Deck 6: Receptor-Mediated Toxicities on the Outside of Cells

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Question
How does the Scatchard plot determine the potency of a given toxicant?
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Question
How does kainic acid cause toxicity to mammalian neuronal cells? What common local anesthetic agent do something opposite?
Question
Why does targeting tyrosine kinase receptors lead to either cell proliferation or cell damage/death?
Question
How can cAMP made by G-protein pathway be immunostimulatory or immunosuppressant?
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Deck 6: Receptor-Mediated Toxicities on the Outside of Cells
1
How does the Scatchard plot determine the potency of a given toxicant?
High affinity toxicants will be more potent in their toxic action as they bind as agonists or antagonists to the target receptor.
2
How does kainic acid cause toxicity to mammalian neuronal cells? What common local anesthetic agent do something opposite?
Kainic acid targets glutamate receptors increasing Na+ movement into these cells (overstimulates). Lidocaine blocks Na+ channels and would have opposite effects at concentrations that were anesthetic.
3
Why does targeting tyrosine kinase receptors lead to either cell proliferation or cell damage/death?
The tyrosine kinase pathway leads to cell proliferation as shown by the effect of the appetite suppression peptide obestatin on a gastric cancer cell line. However, pertussis toxin (whooping cough) has opposite effects as indicated by its partial ability to block the action of obestatin via inhibition of phosphoinositide 3-kinase.
4
How can cAMP made by G-protein pathway be immunostimulatory or immunosuppressant?
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