RESUMEN
Sodium azide is a white crystalline powder used as a broad-spectrum biocide in agriculture and as a preservative in aqueous laboratory reagents. The aim of this study was to determine the effect of sodium azide on the corpus striatum and the possible protection by L-carnitine. Twenty-four adult male albino rats, weighing 150-200 g, were used in this study. The animals were divided equally into four groups. Group I was the control group. Group II received sodium azide at a dose of 20 mg/kg/day orally for 60 consecutive days. Group III received sodium azide at the same previous dose in addition to L-carnitine at a dose of 100 mg/kg/day intraperitoneally for 60 consecutive days. Group IV received only L-carnitine at the same previous dose once daily for 60 consecutive days. At the end of the experiment, all the animals were anesthetized, the brain was dissected out and the regions of the corpus striatum were subjected to light and electron microscopic examination. Moreover, the number of degenerated nerve cells was counted and the results were analyzed statistically. By light and electron microscope, the nerve cells [pyramidal cells and granular cells] of group II animals showed degenerative changes in the form of shrunken darkly stained and hyperchromatic nuclei. Some apoptotic cells were observed. There were multinucleated giant cells in some areas and small vacuoles in the neuropil. Also, cytoplasmic vacuolations and swollen mitochondria with indistinct cristea were detected. The neuropil in some areas contained extravasation of blood elements. The nerve fibers showed fragmentation, thickening, aggregation, and defective myelination. Statistically, there was a highly significant increase in the mean number of degenerated neurons. In group III, L-carnitine preserved most of the histological and ultrastructural profile of the corpus striatum [nerve cells and nerve fibers], with a significant decrease in the rate of neuronal loss. The results of the current study showed that the administration of L-carnitine might protect against neurotoxicity produced by exposure to sodium azide