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forensic toxicology - mechanisms of toxicity - Statistics
General Stats
- This quiz has been taken 2 times
- The average score is 26 of 48
Answer Stats
| Hint | Answer | % Correct |
|---|---|---|
| what do dying cells do during necrosis? | membrane integrity is lost and the cell body swells and bursts open | 100%
|
| what is apoptosis? | programmed cell death | 100%
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| what causes oxidative stress? | reactive oxygen (ROS) and reactive nitrogen (RNS) species | 100%
|
| activation of Ca2+-dependent hydrolytic enzymes (leads to disintegration of membranes, proteins etc.) | 50%
| |
| activation of Ca2+-dependent proteases (convert xanthine dehydrogenase to xanthine oxidase, which also produces superoxide and hydrogen peroxide) | 50%
| |
| activation of constitutively-expressed nitric oxide synthases in neuronal and endothelial cells (increases NO production, which reacts with superoxide to form highly reactive peroxynitrite) | 50%
| |
| how are these species generated indirectly? | activation of cytochrome P450, increased intracellular Ca2+ | 50%
|
| how do these species cause oxidative stress? | activation of dehydrogenases in the TCA cycle (increases electron output via the electron transport chain, causing increased production of superoxide) | 50%
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| what is Ca2+ involved in? | activation of enzymes (e.g. TCA cycle), cytoskeletal polymerisation, muscle contraction, neurotransmission, regulation of signal transduction and exocytosis, transporters | 50%
|
| how are these species generated directly? | activation of foreign compounds (e.g. benzene), redox cycling (e.g. paraquat), transition metals, inhibition of mitochondrial electron transport (blocking the electron transport chain) | 50%
|
| what do we need ATP for? | active transport, especially ion transport, biosynthetic reactions, cell division, cell morphology, cytoskeletal polymerisation, essential part of DNA, muscle contraction, regulation of signal transduction | 50%
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| what other issues can these species cause? | affecting the function of oxidise proteins, mutate DNA causing cellular dysfunction and reducing ATP synthesis, lipid peroxidation, cell swelling, cell lysis | 50%
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| when does calcium become toxic in the cytoplasm? | at high levels | 50%
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| what are the 3 primary causes of necrosis? | ATP depletion | 50%
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| why are the levels of calcium ions tightly regulated within a cell? | because it is so important and so reactive | 50%
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| what are four consequences ofexcitotoxicity? | depletion of ATP (Mitochondrial ATP production is decreased; activation of Ca2+ ATPase uses ATP) | 50%
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| what kind of 'essential function disruption' are these causes? | disruption to energy generation & protein synthesis | 50%
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| what do these species do to ATP? | drain the ATP reserves | 50%
|
| endoplasmic reticulum Ca2+ ATPase | 50%
| |
| what eventuates? | eventually the lipid fragments release reactive aldehydes and more free radicals | 50%
|
| excitotoxicity | 50%
| |
| what is the consequence of increased intracellular Ca2+? | excitotoxicity | 50%
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| what are the 4 mechanisms of calcium removal from the cell? | extracellular Ca2+ ATPase | 50%
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| extracellular Na+/Ca2+ exchanger | 50%
| |
| what will dying cells do during apoptosis? | fragment into membrane-bound apoptotic bodies | 50%
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| inhibition of ADP phosphorylation (eg. DDT) | 50%
| |
| what are the 4 key mechanisms by which ATP can be depleted? | inhibition of electron transport (eg. cyanide inhibits cytochrome oxidase) | 50%
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| inhibition of oxygen delivery to the ETC (eg. cocaine, carbon monoxide) | 50%
| |
| how can oxidative stress be avoided within a cell? | it can be quenched by enzymes | 50%
|
| what affect will this have on neighbouring cells? | it can trigger an inflammatory response or long term inflammation | 50%
|
| how does it stop oxidative stress? | it converts the superoxide radical (O2-) into H2O2 using metals such as Cu, Fe, Mn, or Ni. H2O2 is then degraded to H2O by catalase | 50%
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| what is the role of ion gradients in necrosis? | it sets off a positive feedback loop of Na+ and Ca2+ entering the cell, opening voltage-gated channels, which lets more ions enter etc. | 50%
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| what does this ion gradient cause that leads to necrosis? | loss of volume control: water influx & cell swelling until the cell lyses (dies) | 50%
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| microfilament dysfunction (disrupted morphology and function, impaired motility) | 50%
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| mitochondrial Ca2+ uniporter | 50%
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| what are oxidants? | molecules that can accept an electron | 50%
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| what are antioxidants? | molecules that can donate an electron | 50%
|
| what affect will this have on neighbouring cells? | none, the membrane makes it so cellular contents are not released, so cannot effect neighbouring cells | 50%
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| what is necrosis? | non-programmed cell death | 50%
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| which is more reactive? | oxidants | 50%
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| oxidative stress | 50%
| |
| what is lipid peroxidation? | peroxidative degradation of lipids by removal of hydrogen from fatty acids, producing a lipid radical. | 50%
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| physical damage to mitochondria (eg. chronic ethanol abuse) | 50%
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| production of reaction oxygen and nitrogen species (leads to disintegration of membranes, proteins etc.) | 50%
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| which is most important? | superoxide dismutase (SOD) | 50%
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| what is narcosis? | the bigger picture, downstream cellular effects that toxins can have | 50%
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| how is this further broken down? | this can be further broken down by reaction w oxygen, forming a lipid peroxyl radical | 50%
|
| what is oxidative stress? | when the balance of oxidants and antioxidants is disrupted, meaning that more oxidants are present | 50%
|
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