Glutamate uptake by astrocytes is inhibited by reactive oxygen intermediates but not by other macrophage-derived molecules including cytokines, leukotrienes or platelet-activating factor

J Neuroimmunol. 1993 Oct;48(1):99-104. doi: 10.1016/0165-5728(93)90063-5.

Abstract

By their property to release glutamate and reactive oxygen intermediates, macrophages may play an important role in neurotoxicity. In the present study we have investigated whether macrophage-derived molecules also impair the detoxification of glutamate by astrocytes. Cytokines, including interleukin (IL)-1, 6 and 10, interferon (IFN)-alpha/beta, tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta 1, as well as leukotriene (LT) B4 and C4, prostaglandin (PG) E2 and nitric oxide radicals had no effect on the uptake of [3H]glutamate by murine astrocytes in culture. In contrast, exposure of astrocytes to the enzyme glucose oxidase (100-200 mU ml-1), which maintains steady-state levels of hydrogen peroxide, reduced glutamate uptake by 30-50%. By their dual effect, comprising secretion of glutamate and inhibition of its detoxification by astrocytes, activated macrophages and microglial cells may contribute to exacerbate excitotoxic mechanisms in neurological diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / metabolism*
  • Cells, Cultured
  • Cytokines / pharmacology
  • Glutamates / metabolism*
  • Glutamic Acid
  • Leukotrienes / pharmacology
  • Macrophages / physiology*
  • Mice
  • Mice, Inbred ICR
  • Platelet Activating Factor / pharmacology
  • Reactive Oxygen Species / pharmacology*

Substances

  • Cytokines
  • Glutamates
  • Leukotrienes
  • Platelet Activating Factor
  • Reactive Oxygen Species
  • Glutamic Acid