Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Metabolomic investigation of cisplatin-induced acute kidney injury in paediatric cancer patients.

British journal of clinical pharmacology·2026
Same author

Difference of Admission Neutrophil Gelatinase-Associated Lipocalin Concentration Between Patients Developing and Not Developing Acute Kidney Injury or Need for Acute Dialysis: An Ancillary Individual-Study Data Meta-Analysis (INDICATE-AKI).

Kidney medicine·2026
Same author

Physiological role of gamma-glutamyl transpeptidase: Demise of the gamma-glutamyl cycle.

Analytical biochemistry·2026
Same author

Urine Olfactomedin 4 Predicts Furosemide Response and Kidney Replacement Therapy in Critically Ill Children.

Critical care explorations·2025
Same author

The Renal Activity Index for Lupus: Validation for Prediction of Kidney Inflammation in Adult Patients With Lupus Nephritis.

The Journal of rheumatology·2025
Same author

The Renal Activity Index for Lupus Identifies Active Renal Disease and Treatment Response in Adult Patients With Systemic Lupus Erythematosus and Lupus Nephritis.

Arthritis care & research·2025

Related Experiment Video

Updated: Jul 8, 2026

Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
13:25

Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish

Published on: May 15, 2021

Cisplatin nephrotoxicity: molecular mechanisms.

Marie H Hanigan1, Prasad Devarajan

  • 1Department of Cell Biology, University of Oklahoma Health Sciences Center.

Cancer Therapy
|January 11, 2008
PubMed
Summary

Cisplatin chemotherapy can cause kidney damage (nephrotoxicity), limiting its cancer treatment effectiveness. This review explores new insights into cisplatin

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Cisplatin is a vital chemotherapy drug for various cancers.
  • Its efficacy is dose-dependent, but nephrotoxicity often restricts optimal dosing.
  • Understanding cisplatin's kidney toxicity mechanisms is crucial for improving cancer therapy.

Purpose of the Study:

  • To review recent advances in understanding cisplatin nephrotoxicity mechanisms.
  • To highlight distinct toxicity pathways in tumor cells versus kidney cells.
  • To explore novel therapeutic targets for mitigating kidney damage.

Main Methods:

  • Review of current scientific literature on cisplatin nephrotoxicity.
  • Analysis of biochemical and molecular mechanisms of renal cell injury.

More Related Videos

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
15:43

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

Related Experiment Videos

Last Updated: Jul 8, 2026

Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
13:25

Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish

Published on: May 15, 2021

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
15:43

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

  • Examination of studies on apoptosis and intracellular signaling pathways.

    • Main Results:

    • Cisplatin exhibits different toxicity mechanisms in tumor cells and renal proximal tubular cells.
    • Gamma-glutamyl transpeptidase plays an unexpected role in cisplatin nephrotoxicity.
    • Proximal tubular cells can metabolize cisplatin into a nephrotoxic agent.
    • Apoptosis is a key mechanism in cisplatin-induced kidney cell damage.

    Conclusions:

    • Novel therapeutic strategies may emerge from understanding these mechanisms.
    • Minimizing nephrotoxicity can enhance cisplatin's anti-cancer efficacy.
    • Targeting specific pathways could protect kidneys during cisplatin treatment.