Probenecid
Probenecid - Related Videos
10:39
Single Cell Measurements of Vacuolar Rupture Caused by Intracellular Pathogens
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Cited by 22 •
2013
We describe a method for tracking the endomembrane rupture elicited by the intracellular bacteria Shigella flexneri and Mycobacterium tuberculosis upon host cell invasion. Our assay makes use of CCF4, a host cytoplasmic FRET probe in live or fixed cells. This reporter is degraded by an enzyme activity present on the bacterial surface.
11:17
Monitoring Changes in Membrane Polarity, Membrane Integrity, and Intracellular Ion Concentrations in Streptococcus pneumoniae Using Fluorescent Dyes
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Cited by 44 •
2014
Unlike that seen for eukaryotes, there is a paucity of studies that detail membrane depolarization and ion concentration changes in bacteria, primarily as their small size makes conventional methods of measurement difficult. Here, we detail protocols for monitoring such events in the significant Gram-positive pathogen Streptococcus pneumoniae utilizing fluorescence techniques.
10:29
Applying Fluorescence Resonance Energy Transfer (FRET) to Examine Effector Translocation Efficiency by Coxiella burnetii during siRNA Silencing
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Cited by 15 •
2016
Investigating the interactions between bacterial pathogens and their hosts is an important area of biological research. Here, we describe the necessary techniques to measure effector translocation by Coxiella burnetii during siRNA gene silencing using BlaM substrate.
FAQs
At the proximal tubule, URAT1 normally reabsorbs urate from forming urine back into the body. Probenecid inhibits this transporter, so less urate is returned and more is eliminated in urine. This mechanism links transporter activity with serum urate regulation and explains why the drug is important for studying renal transport and uric acid biology.
Probenecid also affects organic anion transporters involved in renal drug secretion. When secretion is reduced, certain compounds may be cleared from the body more slowly. This effect is particularly relevant to penicillins, because modifying their renal handling can prolong their activity and demonstrates how transporter interactions influence drug disposition.
Transporter interactions can change how quickly a drug leaves the body, even when the drug’s primary biological target is elsewhere. Probenecid provides a way to examine this relationship through its effects on organic anion transporters and renal secretion. Studying these changes helps connect membrane transport processes with altered drug clearance.
Researchers can use probenecid as a transporter-modifying experimental tool because it perturbs defined renal handling pathways, including URAT1-mediated urate reabsorption and organic anion transport. Observing changes in urate excretion or drug clearance can help relate transporter activity to measurable biological outcomes and clarify the contribution of renal membranes to disposition.
The clinical objective is to lower serum urate and help prevent recurrent gout. Increasing urinary uric acid excretion changes the balance between circulating urate and renal elimination. This application illustrates how a renal transport mechanism can be used therapeutically while also providing a practical context for studying urate regulation in biology.
Probenecid can reduce the renal secretion of certain antibiotics, including penicillins, thereby slowing their clearance from the body. The resulting prolongation of antibiotic activity makes the interaction useful in selected treatment contexts. Biologically, this example shows how one compound’s effects on organic anion transport can modify another compound’s duration of action.