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Methylmalonate administration decreases Na+,K+-ATPase activity in cerebral cortex of rats

A T Wyse1, E L Streck, S V Barros

  • 1Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

Neuroreport
|August 3, 2000
PubMed

Insights

Methylmalonate (MMA) exposure in rats reduced Na+,K+-ATPase activity in brain membranes. This effect appears linked to oxidative damage, as glutathione prevented the enzyme inhibition.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Toxicology

Background:

  • Methylmalonate (MMA) is a metabolite implicated in certain metabolic disorders.
  • The impact of MMA on specific neuronal enzyme functions, particularly Na+,K+-ATPase, requires detailed investigation.

Purpose of the Study:

  • To investigate the in vivo and in vitro effects of methylmalonate (MMA) on Na+,K+-ATPase and Mg2+-ATPase activities in rat cerebral cortex.
  • To explore the potential mechanisms underlying MMA-induced alterations in enzyme activity.

Main Methods:

  • Chronic and acute subcutaneous administration of buffered methylmalonate (MMA) or saline to rats at different ages and intervals.
  • Biochemical assays to determine Na+,K+-ATPase and Mg2+-ATPase activities in isolated synaptic plasma membranes from rat cerebral cortex.
  • In vitro incubation of brain homogenates with MMA, with and without glutathione, prior to enzyme activity assessment.

Main Results:

  • Subcutaneous MMA administration significantly reduced Na+,K+-ATPase activity by 30-40% in rat cerebral cortex synaptic membranes.
  • Mg2+-ATPase activity remained unaffected by MMA treatment.
  • In vitro incubation of brain homogenates with MMA decreased Na+,K+-ATPase activity, an effect mitigated by glutathione, suggesting oxidative damage.

Conclusions:

  • In vivo methylmalonate exposure impairs Na+,K+-ATPase activity in the rat brain.
  • The observed reduction in Na+,K+-ATPase activity is likely mediated by oxidative stress or damage to enzyme thiol groups.
  • These findings highlight a potential neurotoxic mechanism of methylmalonate relevant to conditions involving its accumulation.

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