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Renal Toxicology (Screening for damage (Has vol of urine changed from…

- - - - Major target organ for toxicity
  - - - [Gentamycin] in these cells can be 10-100x more conc than blood. 5-6 days half life in cell in kidney
    - - Secondary
        
        Changes in cytoskeleton results in Ca2+ entering the cell
        
        mitochondrial damage electron transport chain takes place but no atp is produced and Ca2+ is realeased
        
        10K fold difference in [Ca2+] inside and outside the cell
        
        Increase in Ca2+ in cell:
        degrades cytoskeleton
        activates phospholipases which breakdown mitochondrial membranes, proteases degrading proteins
        endonucleases degrading DNA.
        
        Decreases ATP production. Activates apoptosis pathways. increases ROS generation
      - Tertiary
        
        Steatosis - fatty acid droplets in liver
        
        Blebbing - blisters on plasma membrane
        
        Necrosis - uncontrolled chaotic cell death
      - Primary
        
        Cell can survive lipid peroxidation
        NAPQI covalently binding to proteins
        
        Thiol - Glutathione (GSH) contains thiol group
        Thiol group allows binding of toxin instead of to proteins. Removes hydrogen
        
        When GSH runs out, N-aetylcysteine is used as a replacement via antidote
        
        Also contains thiol group and can help make GSH (antioxidant)
        
        Reduces levels of primary toxification