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• W4246767939 abstract "A number of studies suggest that epileptic seizures are related to certain harmful functions of nitric oxide (Tsuda et al. 1998). This disorder can be induced with pentylenetetrazole, a drug that causes generalized seizures with abnormal levels of nitric oxide and serotonin (5-HT) (Balakrishnan et al. 1999). Analogous to pentylenetetrazole, carbodiimide participates in the biochemical metabolism of nitric oxide (Rotzingers et al. 1995), even though its mechanism of action remains unknown. Since nitric oxide is an unstable and gaseous free radical with a short half-life, its indirect measurement is possible as a result of the calculation of nitrites or nitrates. Diseases associated with epileptic seizures involve the role played by oxidative stress generated by the effect of free radicals (Bashkatova et al. 2003), where unknown biochemical mechanisms are related with lipid peroxidation levels (Ischiropoulos & Beckman 2003). The aim of the present study is to evaluate the effect of pentylenetetrazole and carbodiimide on some biochemical markers of oxidative stress as nitric oxide metabolites, 5-HT, Na+ K+ ATPase and thiobarbituric acid in rat brain. Twenty-four Wistar male adult rats (350 g) were divided into 3 groups of 8 animals: group I, control group 0.9% NaCl was given; group II treated with carbodiimide (20 mg/kg), and group III, treated with pentylenetetrazole (40 mg/kg), drugs were administered in a single intraperitoneal dose. After 10 min. the animals were decapitated and dissected in sagittal section: the tissue of left-sided section was used for the Na+, K+-ATPase, and total ATPase assays, lipid peroxidation (TBARS), and levels of nitrites and nitrates. The right-sided section was used for determination of serotonin (5-HT). The inorganic phosphorus (Pi) content was measured using the method proposed by Balbonting et al. (1961), the difference of inorganic phosphorus content between test solutions in the presence and absence of ouabain was considered as the activity of Na+, K+-ATPase and total ATPase, respectively, expressed in nmol inorganic phosphorus/mg protein/min. Lipid peroxidation was determined as substances reacting to thiobarbituric acid (Gutteridge & Halliwell 1990) reported in μmol of malondialdehyde/g of wet tissue. The levels of nitrites and nitrates were determined by liquid chromatography (HPLC) (Smith et al. 2002) using 5 mM K2HPO4 and 25 mM KH2PO4, pH 3.0 as mobile phase at flow rate of 1.0 ml/min. and detected at 214 nm. A stainless steel μBondapack C18 (3.9×300 mm) column was used (Waters Asoc). The levels of 5-HT were determined by HPLC (Calderón et al. 2004). Samples were passed through a Millex HV filter (Sep-Pack C13) and 20 μl were injected into chromatographic system. Amine values were interpolated in a previously standarized curve. 5-HT levels in brain treated with carbodiimide and pentylenetetrazole were partially increased in group II and reduced in group III, both compared to the control group (P>0.05). No significant differences were noted in the activity of Na+, K+ ATPase of rats treated with carbodiimide and pentylenetetrazole (P>0.05), neither in total ATPase activity in both groups, only there was slight increase in activity in both groups compared to the control. The levels of nitrites and nitrates were reduced in carbodiimide and pentylenetetrazole groups in relation to control group, however, no significant differences were found in either group (P>0.05). A considerable increase of lipid peroxidation levels was observed in the group pentylenetetrazole compared to control and group carbodiimide (P=0.0001) as is shown in table 1. In the present study, 5-HT levels exhibited a slight increased after administration of carbodiimide. This finding is consistent with the results reported by Obach et al. (1986) who suggested that 5-HT brain levels do not change after administration of carbodiimide. However, Echizen & Fredd (1984) suggested that 5-hydroxyindole acetic acid (5-HIAA) increases in response to the effect of experimentallyinduced hypertension. The pentylenetetrazole-treated group showed less significant nitrite oxidation than the carbodiimide group when brain nitrate levels were increased. These results are consistent with the studies by Kuhn & Arthur (1996), who suggested that nitric oxide acts on the enzyme tryptophane-5-hydroxylase, which is responsible for 5-HT production, specifically when it affects the groups containing iron sulphur in their proteins, causing their nitrosylation and inactivation. D'vakonova (2002) suggested that 5-HT and nitric oxide have a common control effect on the brain serotonergic system, although its mechanism of action remains unknown. Increased thiobarbituric acid levels observed in the pentylenetetrazole group of the present study perhaps was as result of drug interaction with lipids comprising the brain, as suggested by Bashkatova et al. (2003) who stated that the increased and nitric oxide levels may play an important role in the pathophysiology of epileptic seizures due to their marked effect on the CNS. Regarding carbodiimide, the thiobarbituric acid levels were slightly reduced, perhaps as a result of the activation of antioxidant mechanisms involving a catalase (Nagasawa et al. 1990). On the other hand, enzyme activity of Na+, K+ ATPase and total ATPase increased to some extent after administration of pentylenetetrazole and carbodiimide, which indicates that this effect may be caused by the impaired smoothness of the membrane induced by both compounds, as has been previously mentioned. Based on the results of the present study, the authors suggest that pentylenetetrazole induces oxidative injury on brain lipids due to their marked effect on the CNS." @default.
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• W4246767939 date "2005-06-01" @default.
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• W4246767939 title "Effect of Pentylenetetrazole and Carbodiimide on Oxidation Stress Markers in Rat Brain" @default.
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• W4246767939 doi "https://doi.org/10.1111/j.1742-7843.2005.pto_16.x" @default.
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