Organ selective toxicity
8 important questions on Organ selective toxicity
What is molecular homology?
What is an example of liver selective transcription factors?
HNF1alpha is abundantly expressed in liver and HNF1Beta in kidney.
What are the mechanisms behind DES induced developmental changes?
- DES can methylate the DNA wherby DES is able to sensitize the target cells. like cells from the mullerian duct.
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Why can only DES induce embryotoxicity and not normal estrogen?
- DES is an extremely potent ligand of the ER compared with estradiol.
- maybe there are more factors involved like receptor conformational changes. Differential binding to response elements on DNA, recruitment of coregulatory proteins and cross talk with signaling systems.
- Some of the effects of DES are caused by non-ER mechanisms
What are the mechanims behind the plasiticizer DEHP liver toxicity in rodents?
- Most humans express mutated forms of PPARalpha (truncated) which are functionaly inactive.
Why are liver and kidneys so often involved in toxicity?
- both organs have a large variety of metabolizing enzymes including p450
- both organs contain polarized cells. both cell types have excretory function. Such primary or secondary transport systems can highly upconcentrate xenobiotics or their metabolites in certain compartments.
- The liver also harbors high amounts of Kupffer cells that can induce immune mediated toxicity.
What is the role of CYP2E1 in the toxic respons of APAP?
What are mechanisms underlying the cephalosporin nephrotoxicity?
- It is rapidly transported across the basolateral membrane via OAT1.
- cephalosporin has a low affinity for OAT4 at the apical membrane.
- result accumulation.
- Downstream consequences: redox cycling of the pyridine ring, acylation and inactivation of tubular cell proteins through spontaneous reactivity of the beta lactam ring and inhibition of the mitochondrial fatty acyl carnitine transport.
- inhibition of complex 4 in the mitochondria.
- Other xenobiotics have similar toxic mechanisms.
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