Abstract
In our previous study the pattern of glutathione peroxidase (GPX) activity in the course of steroid–sensitive nephrotic syndrome (SSNS) in children suggested a defect in antioxidant defense. In the present report the serum selenium (Se) level, an essential component of GPX activity, was measured in a comparable group of children with SSNS at the same clinical stages at which GPX activity was determined in the previous study. Nephrotic children had normal serum Se levels during the edematous stage, at the end of prednisone treatment, and in remission. At the end of high-dose prednisone treatment, the serum Se level increased (P<0.01) simultaneously with enhanced activity of GPX. These results suggest that children with SSNS have a persistent defect in the antioxidant defense at the important stage of hydrogen peroxide and fatty acid hydroperoxide decomposition. This defect is transiently alleviated by high-dose prednisone treatment.
References
Diamond JR, Bonventre JV, Karnovsky MJ (1986) A role for oxygen free radicals in aminonucleoside nephrosis. Kidney Int 29:478–483
Yoshioka T, Ichikawa J, Fogo A (1991) Reactive oxygen metabolites cause massive, reversible proteinuria and glomerular sieving defect without apparent ultrastructural abnormality. J Am Soc Nephrol 2:902–912
Fydryk J, Jacobson E, Kurzawska O, Małecka G, Gonet B, Urasiński T, Brodkiewicz A, Bukowska H (1998) Antioxidant status of children with steroid-sensitive nephrotic syndrome. Pediatr Nephrol 12:751–754
Burk RF (1983) Biologic activity of selenium. Annu Rev Nutr 3:53–70
Danch A, Drozdz M (1996) Uproszczona metoda oznaczania Se w materiale biologicznym. Diag Lab 32:529–534
Rotruck JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hoekstra WG (1973) Selenium: biochemical role as a component of glutathione peroxidase. Science 179:588–590
Kawamura T, Yoshioka T, Bills T, Fogo A (1991) Glucocorticoid activates glomerular antioxidant enzymes and protects glomeruli from oxidant injuries. Kidney Int 40:291–301
Kawaguchi M, Yamada M, Wada H, Okigaki T (1992) Roles of active oxygen species in glomerular epithelial cell injury in vitro caused by puromycin aminonucleoside. Toxicology 72:329–340
Wetzels JFM, Sluiter HE, Hoitsma AJ, Munster PJJ van, Koene RAP (1988) Prednisolone can increase glomerular permeability to proteins in nephrotic syndrome. Kidney Int 33:1169–1174
Goldberg A, Tischler M, Demartino G, Griffin G (1980) Hormonal regulation of protein degradation and synthesis in skeletal muscle. Fed Proc 39:31–36
Simmons PS, Miles JM, Gerich JH, Haymond MW (1984) Increased proteolysis. An effect of increases in plasma cortisol within the physiologic range. J Clin Invest 73:412–420
Svec F, Rudis M (1981) Glucocorticoids regulate the glucocorticoid receptor in the AtT-20 cell. J Biol Chem 256:5984–5987
Sapolsky RM, Krey LC, McEwen BS (1984) Stress down-regulates corticosterone receptors in a site-specific manner in the brain. Endocrinology 114:287–292
Baliga R, Baliga M, Shah SV (1992) Effect of selenium-deficient diet in experimental glomerular disease. Am J Physiol 263:F56–F61
Yoshimura S, Takekoshi S, Watanabe K, Fujii-Kuriyama Y (1988) Determination of nucleoside sequence of cDNA coding rat glutathione peroxidase and diminished expression of the m RNA in selenium deficient rat liver. Biochem Biophys Res Commun 154:1024–1028
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Fydryk, J., Olszewska, M., Urasiński, T. et al. Serum selenium level and glutathione peroxidase activity in steroid-sensitive nephrotic syndrome. Pediatr Nephrol 18, 1063–1065 (2003). https://doi.org/10.1007/s00467-003-1237-7
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DOI: https://doi.org/10.1007/s00467-003-1237-7