2003Zhonghua neifenmi daixie zazhiRequires access

Inhibitory effect of melatonin on oxidative stress i n kidneys of diabetic rats

Libin Zhang

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Abstract

Objective To in ve stigate the effects of melatonin on oxidative stress and renal function in kidne ys of diabetic rats. Methods Diabetic model of rats was induced by streptozocin. Male diabetic SD rats were assigned to 3 group s: (1) Untreated (DMC); (2) DM+Mel 1, melatonin 0.2 mg·kg -1 ·d -1 b y gavage, and (3) DM+Mel 2, melatonin 5 mg·kg -1 ·d -1 by gavage, se ven rats were in each group. Seven normal rats were assigned to normal control ( NC) group. Eight weeks later, systemic and renal intrinsic anti-oxidant enzyme activities, lipid peroxide levels and urinary protein excretion, creatinine clea rance rate and kidney weight were evaluated. Results Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were lower and lipid peroxide levels were higher in renal cortex of diabetic ra ts than those in NC group. SOD and GSH-Px activities in renal cortex increased and plasma triglycerides level and urinary protein excretion decreased in DM+Mel 1 group. DM+Mel 2 group showed changes similar to DM+Mel 1 group. These dose s also reduced lipid peroxide levels in renal cortex and kidney weight/body weig ht ratio of diabetic rats. Moreover, larger dose melatonin reversed the lowered SODactivitiesine rythrocytesand the raised lipid peroxide levels in plasma of dia betic rats. Conclusion Melatonin may inhibit oxi dative stress in kidneys and improve renal function in diabetic rats. Overproduc tion of reactive oxygen free radicals and insufficieny in intrinsic anti-oxidan t enzymes may contribute to the development of diabetic nephropathy.

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Objective To in ve stigate the effects of melatonin on oxidative stress and renal function in kidne ys of diabetic rats. Methods Diabetic model of rats was induced by streptozocin. Male diabetic SD rats were assigned to 3 group s: (1) Untreated (DMC); (2) DM+Mel 1, melatonin 0.2 mg·kg -1 ·d -1 b y gavage, and (3) DM+Mel 2, melatonin 5 mg·kg -1 ·d -1 by gavage, se ven rats were in each group. Seven normal rats were assigned to normal control ( NC) group. Eight weeks later, systemic and renal intrinsic anti-oxidant enzyme activities, lipid peroxide levels and urinary protein excretion, creatinine clea rance rate and kidney weight were evaluated. Results Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were lower and lipid peroxide levels were higher in renal cortex of diabetic ra ts than those in NC group. SOD and GSH-Px activities in renal cortex increased and plasma triglycerides level and urinary protein excretion decreased in DM+Mel 1 group. DM+Mel 2 group showed changes similar to DM+Mel 1 group. These dose s also reduced lipid peroxide levels in renal cortex and kidney weight/body weig ht ratio of diabetic rats. Moreover, larger dose melatonin reversed the lowered SODactivitiesine rythrocytesand the raised lipid peroxide levels in plasma of dia betic rats. Conclusion Melatonin may inhibit oxi dative stress in kidneys and improve renal function in diabetic rats. Overproduc tion of reactive oxygen free radicals and insufficieny in intrinsic anti-oxidan t enzymes may contribute to the development of diabetic nephropathy.

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Available abstract

Objective To in ve stigate the effects of melatonin on oxidative stress and renal function in kidne ys of diabetic rats. Methods Diabetic model of rats was induced by streptozocin. Male diabetic SD rats were assigned to 3 group s: (1) Untreated (DMC); (2) DM+Mel 1, melatonin 0.2 mg·kg -1 ·d -1 b y gavage, and (3) DM+Mel 2, melatonin 5 mg·kg -1 ·d -1 by gavage, se ven rats were in each group. Seven normal rats were assigned to normal control ( NC) group. Eight weeks later, systemic and renal intrinsic anti-oxidant enzyme activities, lipid peroxide levels and urinary protein excretion, creatinine clea rance rate and kidney weight were evaluated. Results Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were lower and lipid peroxide levels were higher in renal cortex of diabetic ra ts than those in NC group. SOD and GSH-Px activities in renal cortex increased and plasma triglycerides level and urinary protein excretion decreased in DM+Mel 1 group. DM+Mel 2 group showed changes similar to DM+Mel 1 group. These dose s also reduced lipid peroxide levels in renal cortex and kidney weight/body weig ht ratio of diabetic rats. Moreover, larger dose melatonin reversed the lowered SODactivitiesine rythrocytesand the raised lipid peroxide levels in plasma of dia betic rats. Conclusion Melatonin may inhibit oxi dative stress in kidneys and improve renal function in diabetic rats. Overproduc tion of reactive oxygen free radicals and insufficieny in intrinsic anti-oxidan t enzymes may contribute to the development of diabetic nephropathy.

Key concepts: Endocrinology, Internal medicine, Melatonin, Lipid peroxide, Chemistry, Oxidative stress, Glutathione peroxidase, Renal cortex

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