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Sokurenko L. M.1, Chaikovsky Yu.B.1, Andrusishina I.M.2
O.O.Bogomolets National Medical University, Kyiv, Ukraine,
Institute for Occupational Health of AMS of Ukraine, , Kyiv, Ukraine
Research was carried out on Wistar rats weighing 150-200 g, which were
kept in standard vivarium conditions. Animals were divided into 3 groups (total 30
animals). The first (I) group was studied as control, in the second and third groups
- intraperitoneal administration of mercury chloride in a dose 1/100 LD50 (shortterm and long-term exposure) for 2 and 10 weeks was performed. Lumbar and
sacral segments of the spinal cord that form efferent component of the sciatic nerve
and belong to all six neuronal populations of the IX Rexed plate were studied
electron microscopically. Concentration of Mg, Cu, K, Zn, Se, Li were defined.
Statistical processing of the results was carried out by methods of variation
statistics using Microsoft Excel software and "Statistica 4.0" (Statistica Inc. USA).
Results and discussion. Processes of compensatory changes in spinal cord
neurons in short-term exposure (release of protein synthesis products in
organelles), and in the long-term – processes of decompensation (destructuring of
endoplasmic reticulum, ribosomes and polysomes, increase in number of
secondary lysosomes and destruction of the structure of mitochondria, which
accumulate, according to the literature, the ions of mercury) were determined.
Ultrastructural changes reflect stages of the pathological process characterized by
compensation stage, pronounced changes and decompensation.
Under the influence of low concentrations of mercury reduction of such
important for the nervous tissue elements functioning such as magnesium, zinc and
copper in the rats spinal cord was detected. Lower magnesium, which is a marker
of apoptotic nerve cells, influences the activity of the neurotransmitter glycyne,
which is involved in maintaining the accuracy of motion, fine motor skills,
maintenance of posture and causes the clinical picture of micromercurialism. Data
on the growth of vascular motility at lower levels of magnesium allow to perceive
degenerative changes of neurons and glia not only as immediate damage by
mercury chloride, but also as an indirect effect due to pathological changes of
vessel walls. Reduction of magnesium also affects the nerve fibers and cell-cell
contacts, as confirmed ultramicroscopically in the spinal cord and sensitive ganglia
of animals.
Zinc is involved in the regulation of the enzyme (tyrosine kinase), which is
the signal of neurotrophic factors to the growth signaling systems in neurons and
glia, and protects neurons against excess nitric oxide. On the other hand, zinc
which is released from the cells in the intercellular substance has toxic effects on
neurons. It gives the right to consider this process as well as one of the
pathological mechanisms of micromercuryalism. Moreover, according to the
literature nuclear fraction of zinc suffers first, which leads to disruption abilities to
learning and memory, and therefore reflects the period of micromercuryalism when
the clinical picture is difficult to diagnose.
Antagonist of mercury - selenium concentration was almost zero, indicating
a high competitive ability of mercury binding sites in sulfur-containing enzymes
and proteins. Since selenium is an inhibitory factor in autoimmune processes, the
reduction of its concentration may provide another mechanism of pathological
action of mercury - an autoimmune.
Lithium content increases at short exposure of mercury chloride, but was
significantly reduced in long-term, which is likely due to the competitive binding
of metalolihand domains of proteins G1-subunits and neuroprotective effect on
neurons that was found at lower concentrations of potassium in the spinal cord.
Lithium is involved in the metabolism of neurotransmitters and this may explain
the compensatory responses of neurons in the short exposure to mercury chloride
(activation of synthetic processes in organelles of neurons and intense release of
neurotransmitters), and the long-term processes of attrition, which correspond to
the decrease of lithium.
The level of copper, which is zinc antagonist, respectively decreases. As we
know from scientific sources, copper, as well as selenium, organize metal-forming
clusters in the catalytic center of superoxide dismutase and thus is involved in
antioxidant reactions of neurons and glia. Copper, like zinc and selenium,
stabilizes neurofilaments and neurotubules in cytoskeleton of neuron that support
intercellular exchange and ante- and retrograde movement of substances,
neurotransmitters and organelles along axons.
Conclusions. Morphofuntional transformations of neurons and glia are the
main cause of neurological disorders in prolonged exposure to small doses of
mercury compounds. Comparing the data with literature, assumption was made
about mercury salts influence in relation to reversible and irreversible changes of
spinal cord motoneurons.