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Effects of L-NAME, a non-specific nitric oxide synthase inhibitor, on AlCl3-induced toxicity in the rat forebrain cortex.

Stevanović ID, Jovanović MD, Jelenković A, Colić M, Stojanović I, Ninković M - J. Vet. Sci. (2009)

Bottom Line: Crude mitochondrial fraction preparations of forebrain cortices were used for the biochemical analyses: nitrite levels, superoxide production, malondialdehyde concentrations, superoxide dismutase (SOD) activities and reduced glutathione contents.AlCl(3) injection resulted in increased nitrite concentrations, superoxide anion production, malondialdehyde concentrations and reduced glutathione contents in the forebrain cortex, suggesting that AlCl(3) exposure promoted oxidative stress in this brain structure.These results revealed that NO-mediated neurotoxicity due to intrahippocampal AlCl3 injection spread temporally and spatially to the forebrain cortex, and suggested a potentially neuroprotective effect for L-NAME.

View Article: PubMed Central - PubMed

Affiliation: Military Medical Academy, Institute for Medical Research, Crnotravska 17, Belgrade, Serbia. ivanav13@yahoo.ca

ABSTRACT
The present experiments were done to determine the effectiveness of a non-specific nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on oxidative stress parameters induced by aluminium chloride (AlCl(3)) intrahippocampal injections in Wistar rats. Animals were sacrificed 3 h and 30 d after treatments, heads were immediately frozen in liquid nitrogen and forebrain cortices were removed. Crude mitochondrial fraction preparations of forebrain cortices were used for the biochemical analyses: nitrite levels, superoxide production, malondialdehyde concentrations, superoxide dismutase (SOD) activities and reduced glutathione contents. AlCl(3) injection resulted in increased nitrite concentrations, superoxide anion production, malondialdehyde concentrations and reduced glutathione contents in the forebrain cortex, suggesting that AlCl(3) exposure promoted oxidative stress in this brain structure. The biochemical changes observed in neuronal tissues showed that aluminium acted as a pro-oxidant. However, the nonspecific nitric oxide synthase (NOS) inhibitor, L-NAME, exerted anti-oxidant actions in AlCl(3)-treated animals. These results revealed that NO-mediated neurotoxicity due to intrahippocampal AlCl3 injection spread temporally and spatially to the forebrain cortex, and suggested a potentially neuroprotective effect for L-NAME.

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The effects of intrahippocampal drug injection on SOD activities (U/mg proteins) in the rat ipsilateral and contralateral forebrain cortex at different survival times: 3 h (A) and 30 d (B). Results are means ± SD of 10 animals. *Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and control (sham-operated) animal (p < 0.05). •Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and AlCl3-treated animals (p < 0.05). ♦Indicates a statistically significant difference between L-NAME-treated and L-NAME + AlCl3-treated animals (p < 0.05).
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Figure 4: The effects of intrahippocampal drug injection on SOD activities (U/mg proteins) in the rat ipsilateral and contralateral forebrain cortex at different survival times: 3 h (A) and 30 d (B). Results are means ± SD of 10 animals. *Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and control (sham-operated) animal (p < 0.05). •Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and AlCl3-treated animals (p < 0.05). ♦Indicates a statistically significant difference between L-NAME-treated and L-NAME + AlCl3-treated animals (p < 0.05).

Mentions: The results in Fig. 4 show the bilateral SOD activities (U/mg proteins) in the forebrain cortex homogenates at 3 h (A) and 30 d (B) after the treatments. At 3 h and 30 d after AlCl3 injection, there was lower SOD activity compared to the control group, although this was not significantly different. At 3 h and 30 d after L-NAME + AlCl3 injection, there was lower SOD activity compared to both the controls and the AlCl3-treated group (p < 0.05). At 3 h and 30 d, L-NAME injection resulted in lower bilateral SOD activity in the forebrain cortex compared to both controls and the AlCl3-treated animals. However, higher SOD activities were measured in both the ipsi- and contralateral forebrain cortices compared to the L-NAME + AlCl3-treated group (Fig. 4).


Effects of L-NAME, a non-specific nitric oxide synthase inhibitor, on AlCl3-induced toxicity in the rat forebrain cortex.

Stevanović ID, Jovanović MD, Jelenković A, Colić M, Stojanović I, Ninković M - J. Vet. Sci. (2009)

The effects of intrahippocampal drug injection on SOD activities (U/mg proteins) in the rat ipsilateral and contralateral forebrain cortex at different survival times: 3 h (A) and 30 d (B). Results are means ± SD of 10 animals. *Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and control (sham-operated) animal (p < 0.05). •Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and AlCl3-treated animals (p < 0.05). ♦Indicates a statistically significant difference between L-NAME-treated and L-NAME + AlCl3-treated animals (p < 0.05).
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2801103&req=5

Figure 4: The effects of intrahippocampal drug injection on SOD activities (U/mg proteins) in the rat ipsilateral and contralateral forebrain cortex at different survival times: 3 h (A) and 30 d (B). Results are means ± SD of 10 animals. *Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and control (sham-operated) animal (p < 0.05). •Indicates a statistically significant difference between treated (L-NAME + AlCl3- and L-NAME-treated) and AlCl3-treated animals (p < 0.05). ♦Indicates a statistically significant difference between L-NAME-treated and L-NAME + AlCl3-treated animals (p < 0.05).
Mentions: The results in Fig. 4 show the bilateral SOD activities (U/mg proteins) in the forebrain cortex homogenates at 3 h (A) and 30 d (B) after the treatments. At 3 h and 30 d after AlCl3 injection, there was lower SOD activity compared to the control group, although this was not significantly different. At 3 h and 30 d after L-NAME + AlCl3 injection, there was lower SOD activity compared to both the controls and the AlCl3-treated group (p < 0.05). At 3 h and 30 d, L-NAME injection resulted in lower bilateral SOD activity in the forebrain cortex compared to both controls and the AlCl3-treated animals. However, higher SOD activities were measured in both the ipsi- and contralateral forebrain cortices compared to the L-NAME + AlCl3-treated group (Fig. 4).

Bottom Line: Crude mitochondrial fraction preparations of forebrain cortices were used for the biochemical analyses: nitrite levels, superoxide production, malondialdehyde concentrations, superoxide dismutase (SOD) activities and reduced glutathione contents.AlCl(3) injection resulted in increased nitrite concentrations, superoxide anion production, malondialdehyde concentrations and reduced glutathione contents in the forebrain cortex, suggesting that AlCl(3) exposure promoted oxidative stress in this brain structure.These results revealed that NO-mediated neurotoxicity due to intrahippocampal AlCl3 injection spread temporally and spatially to the forebrain cortex, and suggested a potentially neuroprotective effect for L-NAME.

View Article: PubMed Central - PubMed

Affiliation: Military Medical Academy, Institute for Medical Research, Crnotravska 17, Belgrade, Serbia. ivanav13@yahoo.ca

ABSTRACT
The present experiments were done to determine the effectiveness of a non-specific nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on oxidative stress parameters induced by aluminium chloride (AlCl(3)) intrahippocampal injections in Wistar rats. Animals were sacrificed 3 h and 30 d after treatments, heads were immediately frozen in liquid nitrogen and forebrain cortices were removed. Crude mitochondrial fraction preparations of forebrain cortices were used for the biochemical analyses: nitrite levels, superoxide production, malondialdehyde concentrations, superoxide dismutase (SOD) activities and reduced glutathione contents. AlCl(3) injection resulted in increased nitrite concentrations, superoxide anion production, malondialdehyde concentrations and reduced glutathione contents in the forebrain cortex, suggesting that AlCl(3) exposure promoted oxidative stress in this brain structure. The biochemical changes observed in neuronal tissues showed that aluminium acted as a pro-oxidant. However, the nonspecific nitric oxide synthase (NOS) inhibitor, L-NAME, exerted anti-oxidant actions in AlCl(3)-treated animals. These results revealed that NO-mediated neurotoxicity due to intrahippocampal AlCl3 injection spread temporally and spatially to the forebrain cortex, and suggested a potentially neuroprotective effect for L-NAME.

Show MeSH
Related in: MedlinePlus