Gentamicin Injury
Gentamicin Injury - Related Videos
06:25
Kidney Regeneration in Adult Zebrafish by Gentamicin Induced Injury
0 Views •
Cited by 27 •
2015
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.
07:58
Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury
0 Views •
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.
07:28
Controlled Cervical Laceration Injury in Mice
0 Views •
Cited by 17 •
2013
A novel technique to create a reproducible in vivo model of cervical spinal cord laceration injury in the mouse is described. This technique is based on spine stabilization by fixation of the cervical facets and laceration of the spinal cord using an oscillating blade with an accuracy of ±0.01 mm.
15:55
Intravenous Microinjections of Zebrafish Larvae to Study Acute Kidney Injury
0 Views •
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.
04:19
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
0 Views •
Cited by 16 •
2017
Athletes absorb several hundred mild traumatic brain injuries (mTBI)/concussions every year; however, the consequence of these on the brain is poorly understood. Therefore, an animal model of single and repetitive mTBI that consistently replicates clinically relevant symptoms provides the means to advance the study of mTBI and concussion.
FAQs
Following uptake, gentamicin can accumulate within cells and disturb organelle function. This disruption is associated with increased production of reactive oxygen species, chemically reactive molecules that can damage cellular components. The resulting stress may activate apoptosis, a regulated form of cell death. Tracking these linked events helps researchers connect intracellular drug accumulation with tissue-level injury.
Reactive oxygen species provide a mechanistic link between organelle disruption and apoptosis during gentamicin injury. Their increase signals cellular stress and can precede activation of pathways that eliminate damaged cells. Measuring this response allows investigators to distinguish general tissue damage from specific stress-related processes and to evaluate whether a genetic or pharmacological factor changes cellular vulnerability.
Renal cells and sensory hair cells represent two important injury contexts associated with gentamicin exposure: nephrotoxicity and ototoxicity. Studying both systems enables comparison of tissue-specific damage, cell death, and recovery responses. In developmental biology, these models also reveal how developing tissues respond to toxic stress and whether regeneration or protective mechanisms modify the outcome.
Developmental models can show that tissue responses depend on cellular and tissue context rather than exposure alone. Controlled injury in embryos or larvae allows researchers to examine which tissues undergo cell death, which display protective responses, and whether damaged regions recover through regeneration. These observations help connect developmental state with susceptibility and repair.
Researchers use controlled gentamicin exposure in embryos or larvae to create a consistent model of drug-induced tissue damage. They can then examine cellular injury, apoptosis, tissue vulnerability, regeneration, and protective responses within a developing organism. This approach is useful because it links molecular and cellular events to visible changes in developing tissues and recovery over time.
Gentamicin injury models support investigation of genetic, cellular, and pharmacological factors that influence damage and recovery. A study may compare how these factors alter cell death, tissue vulnerability, protective responses, or regeneration after exposure. Such comparisons help identify variables associated with nephrotoxicity or ototoxicity and clarify why outcomes differ among experimental conditions.