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Magnesium supplementation prevents chronic cyclosporine nephrotoxicity via adjusting nitric oxide synthase activity

J Yuan1, J Zhou, B C Chen

  • 1Key Laboratory of Organ Transplantation (Huazhong University of Science and Technology), Ministry of Education, Institute of Organ Transplantation, Tongji Hospital, Wuhan, China.

Transplantation Proceedings
|May 28, 2005
PubMed
Abstract

Insights

Magnesium supplementation improved kidney function and reduced damage caused by cyclosporine (CsA) in rats. This effect was linked to altered nitric oxide synthase (NOS) activity, suggesting a protective role for magnesium in CsA-induced nephrotoxicity.

Area of Science:

  • Nephrology
  • Pharmacology
  • Biochemistry

Background:

  • Nitric oxide synthase (NOS) plays a protective role in chronic cyclosporine (CsA) nephrotoxicity by regulating nitric oxide (NO) production.
  • Understanding the role of NOS in magnesium's effect on CsA-induced kidney damage is crucial for developing preventative strategies.

Purpose of the Study:

  • To investigate the role of nitric oxide synthase (NOS) in the protective effect of magnesium supplementation against chronic cyclosporine (CsA) nephrotoxicity.

Main Methods:

  • Rats were administered CsA (15 mg/kg/day) with or without dietary magnesium (0.6% MgCl2) supplementation for 28 days.
  • Evaluated plasma magnesium, creatinine, renal NOS activity, and NO content.
  • Assessed renal expression of eNOS and iNOS via immunohistochemistry and histological lesions using HE, PAS, and electron microscopy.

Main Results:

  • CsA induced characteristic nephrotoxicity lesions, including arteriolopathy, tubular atrophy, and fibrosis, along with increased constitutive NOS (cNOS) activity but not NO levels.
  • Magnesium supplementation ameliorated CsA-induced histological damage, normalizing cNOS activity and increasing NO levels compared to CsA-only group.
  • Neither CsA nor magnesium supplementation affected inducible NOS (iNOS) activity.

Conclusions:

  • Dietary magnesium supplementation appears to improve renal function and mitigate CsA-induced histological damage.
  • The protective effect is likely mediated by modulating the abnormal activation of constitutive nitric oxide synthase (cNOS) in this CsA nephrotoxicity model.

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