C- and N-bearing species in reduced fluids weree studied experimentally in C–O–H–N and muscovite–C–O–H–N systems and in natural carbonate-bearing samples at mantle P–T parameters. The experiments reproduced three types of reactions leading to formation of hydrocarbons (HCs) at 3.8–7.8 GPa and 800–1400 C and at hydrogen fugacity (fH2) buffered by the Fe–FeO (IW) + H2O or Mo–MoO2 (MMO) + H2O equilibria: (i) Thermal destruction of organic matter during its subduction into the mantle (with an example of docosane), (ii) hydrogenation of graphite upon interaction with H2‑enriched fluids, and (iii) hydrogenation of carbonates and products of their reduction in metamorphic clayey rocks. The obtained quenched fluids analyzed after the runs by gas chromatography-mass spectrometry (GC–MS) and electronic ionization mass-spectrometry (HR–MS) contain CH4 and C2H6 as main carbon species. The concentrations of C2-C4 alkanes in the fluids increase as the pressure and temperature increase from 3.8 to 7.8 GPa and from 800 to 1400 C, respectively. The fluid equilibrated with the muscovite–garnet–omphacite–kyanite–rutile ± coesite assemblage consists of 50–80 rel.% H2O and 15–40 rel.% alkanes (C1 > C2 > C3 > C4). Main N-bearing species are ammonia (NH3) in the C–O–H–N and muscovite–C–O–H–N systems or methanimine (CH3N) in the fluid derived from the samples of natural pelitic rocks. Nitrogen comes either from air or melamine (C3H6N6) in model systems or from NH4+ in the runs with natural samples. The formula CH3N in the quenched fluid of the C–O–H–N system is confirmed by HR–MS. The impossibility of CH3N incorporation into K-bearing silicates because of a big CH3NH+ cation may limit the solubility of N in silicates at low fO2 and hence may substantially influence the mantle cycle of nitrogen. Thus, subduction of slabs containing carbonates, organic matter, and N-bearing minerals into strongly reduced mantle may induce the formation of fluids enriched in H2O, light alkanes, NH3, and CH3N. The presence of these species must be critical for the deep cycles of carbon, nitrogen, and hydrogen.

A mini review of literature data on the mechanisms of formation of the stock of free amino acids and their derivatives in liver pathology and methods for correcting metabolic imbalance.The importance of amino acids in the biosynthesis of protein and highly active biological compounds was the main prerequisite for numerous studies of their content in body fluids and tissues in a wide variety of experimental and pathological situations. In the intermediate metabolism of amino acids and their derivatives, a connecting role is played by in the integration of the main metabolic flows [1][2][3][4]. The pool of free amino acids is represented by a rich set of metabolically and functionally interconnected compounds, with the concentrations being a regulatory factor at many key steps of metabolism [5,6].In connection with the foregoing, study of the mechanisms of formation of the free amino acid pool in vivo is part of the most important problem of contemporary biochemistry and clinical medicine associated with targeted regulation of metabolic processes in the human body by biologically active natural compounds.Currently, the number of patients with pathology continues to grow, with metabolic disorders playing a leading role in the genesis of these pathologic states [4][5][6]. The most urgent in this case is the problem of the pathogenetic role of disorders in the metabolism of amino acids in hepatobiliary pathology, as well as the optimization of the use of individual amino acids or their artificial mixtures not only for replacement therapy, but also for targeted metabolic correction of liver diseases [6][7][8][9][10][11][12][13][14][15][16][17]. In addition to disturbances in the chain of reactions of carbohydrate, lipid and protein metabolisms characteristic of liver damage, a pronounced amino acid imbalance is observed in physiological fluids and tissues [18][19][20].Thus, it was shown that an increase in blood methionine level and a decrease in its excretion during exogenous loads with this amino acid clearly correlate with clinical manifestations of diseases accompanied by impaired liver function [21][22][23][24]. In addition, the blood of patients with liver damage shows a decrease in the concentration of the most important methionine degradation product, cysteine, and a dramatic increase in the toxicity of methionine [25,26]. Normally, up to 10 g of S-adenosylmethionine