Abstract:
Objective To study the pathological and biochemical effect of toluene on the central nervous system of exposed rats.
Methods Altogether 75 healthy male adult rats were chosen, and randomly devided into 5 groups (blank control group, excipient control group, low dose group, medium dose group and high dose group). With intraporitoneal administration of toluene(75 mg/kg body weight for low dose group, 150 mg/kg body weight for medium dose group, and 300 mg/kg body weight for high dose group) every other day for 30 d, the rats were killed, and their cortex and hippocampus were collected. Dyeing with heamatoxylin and eosin(HE), the specimens were observed under microscope and electron microscope for the pathological change of the brain. At the same time, the hippocampus was selected to measure the function of glutamate transporter of the brain.
Results Microscopic observation showed that a light degeneration around neurons and gliacytes occurred in rats's cortex of high dose group and vessel rift(VR) became broadened. Vacuole degeneration happened around some hippocampal neurons of high dose group. Neurons arrayed irregularly, but no degeneration and necrosis were seen in the neurons and gliacytes. Electron microscope examination found that in the toluene exposed groups, nerve cells began apoptosis characterized with disintegration of cell membrane, decrease of organelle's amoun(t ribosome, Golgi body and mitochondria), withdrawing of mitochondrial ridges, nucleus pyknosis, discontinuation of nucleus's membrane, increase of electron density and mass distribution of chromatin. The apoptosis of blood endothelia cells was also found. No such changes were found in the control groups. Function of glutamate transporter of the nerve cells in the high dose group decreased by 49% significantly compared with that in control groups (P<0.01). The function of glutamate transporter in the other dose groups declined too but not significant compared with the control groups.
Conclusion Toluene could induce the pathological change and decline of function of glutamate transporter in exposed rat's brain. Key Words: