Nanotoxicology Flashcards

1
Q

why is nanoparticle size important for nanotoxicology?

A

diameter dependent excretion
e.g. zwitterionic cysteine coated quantum dots
e.g. PMAM-gold NPs accumulate in the blood = increase size

  • larger size found in liver and spleen/ smaller size excreted in the urine
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2
Q

why is nanoparticle surface charge important for nanotoxicology?

A

increase conc of [DOPC:DOTAP:CHOL] in DOPC:DOTAP:CHOL:PEG liposomes

DOPC:DOTAP:CHOL = positive charge

charged liposomes = cleared quickly

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3
Q

what does DOPC:DOTAP:CHOL do to liposomes?

A

give it a/increase positive charge = aggregate with proteins in the blood = lung accumulation

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4
Q

where do DOPC:DOTAP:CHOL liposomes deliver drugs? why?

A

lung
due to protein aggregation due to their positive charge

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5
Q

how does PEG improve nanotoxicology?

A

mask surface charge = stop lung accumulation and fast excretion
= increasing the liposomes half life

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6
Q

why is nanoparticle shape important for nanotoxicology?

A

important for phagocytosis

pointed end of elliptical disc = fast phagocytosis (few minutes)
contact with flat region = slow phagocytosis (over 12hours)

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7
Q

why is it hard to use traditional toxicology assays for NPs?

A

e.g. CNTs - π–π stacking between CNT and reagents in the toxicology assays like MTT and LDH assay

π–π stacking with polycyclic nature/rings = blocks absorbance and fluorescent readings

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8
Q

what are traditional toxicology assays?

A

MTT - mitochondrial succinate dehydrogenase
LDH- lactate dehydrogenase

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9
Q

what reagents are used in traditional toxicology assays?

A

polycyclic nature/rings

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10
Q

how does LDH- lactate dehydrogenase work?

A

LDH releases when cells have defects in the membrane
= LDH detection
= toxicology reported

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11
Q

what is the toxic effect of NPs we are worried about?

A

biological side effects
environmental/workplace exposure of CNTs - lung and skin exposure

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12
Q

name NP affects

A
  1. NP inhalation
    - brain - parkinson’s/alzheimer’s
    - lung - asthma/bronchitis/emphysema/cancer
    - circulatory - artherosclerosis/ vasoconstriction/ thrombus/ high bP
    - heart - arrhythmia/ heart disease/ death
    - lymphatic system - kaposi’s sarcoma
    - skin - auto-immune diseases
  2. NP ingestion
    - GI - crohn’s disease/colon cancer
    - orthopedic implants wear debris - auto-immune diseases/dermatitis/ urticaria/vasculitis
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13
Q

what type of NPs are less toxic?

A

chemically functionalised CNTs

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14
Q

what type of chemical functionalisations can you make to MWNTs?

A
  1. addition of alkyl chain - hydrophobic
  2. addition of ammonium chain - hydrophobic, increase dispersibility
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15
Q

how are inflammatory reactions notices with CNTs?

A

granuloma formation
- mass of immune cells that forms when the immune system attempts to eliminate substances

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16
Q

whats the difference between NT2 pristine and NT2 alykl/TEG?

A

NT2 alkyl and NT2 TEG had lower amounts of granulation than NT2 pristine

17
Q

why does NT2 alkyl and NT2 TEG have lower amounts of granulation than NT2 pristine?

A

NT2 pristine- after sonication still forms long and hydrophobic needles
NT2 alkyl and NT2 TEG- after sonication forms smaller CNTs easier to be phagocytosed by the cell

18
Q

how are CNTs degraded?

A

horseradish peroxidase (HRP) enzyme with low conc. hydrogen peroxide
myeloperoxidases (MPO)

19
Q

what is horseradish peroxidase (HRP) enzyme with low conc. hydrogen peroxide be used for?

A

degrading CNTs - SWCNT and MWCNTs

20
Q

what is myeloperoxidases (MPO) used for ?

A

CNT degradation

21
Q

what is hMPO used for ?

A

implantable polymer degradation