The effect of inhibition of nitric oxide synthase on aluminium-induced toxicity in the rat brain.

نویسندگان

  • Ivana D Stevanović
  • Marina D Jovanović
  • Ankica Jelenković
  • Milica Ninković
  • Mirjana Dukić
  • Ivana Stojanović
  • Miodrag Colić
چکیده

The goal of the present study was to examine the effectiveness of a non-specific nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) to modulate the toxicity of aluminium chloride (AlCl3). Rats were killed at 3 h and at 30 days after treatments and the striatum was removed. Nitrite, superoxide, superoxide dismutase activity, malondialdehyde and reduced glutathione were determined. AlCl3 exposure promoted oxidative stress in the striatum. The biochemical changes observed in neuronal tissues show that aluminium acts as pro-oxidant, while the NOS inhibitor exerts antioxidant action in AlCl3-treated rats. We conclude that L-NAME can efficiently protect neuronal tissue from AlCl3-induced toxicity.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Inhibition of nitric oxide synthase activity improves focal cerebral damage induced by cerebral ischemia/reperfusion in normotensive rats

Introduction: Nitric oxide seems to play a dual role in ischemia/reperfusion injury. Few studies have investigated whether it exacerbates or improves brain edema. In the present study, we inhibited the activity of nitric oxide synthase by L-NAME and evaluated the cerebral infarct volume, tissue swelling and brain edema, alongside the measurement of blood flow of the ischemic region. Methods...

متن کامل

Role of matrix metalloproteinase II on analgesic effect of nitric oxide inhibition in rat

Abstract Introduction: Matrix metalloproteinase 2 is one of the inflammatory mediators that is involved in nociceptive processing and its production is regulated by many inflammatory factors such as nitric oxide. We studied the role of MMP-2 on the analgesic effects of nNOS inhibitor. Methods: Considering that nitric oxide has many roles in pain processing, we studied the CSF levels of MMP-2 ...

متن کامل

The Effect of Dexamethasone on Expression of Inducible Nitric Oxide Synthase Gene During Liver Warm Ischemia-reperfusion in Rat

Background: Liver ischemia / reperfusion Injury (IRI) is one of the major causes of liver failure during various types of liver surgery, trauma and infections. The present study investigates the effect of dexsamethasone on the liver injury and inducible nitric oxide synthase gene expression during hepatic warm ischemia/reperfusion in rats. Materials and Methods: 24 male Wistar rats (200-250 g)...

متن کامل

Therapeutic effect of valsartan against doxorubicin-induced renal toxicity in rats

Objective(s): Doxorubicin (DXR)-induces glomerular atrophy and fibrosis in rat kidneys. The objective of the current study was to investigate the protective effects of valsartan on DXR-induced glomerular toxicity and its mechanisms of actions in rats. Materials and Methods: Male Sprague-Dawley (SD) rats were divided into four groups, and each group contains ten rats. First group was control and...

متن کامل

Contribution of Nitric Oxide Synthase (NOS) Activity in Blood-Brain Barrier Disruption and Edema after Acute Ischemia/ Reperfusion in Aortic Coarctation-Induced Hypertensive Rats

Background: Nitric oxide synthase (NOS) activity is increased during hypertension and cerebral ischemia. NOS inactivation reduces stroke-induced cerebral injuries, but little is known about its role in blood-brain barrier (BBB) disruption and cerebral edema formation during stroke in acute hypertension. Here, we investigated the role of NOS inhibition in progression of edema formation and BBB d...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • General physiology and biophysics

دوره 28 Spec No  شماره 

صفحات  -

تاریخ انتشار 2009