RESEARCH OF REPARATIVE MECHANISMS IN THE OPTIC NERVE IN TOXIC NEUROPATHY CAUSED BY Cr (VI)

Abstract

Intoxication lesions of the optic nerve (toxic optic neuropathy, TON) most often occur under the influence of exogenous factors, including heavy metals. Сell survival under stress have involves heat shock proteins (HSPs). The aim of the research. To assess the optic nerve’s immunoreactivity to heat shock proteins of the HSP70 and HSP90α families and reveal its relationship with the severity of morphological changes in toxic optic neuropathy caused by Cr (VI). Materials and methods. The study was conducted on 48 mature male rats. The experimental groups were given to drink water with Cr(VI) for 20, 40 and 60 days. This type of water is typical for the water basins in the northern districts of the Sumy region. Optic nerves сhanges under the influence of Cr(VI) have investigated by the morphometric method. Neuroglial cells and capillary endothelial cells were assessed by immunohistochemistry by HSP70α and HSP90 expression for intensity and spatial distribution. Results. The data analysis revealed that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. The dynamics of HSP70 immunoexpression in the endothelium of the optic nerve capillaries of rats on 20 and 40 experimental days was characterized by stable values and was 1.5 times higher than the control. The maximum number of positively stained cells for the HSP70 marker was detected in endothelial cells of the microvasculature for 60 days – 82.44±12.42 %. HSP70 levels in neuroglia cells of optic nerve have decreased on day 40 (55.66±11.56% p=0.05) and lower than the control (70.44±4.81 %.) group. Optic nerve capillaries was highest immunoactivity on HSP90 in group II endothelial cells – 51.22±14.57% (p=0.05). The activity of HSP90α protein in optic neuroglia cells was characterized by a gradual increase in the duration of the experiment and was higher by 12, 4 % in experimental group III (81.77±21.67 %) compared with control (71.66±4.95 %). Conclusions. Our study provides an insight into the significant difference in the immunoreactivity of heat shock proteins of the HSP70 and HSP90α families in neuroglia and endothelial cells of the optic nerve capillaries under the influence of Cr(VI). The results obtained suggest that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. A comparison of the dynamics of the development of the dystrophic process in the optic nerve with the results of the immunohistochemical analysis showed, that an increase in the thickness of nerve fibers is accompanied by an increase in immunoreactive neuroglial cells (HSP90α) and endothelial cells (HSP70).