title: Lipid peroxidation and renal tubular damage in chronic pancreatic diseases: is there any relationship?
abstract: Lipid peroxidation is one of the most important expression of oxidative stress induced by oxygen-derived free radicals. Here we evaluate the behavior of malondialdehyde (MDA) in the serum and urine from patients with chronic pancreatic diseases, with respect to patients with extra-pancreatic digestive diseases and glomerulonephritis. Serum and urinary phospholipase A2 (PLA2) activity was also determined, since this enzyme contributes to damage of plasma membranes. MDA and PLA2 levels increased in the sera from most of the patients with pancreatic and extra-pancreatic digestive diseases. In glomerulonephritis, pathological MDA levels (36%), but not PLA2 levels, were found. Serum MDA correlated with gamma-glutamyl transpeptidase (GGT), while PLA2 correlated with alanine-phosphodiesterase (ALP), GGT, alanine-aminotransferase (ALT) and creatinine. In urine, MDA and PLA2 behaved differently from the corresponding serum values. MDA increased in some patients with pancreatic cancer, extra-pancreatic diseases and glomerulonephritis. PLA2 levels did not significantly vary between groups. Urinary MDA correlated with some indicators of renal tubular damage [urinary ribonuclease, beta-2-microglobulin (B-2-M) and N-acetyl-glucosaminidase (NGA)] and with serum bilirubin. Urinary PLA2 correlated only with ribonuclease (RNase). We conclude that serum MDA increases aspecifically in pancreatic and extra-pancreatic diseases, probably reflecting an aspecific phlogistic phenomenon; PLA2, although sharing a similar pattern with MDA, seems mainly related to hepato-biliary damage. Urinary MDA reflects the presence of renal tubular damage, which may be the cause or a consequence of lipid peroxidation; little variations in PLA2 are recorded in urine, and mainly reflect the presence of impaired tubular function.
authors.affiliation: Institute of Laboratory Medicine, University of Padova, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Basso
authors.forename: M P
authors.initials: MP
authors.lastname: Panozzo
authors.forename: M
authors.initials: M
authors.lastname: Plebani
authors.forename: T
authors.initials: T
authors.lastname: Meggiato
authors.forename: M
authors.initials: M
authors.lastname: Zaninotto
authors.forename: A
authors.initials: A
authors.lastname: Piccoli
authors.forename: P
authors.initials: P
authors.lastname: Fogar
authors.forename: C
authors.initials: C
authors.lastname: Ferrara
authors.forename: G
authors.initials: G
authors.lastname: Del Favero
authors.forename: A
authors.initials: A
authors.lastname: Burlina
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002779:Cholestasis; D002908:Chronic Disease; D004066:Digestive System Diseases / Q000378:metabolism / Q000473:pathology; D005260:Female; D005921:Glomerulonephritis / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D007684:Kidney Tubules / Q000473:pathology*; D008054:Lipid Peroxides / Q000097:blood / Q000378:metabolism* / Q000652:urine; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000652:urine; D008875:Middle Aged; D018384:Oxidative Stress; D010179:Pancreas / Q000473:pathology; D010182:Pancreatic Diseases / Q000378:metabolism* / Q000473:pathology*; D010741:Phospholipases A / Q000097:blood / Q000652:urine; D054467:Phospholipases A2
chemical_list: D008054:Lipid Peroxides; D008315:Malondialdehyde; D010741:Phospholipases A; D054467:Phospholipases A2