Title : SOD1, but not SOD3, deficiency accelerates diabetic renal injury in C57BL/6-Ins2(Akita) diabetic mice.

Pub. Date : 2012 Dec

PMID : 22632894






5 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 Superoxide dismutase (SOD) is a major defender against excessive superoxide generated under hyperglycemia. Superoxides superoxide dismutase 1, soluble Mus musculus
2 Increased glomerular superoxide levels were observed in SOD1(-/-)SOD3(+/+) and SOD1(-/-)SOD3(-/-) C57BL/6-Akita mice but not in SOD1(+/+)SOD3(-/-) C57BL/6-Akita mice. Superoxides superoxide dismutase 1, soluble Mus musculus
3 Increased glomerular superoxide levels were observed in SOD1(-/-)SOD3(+/+) and SOD1(-/-)SOD3(-/-) C57BL/6-Akita mice but not in SOD1(+/+)SOD3(-/-) C57BL/6-Akita mice. Superoxides superoxide dismutase 1, soluble Mus musculus
4 Increased glomerular superoxide levels were observed in SOD1(-/-)SOD3(+/+) and SOD1(-/-)SOD3(-/-) C57BL/6-Akita mice but not in SOD1(+/+)SOD3(-/-) C57BL/6-Akita mice. Superoxides superoxide dismutase 1, soluble Mus musculus
5 The present results demonstrate that deficiency of SOD1, but not SOD3, increases renal superoxide in the setting of diabetes and causes overt renal injury in nephropathy-resistant diabetic mice, and that SOD3 deficiency does not provide additive effects on the severity of DN in SOD1-deficient C57BL/6-Akita mice. Superoxides superoxide dismutase 1, soluble Mus musculus