Uranyl acetate
Uranyl acetate is a DNA-binding protein inhibitor that suppresses DNA-binding activity through direct protein-protein interactions. Uranyl acetate stabilizes and fixes DNA and membrane structures in chicken malaria parasite sporozoites via staining. Uranyl acetate induces renal tubular cell apoptosis, regulates the expression of Bcl-2 and Bax, and causes acute renal failure in rats. Uranyl acetate forms stable complexes with ascorbic acid, induces single-strand breaks and relaxation of plasmid DNA in vitro, and exhibits chemical genotoxicity. Uranyl acetate can be used in research related to various diseases such as cancer and acute renal failure.
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- CAS. Nr.: 541-09-3
- Formel: C4H6O6U
- Molecular Weight:388.11
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Speicherung:
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Biologische Aktivität
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Uranyl acetate inhibits the DNA-binding activities of purified zinc finger proteins Aart and Sp1, as well as purified non-zinc finger proteins AP1 and NF-κB in a dose-dependent manner, with complete inhibition achieved at 200 µM; its inhibitory effect on the DNA-binding activities of purified AP1 and Aart is attenuated in the presence of 1% BSA[1].
Uranyl acetate inhibits the DNA-binding activity of purified Aart only when incubated with unbound protein, as it does not disrupt preformed DNA-protein complexes[1].
Uranyl acetate induces dose-dependent single-strand breaks in pBluescript SK+ plasmid DNA in vitro when combined with ascorbic acid, and forms a stable complex with ascorbic acid in D2O at room temperature[4].
Uranyl acetate (0.5%; 20 minutes) preserves and stains membranous structures of Plasmodium gallinaceum sporozoites isolated from Aedes aegypti midgut after glutaraldehyde-OsO4 double fixation in citrate or phosphate buffer, generating intact, distinct trilaminar pellicle, nuclear, mitochondrial, endoplasmic reticulum and dense inclusion body membranes[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Uranyl acetate (5 mg/kg; intravenous injection; administered twice at a 14-day interval) induces significantly milder acute renal failure in male Sprague-Dawley rats[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (male, 240-260 g)[2]
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Dosage:5 mg/kg
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Administration:i.v.; single injection
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Result:Elevated serum creatinine and tubular injury scores, both peaking at day 5 and recovering to baseline by day 14.
Triggered tubular apoptosis verified by electron microscopy and agarose electrophoresis at day 5.
Generated dual TUNEL-positive apoptotic cell peaks at day 5 and day 14, with values returning to baseline at day 21.
Reduced tubular epithelial cell counts to a nadir at day 5; cell numbers rebounded above baseline to peak at day 9 and normalized by day 21.
Maximized BrdU-positive nuclei at day 5 (baseline recovery at day 14) and PCNA-positive nuclei at day 5 (baseline recovery at day 15).
Suppressed Bcl-2 expression at days 5 and 9, with expression peaking at day 14 before normalization.
Slightly raised Bax expression at day 3, lowered expression at day 5, and produced a Bax expression peak at day 14 prior to baseline recovery.
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Animal Model:Sprague-Dawley (male, 240-260 g)[2]
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Dosage:5 mg/kg (first injection); 5 mg/kg (second injection 14 days after the first)
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Administration:i.v.; two injections 14 days apart
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Result:Elevated serum creatinine, peaking at day 3 after the second injection; this peak was milder than that of single-injection rats.
Raised tubular injury scores with a day 3 peak lower than single-injection groups, with full recovery to baseline by day 7.
Boosted TUNEL-positive tubular apoptotic cells starting at day 1, sustained high levels from day 3 to 7 without baseline recovery by day 14, and yielded a weaker peak than single-injection rats.
Maintained higher tubular epithelial cell counts per cross-section than single-injection rats up to day 7 post-second injection.
Slightly raised BrdU-positive nuclei at day 3, which returned to baseline by day 7.
Maximized PCNA-positive nuclei at day 3, followed by baseline restoration at day 7.
Upregulated Bcl-2 expression to an early peak at day 1, declined at day 5, and formed a secondary peak at day 7.
Elevated Bax expression to a peak at day 1 and retained above-baseline Bax levels over the full 14-day observation window.
Chemical Information
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CAS. Nr. 541-09-3
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Molecular Weight 388.11
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Formel C4H6O6U
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SMILES
O=C(O[U](=O)(=O)OC(=O)C)C
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Hartsock WJ, et al. Uranyl acetate as a direct inhibitor of DNA-binding proteins. Chemical research in toxicology. 2007 May;20(5):784-9. [Content Brief]
[2]. Sano K, et al. Role of apoptosis in uranyl acetate-induced acute renal failure and acquired resistance to uranyl acetate. Kidney international. 2000 Apr;57(4):1560-70. [Content Brief]
[4]. Yazzie M, et al. Uranyl acetate causes DNA single strand breaks in vitro in the presence of ascorbate (vitamin C). Chemical research in toxicology. 2003 Apr;16(4):524-30. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Uranyl acetate Related Classifications
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