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Аврова, Н. Ф.; Shestak, K. I.; Захарова, И. О.; Sokolova, T. V.; Leont'ev, V. G.

doi:10.1023/a:1020752101736

Cited by 24 publications

(2 citation statements)

References 28 publications

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“…Moreover, nitric oxide (NO x ) is also an important signaling molecule that not only mediates several physiological functions, including the regulation of neurotransmission, but also regulates many pathological processes [45, 46]. NO x plays a crucial factor in the regulation of Na + /K + -ATPase activities in brain, and less or excess of NO x production can result in neurotoxicity [47, 48]. Acute exposure to high-dose of toxic metals has been indicated to be capable of inhibiting NO x levels in vivo and in vitro [22, 49, 50].…”

Section: Discussionmentioning

confidence: 99%

Exposure to Low Dose of Cinnabar (a Naturally Occurring Mercuric Sulfide (HgS)) Caused Neurotoxicological Effects in Offspring Mice

Huang

Hsu

Liu

et al. 2012

Journal of Biomedicine and Biotechnology

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Cinnabar, a naturally occurring mercuric sulfide (HgS), has long been used in Chinese mineral medicine for more than 2000 years. Although mercury is well-known for its toxicity, whether cinnabar induces neurotoxicity, especially in infants and children, is unknown. The purpose of this study was to explore the neurotoxic effects of low-dose of cinnabar (10 mg/kg/day) on developing mice. The results revealed neurobehavioral defects in F1-C-Cin group, which were associated with Hg accumulation, increased NOx levels in whole blood, and Na+/K+-ATPase activities in brain tissues. F1- and F2-Cin-V groups were found to increase brain Hg contents and prominent neurobehavioral defects compared with F1-C-V group, suggesting that the fetal brain was more susceptible to irreversible effects for cinnabar-induced damage. Moreover, F1- and F2-Cin-Cin groups had severely neurobehavioral dysfunctions, closely correlated with the further alteration of NOx levels and Na+/K+-ATPase activities than F1- and F2-C-Cin groups. Effects in F2-Cin-Cin group were more significant than those in F1-Cin-Cin group. In conclusion, this study demonstrates that exposure to low-dose of cinnabar during the perinatal and developmental stages results in irreversible and severe injuries of the neurotoxicity in offspring, and NOx and Na+/K+-ATPase activities may exist potential and useful biomarkers for neurotoxicity-induced by low-doses of mercuric compounds.

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Section: Discussionmentioning

confidence: 99%

Exposure to Low Dose of Cinnabar (a Naturally Occurring Mercuric Sulfide (HgS)) Caused Neurotoxicological Effects in Offspring Mice

Huang

Hsu

Liu

et al. 2012

Journal of Biomedicine and Biotechnology

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“…The assays were divided into eight groups; group 1 (saline), group 2 (GAA 10 μM, 30 μM, 50 μM and 100 μM), group 3 (1.0 mM trolox), group 4 (GAA + 1.0 mM trolox), group 5 (1.0 mM GSH), group 6 (GAA + 1.0 mM GSH), group 7 (1.0 mM L-NAME) and group 8 (GAA + 1.0 mM L-NAME). After the addition of compounds, erythrocytes or plasma were pre-incubated at 37°C for 1 h. The doses of trolox, GSH and L-NAME utilized were chosen according to Wyse et al 17 , Avrova et al 18 and Qi et al 19 .…”

Section: Drugs Administrationmentioning

confidence: 99%

Guanidinoacetate alters antioxidant defenses and butyrylcholinesterase activity in the blood of rats

Eger¹,

Ferreira²,

Batista³

et al. 2015

cbr

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Introduction: Deficiency of guanidinoacetate methyltransferase, the first described creatine biosynthesis defect, leads to depletion of creatine and phosphocreatine, and accumulation of guanidinoacetate (GAA) in brain and body fluids. The present study aimed to investigate the influence of GAA on the activities of antioxidant enzymes, as well as on thiobarbituric acid-reactive substances (TBARS) and butyrylcholinesterase (BuChE) activity in the blood of rats. We also evaluated the effect of trolox (6-hydr oxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), GSH (glutathione) and L-NAME (NG-nitro-L-arginine methyl ester) on the alterations elicited by GAA. Methods: The rats were randomly divided into 8 groups: (1) control; (2) GAA (10, 30, 50, 100 mM/kg); (3) trolox (1 mM/kg) + control; (4) trolox (1 mM/kg) + GAA (100 mM/kg); (5) GSH (1 mM/kg) + control; (6) GSH (1 mM/kg) + GAA (100 mM/kg); (7) L-NAME (1 mM/kg) + control; (8) L-NAME + GAA (100 mM/kg). After the addition of compounds, erythrocytes and plasma were pre-incubated at 37°C for 1h and tested immediately. Results: GAA enhanced the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in the erythrocytes and BuChE activity. In addition, GAA enhanced TBARS levels in the plasma. Trolox, GSH and L-NAME addition prevented the majority of alterations in oxidative stress parameters and the increase of BuChE activity that were caused by GAA. Data suggest that GAA alters antioxidant defenses and induces lipid peroxidation in the blood, as well altering BuChE activity. However, in the presence of trolox, GSH and L-NAME some of these alterations in oxidative stress and BuChE activity were prevented. Conclusions: Our findings lend support to a potential therapeutic strategy for this condition, which may include the use of appropriate antioxidants for ameliorating the damage caused by GAA.

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The Role of Nitric Oxide in Homocysteine Thiolactone-Induced Seizures in Adult Rats

et al. 2009

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The role of NO in epileptogenesis has been studied in different experimental models, and the reported results have been highly contradictory. The current study aimed to determine the role of NO in mechanisms of D: ,L: -homocysteine-thiolactone (H) induced seizures by testing the action of L: -arginine (NO precursor) and L: -NAME (NOS inhibitor) on behavioral and electroencephalographic (EEG) manifestations of H-induced seizures. The same holds true with the brain Na(+)/K(+)- and Mg(2+)-ATPase activity in adult male Wistar rats. We showed that the pretreatment with L: -arginine (300, 600 and 800 mg/kg, i.p.) in a dose-dependent manner significantly decreased lethality, seizure incidence and a number of seizure episodes and prolonged latency time to the first seizure elicited by a convulsive dose of H (8 mmol/kg, i.p.). L: -Arginine (800 mg/kg) completely reversed the inhibitory effect of H on the Na(+)/K(+)-ATPase activity in the hippocampus, the cortex and the brain stem and decreased the H-induced spike-and- wave discharges (SWD) formation in EEG. On the other hand, pretreatment with L: -NAME (200, 500 and 700 mg/kg, i.p.) potentiated a subconvulsive dose of H (5.5 mmol/kg, i.p) by increasing incidence and severity determined by a descriptive-rating scale (0-4) and shortening the latency time to the first seizure. The L: -NAME reversed H-induced alterations in the Na(+)/K(+)-ATPase activity in the cortex and the brain stem but not in the hippocampus. At last, the potentiated SWD appearance in EEG and an increased number of lethal outcomes occurred. In the present work, the modulation of NO levels, with the NO precursor and NOS inhibitor, was shed more light on its mechanism of action and answered the question whether NO could be included in the list of anticonvulsant agents in the D: ,L: -homocysteine thiolactone experimental model of seizures in adult rats.

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Untitled

Cited by 24 publications

References 28 publications

Exposure to Low Dose of Cinnabar (a Naturally Occurring Mercuric Sulfide (HgS)) Caused Neurotoxicological Effects in Offspring Mice

Exposure to Low Dose of Cinnabar (a Naturally Occurring Mercuric Sulfide (HgS)) Caused Neurotoxicological Effects in Offspring Mice

Guanidinoacetate alters antioxidant defenses and butyrylcholinesterase activity in the blood of rats

The Role of Nitric Oxide in Homocysteine Thiolactone-Induced Seizures in Adult Rats

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