Brain energy metabolism is compromised by the metabolites accumulating in homocystinuria

Streck, Emílio L.; Delwing, Débora; Tagliari, Bárbara; Matté, Cristiane; Wannmacher, Clóvis Milton Duval; Wajner, Moaçir; Wyse, Ângela T. S.

doi:10.1016/s0197-0186(02)00230-9

Cited by 45 publications

(30 citation statements)

References 43 publications

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“…We have demonstrated that Met in vitro reduces brain energy metabolism, induces oxidative stress and inhibits Na + ,K + -ATPase activity in rat hippocampus [22][23][24]. Animal models are useful to better understand the pathophysiology of diseases.…”

Section: Discussionmentioning

confidence: 99%

Hypermethioninemia Increases Cerebral Acetylcholinesterase Activity and Impairs Memory in Rats

et al. 2007

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In the present study we investigated the effect of chronic hypermethioninemia on rat performance in the Morris water maze task, as well as on acetylcholinesterase (AChE) activity in rat cerebral cortex. For chronic treatment, rats received subcutaneous injections of methionine (1.34-2.68 micromol/g of body weight), twice a day, from the 6th to the 28th day of age; control rats received the same volume of saline solution. Groups of rats were killed 3 h, 12 h or 30 days after the last injection of methionine to AChE assay and another group was left to recover until the 60th day of life to assess the effect of early methionine administration on reference and working spatial memory of rats. AChE activity was also determined after behavioral task. Results showed that chronic treatment with methionine did not alter reference memory when compared to saline-treated animals. In the working memory task, we observed a significant days effect with significant differences between control and methionine-treated animals. Chronic hypermethioninemia significantly increased AChE activity at 3 h, 12 h or 30 days after the last injection of methionine, as well as before or after behavioral test. The effect of acute hypermethioninemia on AChE was also evaluated. For acute treatment, 29-day-old rats received one single injection of methionine (2.68 micromol/g of body weight) or saline and were killed 1, 3 or 12 h later. Results showed that acute administration of methionine did not alter cerebral cortex AChE activity. Our findings suggest that chronic experimental hypermethioninemia caused cognitive dysfunction and an increase of AChE activity that might be related, at least in part, to the neurological problems presented by hypermethioninemic patients.

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Section: Discussionmentioning

confidence: 99%

Hypermethioninemia Increases Cerebral Acetylcholinesterase Activity and Impairs Memory in Rats

et al. 2007

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“…However, in vitro studies have begun to identify some of the actions of Met to induce brain damage. In this context, we have previously demonstrated that this amino acid induces oxidative stress, reduces brain energy metabolism and inhibits Na + ,K + -ATPase activity in rat hippocampus in vitro (Stefanello et al, 2005;Streck et al, 2002aStreck et al, , 2003. These alterations may explain the cerebral edema observed in patients with methionine adenosyltransferase deficiency since reduction of Na + ,K + -ATPase caused by hypermethioninemia may lead to an impairment of sodium and potassium membrane transport with a consequent intracellular accumulation of sodium and water (Mudd et al, 2003).…”

Section: Introductionmentioning

confidence: 94%

Chemically induced model of hypermethioninemia in rats

Stefanello

Matté

Scherer

et al. 2007

Journal of Neuroscience Methods

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“…These results suggested an induction oxidative stress in blood of HD patients, and it is associated with the higher HHcy levels and reduced BuChE activity. It has been shown that HHcy increases lipid peroxidation [42], and BuChE can be inhibited by HHcy [3,43] mediated by the generation of free radical formation [44]. Studies show that hydrogen peroxide can inhibit serum cholinesterase.…”

Section: Discussionmentioning

confidence: 99%

Butyrylcholinesterase activity is reduced in haemodialysis patients: Is there association with hyperhomocysteinemia and/or oxidative stress?

Garcia

Wyse

Valentini

et al. 2008

Clinical Biochemistry

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Brain energy metabolism is compromised by the metabolites accumulating in homocystinuria

Cited by 45 publications

References 43 publications

Hypermethioninemia Increases Cerebral Acetylcholinesterase Activity and Impairs Memory in Rats

Hypermethioninemia Increases Cerebral Acetylcholinesterase Activity and Impairs Memory in Rats

Chemically induced model of hypermethioninemia in rats

Butyrylcholinesterase activity is reduced in haemodialysis patients: Is there association with hyperhomocysteinemia and/or oxidative stress?

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