This paper presents the results of the study of the effect of water with deuterium content of 750 ppm, used for simulation of the isotopic composition of water in ice caps at the poles of Mars, on oxidative processes in the liver tissue and blood of laboratory animals. It was found that prolonged consumption of deuterium-enriched water contributed to an increase in the deuterium content in blood plasma up to 487 ppm. As a result, increased antioxidant activity in the liver tissues and blood plasma was observed. In addition, the effect of a medium that contains 487 ppm of deuterium on the secondary structure of bovine serum albumin was also investigated in a model experiment. A decrease in intensity of circular dichroism and intrinsic tryptophan fluorescence spectra was found. This indicates that there are conformational changes in the structure of this protein at a time when the content of deuterium increases in the incubation medium. The results of our research point to the need to explore further the effect of drinking diet with the increased deuterium to (from 700 to 1000 ppm) on living systems, to explain the possibility for life on Mars.

The coordination compound [Mg(HCom)2(H2O)6]·2H2O (I) was obtained by the reaction of comenic acid (H2Com) with magnesium acetate in water. The formation of a new phase was confirmed by powder X-ray diffraction. The molecular formula of the compound was determined from energy dispersive X-ray fluorescence and thermogravimetry data. The thermo-oxidative stability of magnesium comenate was studied by simultaneous thermal analysis in air. The molecular structure of the complex was discussed on the basis of spectral data (NMR, IR, and UV spectroscopy) and studied in detail using X-ray diffraction (CCDC no. 2 207 835). Magnesium comenate crystallizes in the triclinic system, space group P 1̅, the structure is stabilized by intra- and intermolecular hydrogen bonds between the coordinated water molecules, acid anions, and [Mg(H2O)6]2+.

Meconic, comenic, chelidonic, and kojic acids are the main representatives of gamma-pyronic acids. It was found that comenic acid has a neuroprotective effect, and chelidonic acid has a pronounced anti-inflammatory effect. The neuroprotective effect of meconic acid has not been explored. The aim of this study was to investigate the neuroprotective potential of meconic acid on an in vitro ischemic stroke model, as well as on the basis of its physicochemical properties. A primary neuro-glial culture was obtained from the cerebellum of 7- to 8-day-old Wistar rats by mechanical dissociation. The protective effect of meconic acid on the culture of cerebellar neurons was studied using a model of glutamate toxicity and oxygen–glucose deprivation. The antioxidant activity of meconic acid was studied by quantum mechanical calculations and experimentally in the citrate-phosphate-luminol model system by chemiluminescence analysis. The chelating properties of meconic acid with respect to Fe3+ in solutions were studied by the Job’s method. Meconic acid has been found to have a protective effect on in vitro models of ischemia. It caused a decrease in the level of intracellular calcium and restoration of the membrane potential of mitochondria in the culture of cerebellar neurons under glutamate exposure and an increase in the percentage of living cells under oxygen–glucose deprivation. Meconic acid had a high calculated antioxidant potential, as was confirmed experimentally. With an increase in pH of the medium, a stepwise binding of meconic acid with Fe3+ occurred with the formation of complexes of different ligand/metal ratios. At physiological pH, the resulting complex had a composition with the ratio 1 : 3. The revealed antioxidant, chelating, and cytoprotective effects of meconic acid provide a basis for further study of the possible neuroprotective properties of this compound in experiments in vivo; the data on its physicochemical properties can be useful for the synthesis and study of new coordination compounds based on this acid.

Water containing 750 ppm deuterium was used to simulate the isotopic composition of water in ice caps at the poles of Mars and tested for effect on oxidative processes in the liver and blood of laboratory animals. Prolonged consumption of deuterium-rich water was found to increase the deuterium content in the blood plasma to 487 ppm. Higher antioxidant activity was consequently observed the liver and blood plasma. The effect of a medium containing 487 ppm deuterium on the secondary structure of bovine serum albumin (BSA) was additionally studied in a model experiment. Lower intensities were observed in circular dichroism (CD) and intrinsic tryptophan fluorescence spectra, indicating that conformational changes arose in albumin structure when the deuterium content increased in the incubation medium. The study provides a basis for further research of how drinking water with a higher deuterium content (700–1000 ppm) affects living systems, to understand the possibility of life on Mars.

The effects of prolonged (42 day) consumption of deuterium-depleted water by rats on the functional state of their central nervous system under normal conditions and under conditions of normobaric hypercapnic hypoxia have been studied. The consumption of deuterium-depleted water both under normal conditions and after exposure to oxidative stress contributed to a significant reduction in emotional anxiety in animals. Prolonged consumption of deuterium-depleted water before experimental hypoxia (amnesic factor) helped animals to maintain their ability to learn and memory at the control level, i.e., it exerted a pronounced protective antiamnesic effect. Under normal conditions, deuterium-depleted water does not affect the learning ability of animals.

The effects of prolonged (42 days) addition of deuterium-depleted water into rat’s diet on the functional state of the central nervous system in normal conditions and under conditions of normobaric hypoxia with hypercapnia were studied. It was also established that the use of deuterium-depleted water both in normal conditions and after exposure to oxidative stress contributes to a significant reduction in the emotional anxiety of animals. Prolonged use of deuterium-depleted water before hypoxic exposure (amnestic effect) helps to maintain learning and memory at the control level, i.e. it has a pronounced protective antiamnestic effect. In normal conditions, deuterium-depleted water does not affect the learning ability of animals.

Abstract—It is established that a medium with a reduced content of deuterium has no effect on the secondary structure of horseradish peroxidase and bovine serum albumin and caused no conformational changes in the structures of these proteins. The placement of these proteins in a buffer solution prepared based on deuterium-depleted water led to a decrease in the intensity of intrinsic tryptophan fluorescence, while the circular dichroism spectra remained virtually unchanged. A decrease in the content of deuterium in the reaction medium led to a decrease in the activity of the peroxidase oxidation reaction of o-dianisidine and luminal with hydrogen peroxide.

The effect of deuterium-depleted water on oxidative processes in the rat brain under physiological or hypoxic conditions was studied. The results obtained by a tissue culture method that characterize the functional parameters of neurons under stress are also presented. Results on free radical processes in the rat brain tissues demonstrated that consumption of deuterium-depleted water over 2 weeks has a stress effect. The long-term consumption of deuterium-depleted water caused activation of non-specific protective systems. The effect of a saline solution prepared with deuterium-depleted water on a cerebellar tissue culture was also studied. When incubation occurred in a saline solution based on deuterium-depleted water, glucose deprivation and temperature stress (39°C) were found to result in increased cell death in the neuronal culture. The neuron death rates under physiological conditions were similar in the case of both 150 and 50 ppm deuterium. At the same time, the mitochondrial membrane potential of cerebellar neurons decreased in the deuterium-depleted medium. Thus, incubation of cerebellar neurons in the deuterium-depleted saline solution had no cytoprotective effect.

Using the model of cultured spinal ganglia, we demonstrated high neurotrophic activity of comenic acid and its derivatives potassium comenate and calcium comenate both under normal conditions and during oxidative stress. Calcium comenate in the norm as well as potassium and calcium comenates during oxidative stress demonstrate greater neurotrophic potency than comenic acid.

This paper reports an analysis of the effects of sodium comenate on neurite growth from spinal ganglia under the conditions of hydrogen peroxide-induced oxidative stress and on the glutathione antioxidant system in the brain of mice exposed to immobilization stress. It has been demonstrated that sodium comenate at the concentrations of 0.1–0.001 mM stimulates the growth of neurites from spinal ganglia exposed to oxidative stress. The most profound stimulatory effect was observed with 0.001 mM sodium comenate. The administration of sodium comenate at doses of 1, 2, and 4 mg/kg contributed to the maintenance of the GSH content and glutathione peroxidase and glutathione reductase activities at the physiologically normal state level under stress conditions. The results of the study of neurotrophic and antioxidant effects of sodium comenate in oxidative stress suggest that this compound is a highly efficient neuroprotector.

Potassium comenate and comenic acid exhibit manifest and virtually identical antioxidant activity under conditions of hypoxia with hypercapnia. The effects of these drugs on conditioned reflex training with positive reinforcement differ significantly. Potassium comenate promotes retention of the learning capacity and memory in hypoxic rats at the level of intact control, that is, exhibits a pronounced protective antiamnestic effect, while comenic acid only facilitates training of the conditioned reflex with positive reinforcement.

Изучено влияние нового фармакологического соединения кальциевой соли коменовой кислоты (CaK) на генерацию активных форм кислорода в модельной системе ЦФЛ (цитрат фосфатный буфер с добавлением люминола), на токсичность глутамата в диссоциированных культурах нейронов мозжечка крыс, а также его влияние на ростовые процессы культивируемых нейронов спинальных ганглиев эмбрионов кур в условиях окислительного стресса в сравнении с коменовой кислотой (КК). Установлено, что CaK повышает устойчивость культивируемых нейронов мозжечка к глутаматной цитотоксичности, проявляет выраженный нейротрофический эффект — защищает нейроны спинальных ганглиев эмбрионов кур от окислительного воздействия перекиси водорода, значительно снижает содержание свободных радикалов в модельной системе ЦФЛ (на 64,6 %, p < 0,001). Антиокислительные свойства CaK практически не отличаются от КК, в тоже время максимальный нейропротекторный эффект CaK проявляется в более низких (1 и 10 мкМ), чем КК (1000 мкМ) концентрациях, а нейротрофическое действие, в отличие от КК, в более широком диапазоне концентраций: CaK — 0,01 и 0,001 мМ, КК — 0,01 мМ.

We studied antioxidant protective effect of comenic acid and potassium comenate in doses of 2, 4, and 8 mg/kg under conditions of oxidative stress in the brain of mice exposed to immobilization stress. Administration of potassium comenate and comenic acid in the above doses for 3 days before stress prevented the development of oxidative processes in the brain of stressed animals. The antioxidant effect of potassium comenate more pronounced.

The study demonstrated neuroprotective action of novel chemical agent, potassium salt of comenic acid, against the glutamate-induced cytotoxicity on the model of cultured cerebral neurons. Potassium comenate (0.001-1.0 mM) significantly decreased the rate of glutamateinduced neuronal death. The highest viability of the cultured neurons during postglutamate time was observed when potassium comenate was applied in a concentration of 0.1 mM.

We demonstrated an increase in glutamate neurocytotoxicity in cultured cerebellar cells from rat pups subjected to lead poisoning during the prenatal development or early lactation period. The toxic effect of glutamate was weaker, if lead was applied in combination with antioxidant comenic acid. These data are discussed in view of practical use of comenic acid for the therapy of the brain tissues subjected to lead poisoning.

We studied the state of the antioxidant glutathione system ( activity of glutathione peroxidase, glutathione reductase, and content of GSH and GSSG) and the level of lipid peroxidation in the brain of newborn rats, as well as the intensity of neurite growth in the cultured spinal ganglia of these animals after prenatal treatment with lead acetate. Daily addition ( 6 mg/kg) or single addition on the 18th day of pregnancy ( 200 mg/kg) of lead acetate to food of pregnant females resulted in a considerable decrease in the activity of the glutathione system and increase in the levels of GSSG and malonic dialdehyde in the brain tissue. The lead intoxication also inhibited neurite growth in cultured ganglia. In addition, the permanent presence of lead acetate (0.02 mM) in the cultures of ganglia of intact rats on the second and third days in vitro also led to inhibition of neurite growth. The data obtained indicate that oxidative stress, which results in decreased antioxidant activity, may be one of the main mechanisms that underlie toxic injury of central and peripheral neurons after prenatal action of lead.

Software and information tools for cartographic support of transport dispatching service on the basis of electronic regional maps and geographic information systems (GIS) are examined.