Gentamicin Nephrotoxin
Gentamicin Nephrotoxin - Related Videos
07:58
Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury
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Cited by 8 •
2016
Renal injuries incurred from nephrotoxins, which include drugs ranging from antibiotics to chemotherapeutics, can result in complex disorders whose pathogenesis remains incompletely understood. This protocol demonstrates how zebrafish can be used for disease modeling of these conditions, which can be applied to the identification of renoprotective measures.
04:18
Intravenous Microinjection of Nephrotoxins into Zebrafish Embryo: A Technique to Deliver Nephrotoxic Agents into the Bloodstream of Zebrafish Embryo
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This video demonstrates the intravenous microinjection of nephrotoxins into the tail vein of a zebrafish embryo to study their chemical effects on renal function.
06:25
Kidney Regeneration in Adult Zebrafish by Gentamicin Induced Injury
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Cited by 27 •
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Here we present a reliable method to study adult kidney regeneration by inducing acute kidney injury by gentamicin injection. We show that injury is dependent on gentamicin dosage and environmental temperature using in situ hybridization to label lhx1a+ developing new nephrons.
15:55
Intravenous Microinjections of Zebrafish Larvae to Study Acute Kidney Injury
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Cited by 83 •
2010
We describe a technique of microinjecting the aminoglycoside, gentamicin, into 2 days post-fetilization (dpf) zebrafish larvae to induce acute kidney injury (AKI). We also describe a method for whole mount immunohistochemistry, plastic embedding and sectioning of zebrafish larvae to visualize the AKI mediated damage.
13:39
Antibiotic Susceptibility Testing: Epsilometer Tests to Determine MIC Values of Two Antibiotics and Evaluate Antibiotic Synergy
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2023
Source: Anna Bläckberg1, Rolf Lood1 1 Department of Clinical Sciences Lund, Division of Infection Medicine, Biomedical Center, Lund University, 221 00 Lund Sweden Knowledge of the interactions between antibiotics and bacteria is important in understanding how microbes evolve antibiotic resistance. In 1928, Alexander Fleming discovered penicillin, an antibiotic that exerts its antibacterial function by interfering with cell wall regeneration (1). Other antibiotics with diverse mechanisms of...
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Filtered gentamicin reaches proximal tubule cells through megalin- and cubilin-mediated endocytosis, a receptor-associated uptake process. This route helps explain why the drug can accumulate inside these cells rather than remaining only in tubular fluid. The resulting intracellular exposure provides the starting point for studying how an antibiotic produces localized renal cellular injury.
Inside proximal tubule cells, gentamicin accumulates in lysosomes, where it can disturb membrane integrity, mitochondria, and cellular signaling. These changes connect intracellular drug retention with broader cellular dysfunction rather than treating toxicity as a single isolated lesion. Studying several affected compartments helps investigators link organelle-level disruption to impaired tubular performance.
When gentamicin injury disrupts proximal tubule function, tubular reabsorption may decline, while markers of renal dysfunction may rise. Measuring both functional impairment and biochemical indicators gives experiments complementary evidence: one reflects what the tubule can do, and the other signals deterioration of kidney performance. Together, these outcomes characterize consequences beyond cellular damage alone.
A basic study introduces gentamicin into an experimental model and examines consequences at cellular and kidney-function levels. Investigators can look for injury involving proximal tubule cells, changes in tubular reabsorption, and elevated renal dysfunction markers. This design connects the exposure to measurable biological outcomes without relying on a single indicator of nephrotoxicity.
Useful readouts span cellular damage and renal performance. At the cellular level, investigators can examine disruption involving lysosomes, mitochondria, or signaling. At the functional level, they can assess tubular reabsorption and markers of renal dysfunction. Considering these categories together helps distinguish intracellular injury from its consequences for kidney physiology.
By applying a candidate protective compound within a gentamicin injury model, researchers can ask whether it reduces cellular damage or preserves kidney-related function. Evidence may come from less disruption of affected cell components, better tubular reabsorption, or lower renal dysfunction markers. The model therefore supports comparative evaluation of interventions against a defined toxic exposure.
Gentamicin nephrotoxicity links antibiotic exposure to renal physiology and drug-induced acute kidney injury. Its experimental use allows researchers to study how proximal tubule cells respond to intracellular drug accumulation, how that response affects reabsorption, and how renal dysfunction can be detected. The model also provides a setting for evaluating compounds intended to protect kidney function.