Intrastriatal hypoxanthine administration affects Na<sup>+</sup>,K<sup>+</sup>‐ATPase, acetylcholinesterase and catalase activities in striatum, hippocampus and cerebral cortex of rats

Bavaresco, Caren Serra; Chiarani, Fábria; Wajner, Moaçir; Netto, Carlos Alexandre; Wyse, Ângela T. S.

doi:10.1016/j.ijdevneu.2006.08.007

Cited by 7 publications

(2 citation statements)

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“…Impaired energy metabolism may trigger proapoptotic signalling (programmed cell death), oxidative damage to lipids, protein and DNA, and impair mitochondrial DNA repair. 14,15 It has been demonstrated that alterations in energy metabolism seem to be implicated in the pathogenesis of a number of muscle and neurological complications, [16][17][18] metabolic disorders, [19][20][21][22] aging [23][24][25] and neuromuscular diseases. 26,27 Mitochondrial function and structure/integrity is crucial to maintaining the energy supply for optimal function and maintenance of homeostasis in some tissues.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Kolling¹,

Scherer²,

Siebert³

et al. 2012

Cell Biochemistry & Function

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Homocystinuria is a neurometabolic disease caused by a severe deficiency of cystathionine beta-synthase activity, resulting in severe hyperhomocysteinemia. Affected patients present several symptoms including a variable degree of motor dysfunction. In this study, we investigated the effect of chronic hyperhomocysteinemia on the cell viability of the mitochondrion, as well as on some parameters of energy metabolism, such as glucose oxidation and activities of pyruvate kinase, citrate synthase, isocitrate dehydrogenase, malate dehydrogenase, respiratory chain complexes and creatine kinase in gastrocnemius rat skeletal muscle. We also evaluated the effect of creatine on biochemical alterations elicited by hyperhomocysteinemia. Wistar rats received daily subcutaneous injections of homocysteine (0.3-0.6 µmol/g body weight) and/or creatine (50 mg/kg body weight) from the 6th to the 28th days of age. The animals were decapitated 12 h after the last injection. Homocysteine decreased the cell viability of the mitochondrion and the activities of pyruvate kinase and creatine kinase. Succinate dehydrogenase was increased other evaluated parameters were not changed by this amino acid. Creatine, when combined with homocysteine, prevented or caused a synergistic effect on some changes provoked by this amino acid. Creatine per se or creatine plus homocysteine altered glucose oxidation. These findings provide insights into the mechanisms by which homocysteine exerts its effects on skeletal muscle function, more studies are needed to elucidate them. Although creatine prevents some alterations caused by homocysteine, it should be used with caution, mainly in healthy individuals because it could change the homeostasis of normal physiological functions.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Kolling¹,

Scherer²,

Siebert³

et al. 2012

Cell Biochemistry & Function

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Creatine prevents the inhibition of energy metabolism and lipid peroxidation in rats subjected to GAA administration

Kolling

Wyse

2010

Metab Brain Dis

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Guanidinoacetate methyltransferase (GAMT) deficiency is an inherited neurometabolic disorder, biochemically characterized by the tissue accumulation of guanidinoacetate (GAA). Affected patients present epilepsy and mental retardation whose etiopathogeny is unclear. Previous reports have shown that GAA alters brain energy metabolism and that creatine, which is depleted in patients with GAMT deficiency, can act as a neuroprotector; as such, in the present study we investigated the effect of creatine administration on some of the altered parameters of energy metabolism (complex II, Na(+),K(+)-ATPase and creatine kinase) and lipid peroxidation caused by intrastriatal administration of GAA in adult rats. Animals were pretreated for 7 days with daily intraperitonial administrations of creatine. Subsequently, these animals were divided into two groups: Group 1 (sham group), rats that suffered surgery and received saline; and group 2 (GAA-treated). Thirty min after GAA or saline, the animals were sacrificed and the striatum dissected out. Results showed that the administration of creatine was able to reverse the activities of complex II, Na(+),K(+)-ATPase and creatine kinase, as well as, the levels of thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation. These findings indicate that the energy metabolism deficit caused by GAA may be prevented by creatine, which probably acts as an antioxidant since it was able to prevent lipid peroxidation. These data may contribute, at least in part, to a better understanding of the mechanisms related to the energy deficit and oxidative stress observed in GAMT deficiency.

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Alterations on Na+,K+-ATPase and Acetylcholinesterase Activities Induced by Amyloid-β Peptide in Rat Brain and GM1 Ganglioside Neuroprotective Action

et al. 2013

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Alzheimer's disease (AD) is a neurodegenerative disorder whose pathogenesis involves production and aggregation of amyloid-β peptide (Aβ). Aβ-induced toxicity is believed to involve alterations on as Na(+),K(+)-ATPase and acetylcholinesterase (AChE) activities, prior to neuronal death. Drugs able to prevent or to reverse these biochemical changes promote neuroprotection. GM1 is a ganglioside proposed to have neuroprotective roles in AD models, through mechanisms not yet fully understood. Therefore, this study aimed to investigate the effect of Aβ1-42 infusion and GM1 treatment on recognition memory and on Na(+),K(+)-ATPase and AChE activities, as well as, on antioxidant defense in the brain cortex and the hippocampus. For these purposes, Wistar rats received i.c.v. infusion of fibrilar Aβ1-42 (2 nmol) and/or GM1 (0.30 mg/kg). Behavioral and biochemical analyses were conducted 1 month after the infusion procedures. Our results showed that GM1 treatment prevented Aβ-induced cognitive deficit, corroborating its neuroprotective function. Aβ impaired Na(+),K(+)-ATPase and increase AChE activities in hippocampus and cortex, respectively. GM1, in turn, has partially prevented Aβ-induced alteration on Na(+),K(+)-ATPase, though with no impact on AChE activity. Aβ caused a decrease in antioxidant defense, specifically in hippocampus, an effect that was prevented by GM1 treatment. GM1, both in cortex and hippocampus, was able to increase antioxidant scavenge capacity. Our results suggest that Aβ-triggered cognitive deficit involves region-specific alterations on Na(+),K(+)-ATPase and AChE activities, and that GM1 neuroprotection involves modulation of Na(+),K(+)-ATPase, maybe by its antioxidant properties. Although extrapolation from animal findings is difficult, it is conceivable that GM1 could play an important role in AD treatment.

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Intrastriatal hypoxanthine administration affects Na⁺,K⁺‐ATPase, acetylcholinesterase and catalase activities in striatum, hippocampus and cerebral cortex of rats

Cited by 7 publications

References 47 publications

Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Creatine prevents the inhibition of energy metabolism and lipid peroxidation in rats subjected to GAA administration

Alterations on Na+,K+-ATPase and Acetylcholinesterase Activities Induced by Amyloid-β Peptide in Rat Brain and GM1 Ganglioside Neuroprotective Action

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Intrastriatal hypoxanthine administration affects Na+,K+‐ATPase, acetylcholinesterase and catalase activities in striatum, hippocampus and cerebral cortex of rats

Cited by 7 publications

References 47 publications

Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Creatine prevents the inhibition of energy metabolism and lipid peroxidation in rats subjected to GAA administration

Alterations on Na+,K+-ATPase and Acetylcholinesterase Activities Induced by Amyloid-β Peptide in Rat Brain and GM1 Ganglioside Neuroprotective Action

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Intrastriatal hypoxanthine administration affects Na⁺,K⁺‐ATPase, acetylcholinesterase and catalase activities in striatum, hippocampus and cerebral cortex of rats