Contribution of hepatic reticuloendothelial system to glomerular IgA deposition in rat liver injury.
Liver damage was induced in rats by a single dose of dimethylnitrosamine or D-galactosamine. In the dimethylnitrosamine model, marked glomerular IgA deposition occurred between Days 4 and 28, with its peak at Day 14. Serum IgA levels were significantly increased at Days 2 and 4, then gradually decreased, and normalized at Day 14. In the D-galactosamine model, however, no such deposition was observed, though serum IgA levels similarly increased on Days 2 and 4. IgA content in high molecular weight fraction from serum increased at Day 3 in both models. This increment remained at Day 7 only in the dimethylnitrosamine model, in which carbon clearance from the circulation was significantly decreased at Day 3. These data suggest that dysfunction of the hepatic reticuloendothelial system is a factor contributing to glomerular IgA deposition occurring in liver injury.
Ogata
I
I
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Fujiwara
K
K
Nishi
T
T
Kuwata
S
S
Ohta
Y
Y
Nosaka
K
K
Oka
H
H
D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D002244:Carbon / Q000097:blood; D005591:Chemical Fractionation; D056486:Chemical and Drug Induced Liver Injury; D004128:Dimethylnitrosamine / Q000494:pharmacology; D005688:Galactosamine / Q000494:pharmacology; D007070:Immunoglobulin A / Q000032:analysis / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000378:metabolism*; D008099:Liver / Q000503:physiopathology*; D008107:Liver Diseases / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008970:Molecular Weight; D012157:Mononuclear Phagocyte System / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains
D007070:Immunoglobulin A; D002244:Carbon; D005688:Galactosamine; D000410:Alanine Transaminase; D004128:Dimethylnitrosamine