Neurochemical and oedematous changes in 1,3-dinitrobenzene-induced astroglial injury in rat brain from a 1H-nuclear magnetic resonance perspective

Abstract

1,3-Dinitrobenzene (1,3-DNB), an intermediate used in the chemical industry, has toxic effects in the brain and testes. It produces focal lesions with marked astroglial necrosis in the rat brain upon repeated administration. Astrocytic death occurs in parallel with elevated local blood flow and is followed by damage to the cerebral vasculature and neurones. (1)H-nuclear magnetic resonance spectroscopic analysis before the onset of astrocytic damage, showed a global elevation of lactate, whereas choline containing compounds increased in the non-vulnerable cerebral cortex, yet decreased in the vulnerable brainstem. Similarly, glutamate increased in the cerebral cortex, cerebellum and midbrain, but decreased in the susceptible brainstem. In vivo T2-weighted NMR imaging showed high signal intensities in brain nuclei shown to develop astroglial loss by conventional neuropathology at 24 hours after completion of dosing, but not at 6-10 hours. Hence the early neurochemical changes in susceptible areas contribute to the aetiology of degeneration, and those seen elsewhere may represent adaptive responses dependent on the particular phenotype of different cell groups and underlying metabolic relationships.