title: Protective effect of magnesium on renal function in STZ-induced diabetic rats.
abstract: BACKGROUND
  Diabetic nephropathy is a serious complication of T1D (type one diabetes mellitus). Persistent hyperglycemia and subsequent hypomagnesemia is believed to develop kidney damage by activation of oxidative stress. We conducted this study to investigate the renoprotective effect of magnesium sulfate (MgSO4) on renal histopathology and oxidative stress in diabetic rats.
  
  
  METHODS
  The study included 70 male rats. The animals were divided into seven groups: control (CRL), control receiving MgSO4 (CRL + Mg1 & CRL + Mg8), diabetic (DM1 & DM8) and diabetic receiving MgSO4 (DM + Mg1 & DM + Mg8). Rats were given 20 mg/kg (i.p) Streptozocin (STZ) for 5 consecutive days in (MLD) multiple low doses to induce T1D. At day 10 treatment groups were received MgSO4 (10 g/l) in drinking water, for 1 or 8 weeks. The blood glucose, BUN and creatinine levels were measured. Renal tissue levels of malondialdehyde (MDA) were measured by thiobarbituric acid (TBA) method to evaluate the oxidative stress. Renal histopathology was done using H & E staining method.
  
  
  RESULTS
  Treatment with MgSO4 significantly decreased the blood glucose in DM + Mg1 and DM + Mg8 groups as compared with DM1 and DM8. Magnesium treatment also decreased serum BUN and tissue level of MDA significantly in both short and long term treatment. The body weight loss and kidney weight to body weight ratio was improved by MgSO4. Histological results showed there were no differences between DM and DM + Mg groups.
  
  
  CONCLUSIONS
  Our findings showed that diabetic nephropathy is associated with high blood glucose level and oxidative stress (significant increase in MDA level). The renal dysfunction and oxidative stress can be improved by magnesium sulfate administration. It is suggested that protection against development of diabetic nephropathy by MgSO4 treatment involves changes in the blood glucose and oxidative stress.
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Mohammad Reza
authors.initials: MR
authors.lastname: Parvizi
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Mohsen
authors.initials: M
authors.lastname: Parviz
authors.affiliation: Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Seyed Mohammad
authors.initials: SM
authors.lastname: Tavangar
authors.affiliation: Department of Physiology, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
authors.forename: Nepton
authors.initials: N
authors.lastname: Soltani
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Mehri
authors.initials: M
authors.lastname: Kadkhodaee
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Behjat
authors.initials: B
authors.lastname: Seifi
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Yaser
authors.initials: Y
authors.lastname: Azizi
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Mansoor
authors.initials: M
authors.lastname: Keshavarz
keywords: Diabetes mellitus type 1; Diabetic nephropathy; Oxidative stress; Streptozocin