Related Experiment Videos
Polymorphonuclear leukocytes increase glomerular albumin permeability via hypohalous acid
J Z Li1, R Sharma, K N Dileepan
1University of Kansas Medical Center, Department of Medicine, Kansas City.
Kidney International
|October 1, 1994
Summary
Hypohalous acids, generated by hydrogen peroxide and myeloperoxidase, increase glomerular permeability in acute glomerulonephritis. This finding implicates hypohalous acids as key mediators of kidney injury from activated neutrophils.
Area of Science:
- Nephrology
- Immunology
- Biochemistry
Background:
- Acute glomerulonephritis involves neutrophil infiltration and reactive oxygen species (ROS) generation.
- Hydrogen peroxide (H2O2) and hypohalous acids are ROS implicated in neutrophil-mediated kidney injury.
Purpose of the Study:
- To investigate the specific role of ROS in neutrophil-induced glomerular injury.
- To determine if hypohalous acids mediate increased glomerular permeability.
Main Methods:
- Isolated rat glomeruli were incubated with H2O2, H2O2 plus myeloperoxidase (MPO), or activated polymorphonuclear leukocytes (PMNs).
- Glomerular albumin permeability (Palbumin) was measured.
- ROS scavengers (superoxide dismutase, catalase, taurine, sodium azide, dimethyl sulfoxide) were used to assess mechanisms.
Main Results:
- H2O2 alone did not increase Palbumin.
- H2O2 with MPO significantly increased Palbumin.
- Activated PMNs, but not non-activated PMNs, increased Palbumin.
- Superoxide dismutase, catalase, and taurine inhibited the increase in Palbumin, suggesting a role for ROS.
Conclusions:
- Hypohalous acid, generated via the H2O2-MPO-halide system, increases glomerular albumin permeability.
- Hypohalous acid is likely the primary mediator of immediate glomerular protein leakage induced by PMNs in acute glomerulonephritis.