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).
Highlights
IntroductionProblem description Intoxication lesions of the optic nerve (toxic optic neuropathy, TON) most often occur under the influence of exogenous factors [1, 2], including heavy metals [3]
The results of the immunohistochemical examination of optic nerve samples of experimental rats of all groups showed different expression of HSP70 (Fig. 1) and HSP90α (Fig. 2) in neuroglia cells and capillary endothelial cells depending on the duration of the experiment (Table 1)
For the first time, our study describes the features of the immunoexpression of heat shock proteins of the families: HSP70 and HSP90α in optic neuropathy associated with Cr (VI)
Summary
Problem description Intoxication lesions of the optic nerve (toxic optic neuropathy, TON) most often occur under the influence of exogenous factors [1, 2], including heavy metals [3]. Over the past few decades, emissions of pollutants into the environment have increased significantly due to rapid industrialization, urbanization, and overuse of agricultural fertilizers [4, 5]. One of the 14 most toxic heavy metals that pollute the environment, according to the Environmental Protection Agency India, is hexavalent chromium (Cr (VI)), due to its widespread use in the industry [6]. The lack of proper control over the disposal of Cr (VI) waste leads to an increase in the level of Cr (VI) in soil, water, air, polluting the environment [6, 7]. The most common routes of exposure to chromium through these media are ingestion, inhalation, and dermal contact with soil, water, or particulates in the air contaminated with chromium
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