SUPEROXIDE-DISMUTASE ACTIVITY IN HUMAN GLOMERULONEPHRITIS

Citation
A. Kashem et al., SUPEROXIDE-DISMUTASE ACTIVITY IN HUMAN GLOMERULONEPHRITIS, American journal of kidney diseases, 28(1), 1996, pp. 14-22
Citations number
31
Categorie Soggetti
Urology & Nephrology
ISSN journal
02726386
Volume
28
Issue
1
Year of publication
1996
Pages
14 - 22
Database
ISI
SICI code
0272-6386(1996)28:1<14:SAIHG>2.0.ZU;2-U
Abstract
Superoxide dismutase (SOD) in renal tissue biopsy specimens obtained f rom patients with immunoglobulin A nephropathy (13 cases) and non-immu noglobulin A mesangial proliferative glomerulonephritis (nine cases) w as studied at the protein level by an enzyme-linked immunosorbent assa y method and at the mRNA level by the reverse transcriptase-polymerase chain reaction (RT-PCR) assay. Total SOD activity in the tissue super natant was measured by applying an electron paramagnetic resonance/spi n trapping method, Normal renal tissues obtained from kidneys removed for malignancies (six cases) were included as healthy controls. The co pper and zinc form of SOD (Cu,Zn-SOD) activity at both the protein and mRNA levels was lower in the moderately or severely damaged tissues c ompared with that in the normal or mildly damaged tissues. On the othe r hand, manganese SOD (Mn-SOD) values at either the protein level or t he mRNA level did not differ significantly between control and patient samples. In the histochemical study using a polyclonal rabbit anti-Cu ,Zn-SOD antibody, the staining intensity for Cu,Zn-SOD antigen was low er in the areas with advanced histologic damage than in the intact tis sues. A follow-up study showed that renal function deterioration was p roportionately slower in patients whose SOD activity was within the ra nge of healthy tissue levels at the time of biopsy. Our data suggest t hat a lower level of SOD activity, whether as a cause or a consequence of the disease process, might induce a decrease in the scavenger reac tion of superoxide (O-2(-)), thus causing the tissue to become more vu lnerable to oxidative stress. (C) 1996 by the National Kidney Foundati on, Inc.