaperones (HSPs) to mediate folding
  6. Cysteine - contain thiol (-SH) that binds HMs
  7. Helix-turn-helix motifs - sense and bind HMs
25
Q

What are adaptations against protein denaturation and aggregation in high toxicity?

A
  1. Salt bridges
  2. Metal cofactors (eg. Rubredoxins bind Fe+)
26
Q

What are adaptations against loss of enzyme activity in high toxicity?

A
  1. Enzyme redundancy - compensation
  2. Evolution of specific binding motifs for metal ions
27
Q

What are DNA adaptations against high toxicity?

A

Must withstand oxidative stress from high HM presence

  1. Robust DNA repair mechanisms
  2. Metal resistance gene expression
  3. Dps (DNA protection during starvation) proteins - bind and shield DNA
28
Q

What are energy utilisation adaptations in high toxicity?

A
  1. Dissimilatory metal reduction (DMR) - use of HMs as terminal electron acceptors in respiratory chain
  2. Assimilation - uptake and integration of HMs into cellular components for metabolic use
  3. Metabolism adjustment - prioritise ATP production for active transport
  4. Use alternative energy pathways (glycolysis even in presence of o2)
  5. Enhanced redox recycling of HMs - to convert into useable energy
  6. Use anaerobic pathways to cope with o2 lack
  7. Use phosphatase hydrolysis - generates energy for HM sequestration, chelation, transformation
  8. Some use symbiotic relationships
29
Q

Examples of archaea with resistance to heavy metals?

A

Sulfolobus acidocalarius - sulfur-rich geothermal springs
Ferroplasma acidarmanus - acidic mine drainage

30
Q

Examples of bacteria with resistance to heavy metals?

A

Cupriavidus metallidurans - metal-contaminated soils and mines
Acidithiobacillus ferrooxidans - thrives in high Fe2+ and sulfur (mines)

31
Q

Examples of eukaryotes with resistance to heavy metals?

A

Fungi (Aspergillus niger) - contaminated soils
Common sunflower (Helianthus annuus) - metal contaminated soils

32
Q

Earths toxic environments as astrobiological models