Toxicology

  • Created by: SamDavies
  • Created on: 11-01-19 23:40
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  • Toxicology
    • Cellular toxicity
      • GSH is an anti-oxidant
      • GSH also removes paracetamols reactive metabolite from the body
        • Phenols are electron rich - can be oxidised to quinones (highly reactive with GSH)
      • Depletion of GSH, increases reactive oxygen species
    • Liver toxicity
      • Depletion of GSH causes NAPQI accumulation
      • Leads reactions between the excess of quinone with proteins in the liver
      • The exogenous species would cause an anti-inflammatory immune response where liver attacks itself
    • Drug-Drug Interactions
      • CYP450 enzymes
        • Phase I oxidation in the liver
        • CYP450 inhibitors bind strongly to metal centre of haem group
        • CYP450 inhibitors are unhindered aromatic nitrogens
      • CYP450 inhibitors will make CYP450s unavailable to metabolise certain drugs, causing them to accumulate
    • Idiosyncratic toxicity
      • Type B reactions which occur rarely and unpredictably
      • Acyl glucuronides formed from phase II can be unstable, binding to random proteins in the body
        • Formed from -COOH
      • Increases risk of secondary pharmacology
      • This could lead to serious liver injury
    • Genotoxicity
      • Some active metabolites can bind with DNA causing a genetic mutation
      • Anilines and heteroaromatic amines
        • Can become oxidised and bind to DNA
      • Masked anilines
      • Thresholds and margins do not exist for these compounds
    • Off-target effects
      • Highly lipophilic compounds
      • NAIDS block COX2 for anti-inflammatory effects.
      • NSAIDS also block COX1, reducting prostaglandin production

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