Evaluation of the zinc succinate toxic effect on the cerebral cortex of rat

Background. Anthropogenic human activity contributes to the inclusion of zinc compounds in the biological cycle in areas where there is pollution with this metal. This leads to the accumulation of the substance in organs and tissues, which can have a neurotoxic effect on the body. Aim. To evaluate the toxic effect of zinc succinate on the structure and function of the cerebral cortex of laboratory rats. Materials and methods. The study was performed on 12 Wistar male rats aged 2 months. The animals were divided into 2 groups: control and experimental, 6 rats each. Within 30 days, the animals of the experimental group were intragastrically injected with a solution containing zinc succinate in a dose of 100 mg/kg. The rats from group 1 served as intact controls. Fluorescent analysis of coenzyme activity of the brain was performed, for which excitation was used at wavelengths of 365 nm and 450 nm, which corresponds to the reduced form of nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD); morphological analysis of the motor cortex of the cerebral hemispheres.Results. Analysis of fluorescence spectra demonstrated a statistically significant decrease in its intensity in the experimental group for the coenzyme NADH (0.855 [0.092]) compared with the control (0.709 [0.062]); p <0.05. Differences in the intensity of the fluorescence spectra for coenzyme FAD is not found. Morphological analysis revealed the presence of toxic and dystrophic processes in the cerebral cortex in animals of the experimental group: the vessels are predominantly full - blooded, in some places the expansion of the perivascular space is visualized, a small number of neurons in the form of shadow cells. Conclusion. The effect of zinc succinate on the structure of the cerebral cortex is characterized by a decrease in the fluorescence intensity of coenzyme NADH, and the absence of changes in the fluorescence of coenzyme FAD, which may indicate the initiation of mitochondrial dysfunction and impaired oxygenation of neurons. Morphological analysis demonstrates the development of dystrophic changes.