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Updated: Jul 15, 2026
Isolation of Mouse Peritoneal Cavity Cells
Published on: January 28, 2010
A short review of experimental peritoneal sclerosis: from mice to men
L Gotloib1, V Wajsbrot, A Shostak
1Department of Nephrology, Hypertension and the Research Center for Experimental Nephrology, Ha'Emek Medical Center, Afula 18101, Israel. gotloib@012.net.il
Abstract:
Peritoneal sclerosis has been induced in rodents in vivo by exposing the membrane to a variety of experimental interventions: asbestos, 0.1% chlorexidine, iron dextran, glucose degradation products, AGE deposits derived from uremia per se, sodium hypochlorite, lypopolysaccharide, low pH, pure water, silica or zymosan. With a few exceptions (pure water, chlorhexidine and low pH), the other substances mentioned operate setting out different degrees of oxidative stress. This short review describes several experimental interventions in rodents, aimed at acute exfoliation or long-term, sustained injury of the mesothelial monolayer performed by means of intraperitoneal injections of different oxidant agents. Acute exfoliation induced by deoxycholate resulted in a depopulated monolayer coincident with immediate alteration of the peritoneal permeability, evidenced by increased urea D/P ratio, higher glucose absorption rate, elevated albumin losses in the effluent and significant reduction of the ultrafiltration rate. In the long term (30 days), these manifestations of membrane failure persisted and coincided with substantial peritoneal sclerosis. Peritoneal sclerosis was also induced by IP injections of 0.125% trypsin and 6.6 mM/L solution of formaldehyde. Using the doughnut rat model of mesothelial regeneration, exposure to 4.25% glucose or 7.5% icodextrin solutions severely hampered repopulation of the monolayer, which was replaced by a thick sheet of fibrous tissue. It is concluded that peritoneal sclerosis derives mostly from sustained oxidative injury to the peritoneal membrane. Loss of the mesothelial monolayer is the first step in the chain of events leading to this complication.
Insights
Peritoneal sclerosis in rodents is often caused by oxidative stress to the peritoneal membrane. Loss of the mesothelial cell layer is the initial event leading to this serious complication.
Area of Science:
- Nephrology
- Cell Biology
- Toxicology
Background:
- Peritoneal sclerosis is a serious complication of peritoneal dialysis.
- Experimental models are crucial for understanding its pathogenesis.
Purpose of the Study:
- To review experimental interventions inducing peritoneal sclerosis in rodents.
- To elucidate the role of oxidative stress in mesothelial cell injury and sclerosis.
Main Methods:
- Induction of peritoneal sclerosis in rodents using various agents (asbestos, chlorexidine, iron dextran, etc.).
- Assessment of mesothelial monolayer integrity and peritoneal membrane function.
- Evaluation of long-term effects of injury (30 days) and regeneration models.
Main Results:
- Multiple agents, primarily those causing oxidative stress, induced peritoneal sclerosis.
- Acute injury led to increased peritoneal permeability and albumin loss.
- Sustained injury and impaired regeneration resulted in fibrosis and sclerosis.
Conclusions:
- Sustained oxidative injury to the peritoneal membrane is the primary cause of peritoneal sclerosis.
- Loss of the mesothelial monolayer is the initiating event in sclerosis development.
