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Peroxynitrite formation and apoptosis in transgenic sickle cell mouse kidneys
N Bank1, M Kiroycheva, F Ahmed
1Renal and Hematology Divisions, Department of Medicine, Montefiore Medical Center, and the Albert Einstein College of Medicine and Long Island Jewish Medical Center, Bronx, New York, USA.
Kidney International
|December 9, 1998
Summary
Sickle cell disease in mice causes kidney damage through increased reactive oxygen species, leading to protein nitration and cell death. This suggests peroxynitrite formation contributes to kidney injury in sickle cell nephropathy.
Area of Science:
- Nephrology
- Pathology
- Biochemistry
Background:
- Nitric oxide synthases (NOS) are highly expressed in the kidneys of sickle cell disease mouse models.
- NOS activity can lead to peroxynitrite formation when superoxide radicals are abundant.
Purpose of the Study:
- To investigate the presence of nitrotyrosine, a marker of peroxynitrite, in the kidneys of sickle cell mice.
- To assess apoptosis indicators in the kidneys of these mice.
Main Methods:
- Western blot and immunohistochemistry were used to detect nitrotyrosine.
- Agarose gel electrophoresis and TUNEL staining were performed to evaluate apoptosis.
Main Results:
- Increased tyrosine nitration of specific proteins (57 and 22 kD) was observed in sickle cell mouse kidneys.
- Nitrotyrosine and inducible NOS (iNOS) were found in tubular epithelial cells, correlating with DNA damage and apoptosis.
- Apoptosis was more pronounced in sickle cell mice, especially under hypoxic conditions.
Conclusions:
- Peroxynitrite and other reactive oxygen species are likely produced in sickle cell kidneys.
- Ischemia/reperfusion and hypoxia may activate iNOS, leading to reactive oxygen species formation.
- Protein nitration and enhanced apoptosis are consequences of these reactions in sickle cell nephropathy.
