The degree of oxidative stress in the rat brain during ischemia and reperfusion in conditions of correction of the L-arginine-NO system

Abstract

The aim of the present work was to evaluate oxidative stress in the brains of rats during ischemia/reperfusion in conditions of correction of the L-arginine-NO system. Experiments on 128 rats with brain ischemia/perfusion in conditions of modulation of the L-arginine-NO system were used to study changes in the concentrations of (a) lipid peroxidation products, i.e., diene conjugates, malonic dialdehyde, and Schiff bases, and (b) antioxidant protection factors, i.e., retinol, alpha-tocopherol, and SH-groups. Administration of L-arginine and NO synthase inhibitors, i.e., the non-selective inhibitor N(omega)-nitro-L-arginine methyl ester, the selective neuronal NO synthase inhibitor 7-nitroindasole, and the selective inhibitor of inducible NO synthase S-methylisothiourea, established that oxidative stress in rats with brain ischemia/perfusion is NO-dependent. NO formed by the various isoforms of NO synthase had different roles: hyperactivation of neuronal NO synthase was responsible for oxidative stress in both periods of brain ischemia/reperfusion, while increased inducible NO synthase activity was responsible in the late period.

In vivo characterisation of a Nafion®-modified Pt electrode for real-time nitric oxide monitoring in brain extracellular fluid

“…52,53 Other reports confirm the antioxidant effects of L-arginine in the early and late stages of ischemia with deficiencies of the amino acid in brain neurons along with inadequate levels of NO formation within them leading to increases in superoxide formation. 54 Our finding supports the role of L-arginine in the biosynthesis of NO in the body; however, contradictory reports have been published discussing the possible role of L-arginine in one mechanism of NO inhibition. Castellano et al detailed how glutamate-stimulated NO production was markedly increased by 32 nM L-arginine infusion, however, 128 nM infusion had no significant effect on glutamate-evoked NO production as the NO levels were significantly lower than the corresponding value obtained with 32 nM L-arginine.…”

Brain nitric oxide: Regional characterisation of a real-time microelectrochemical sensor

“…Recent studies have demonstrated that arginine availability is an important condition for the physiological functioning of the nitroergic system (Do et al, 2002; and Saul'skaya, 2007). Indirect reports confirm the antioxidant effects of l-arginine in the early and late stages of ischaemia (Maksimovich et al, 2006) and its reduction in brain edema formation and improvement of cortical blood flow in the early phase after a brain trauma (Lundblad and Bentzer, 2007). Previously our group has confirmed in real-time that both systemic and local l-arginine administration significantly increased the NO sensor's signal in the striatum of Wistar rats compared to pre-administration baseline levels (Brown et al, 2009;Finnerty et al, 2012).…”

Resveratrol neuroprotective effects during focal cerebral ischemia injury via nitric oxide mechanism in rats

“…Sham operated animals underwent all surgical procedure except MCA ligation. For examining which NOS was responsible for the neuroprotective effect of resveratrol in FCI injury, we administrated a nonselective NOS inhibitor (L-NAME, 1 mg/kg), 25 a selective nNOS inhibitor (7-nitroindazole, 50 mg/kg), 26 a specific iNOS inhibitor (S-methylisothiourea sulfate, 3 mg/kg), 27 and a selective eNOS inhibitor (L-NIO, 10 mg/kg) 28 15 minutes before MCA occlusion to examine their antagonistic effect with resveratrol. Animals were randomly allocated to each drug treatment and control groups.…”