Evaluating the environmental and therapeutic impacts of dietary supplement (Case study: The supplement Oyox for prevention of environment damages, treatment and disorders in the hepatobilliary system)

Document Type : Research Paper

Authors

Head of the Laboratory of Energy of Biological Systems, Institute of Theoretical and Experimental RA

Abstract

Globally recommended diets are a powerful method for raising the public's awareness of dietary choices. Although dietary choices drive both health and environmental outcomes, these diets make almost no reference to environmental impacts. Besides, Encephalic damage and disorders of the hepatobiliary system occur against the background of metabolic disorders. Metabolic processes largely depend on the activity and the qualitative and quantitative characteristics of sirtuin-type proteins. Protein deficiency can be filled by artificially introducing them into the body through dietary supplements. The study aimed to analyze the possibilities of using the dietary supplement OYOX to prevent environmental harm as well as treating encephalic damage and disorders of the hepatobiliary system. We used theoretical and practical research methods. In particular, the methods of analysis of literature sources, statistical data, results of clinical and preclinical studies were used. The method of generalization, analysis, systematization, classification of the obtained data was used. The results were evaluated 3 and 6 months after taking the dietary supplement. In the group of people taking OYOX, a statistically significant decrease was observed in the percentage of short telomeres (p = 0.029); a decrease in the percentage of senescent cytotoxic (CD8+ / CD28-) T cells (by 1.5%; 4.4%; 8.6% and 7.5% after 3 and 6 months respectively); improvement in lipid and carbohydrate metabolism glycosylated hemoglobin (HbA, 1%) by 4.9% (p = 0.01), total cholesterol 5.7 mmol  L-1 (p = 0.003), low density lipoprotein (LCL-C): 3.82 mmol  L-1 (p = 0.0021), homocysteine: 3.4 mmol L-1  (p = 0.001). In conclusions, dietary supplement OYOX is effectively used to eliminate the deficiency of sirtuin-type proteins SIR1, SIR3, SIR6.
 

Keywords


Abdellatif, M 2012, Sirtuins and pyridine nucleotides, Circulation Research, 111: 642-656.
Brian, J, & Verdin, E 2014, Sirtuins: Sir2-related NAD-dependent protein deacetylases, Genome Biology, 5:  224-243.
Chahirou, Y, Mesfioui, A, Ouichou, A, & Hessni, A 2018, Аdipokines: mechanisms of metabolic and behavioral disorders, Obesity and Metabolism, 15: 14-20, DOI: 10.14341/OMET9430.
Chen, J, Zhou, Y 2015, Mueller-Steiner S, Chen LF, Kwon H, Yi S, Mucke L, Gan L. SIRT1 protects against microglia-dependent amyloid-beta toxicity through inhibiting NF-kappa B signaling, Journal of Biological Chemistry, 280(48): 64-74.
Fefelova, YA, Sergeeva, EY, Novikova, LV & Klimina, GM 2016, Influence of the nature of nutrition on SIRTUIN1-mediated changes in metabolic processes, Nutrition issues, 85: 5-13.
Joshi, D & Adhikari, N 2020, Aflavinines: History, biology and total synthesis. Advanced Journal of Chemistry-Section B, 2: 3-9.
Kawahara, TL, Michishita, E, Adler, AS, Damian, M, Berber, E, Lin, M, McCord, RA, Ongaigui, KC, Boxer, LD, Chang, HY, & Chua, KF 2019, SIRT6 links histone H3 lysine 9 deacetylation to NF-kappa B-dependent gene expression and organismal life span, Cell, 136: 62-74.
Kelly, G 2010, A review of the sirtuin system, its clinical implications, and the potential role of dietary activators like resveratrol: Part 1, Alternative Medicine Review, 15: 245-63.
Kendrick, AA, Choudhury, M, Rahman, SM 2011, Fatty liver is associated with reduced SIRT3 activity and mitochondrial protein hyperacetylation, Biochemical Journal, 33: 505-514.
Kennedy, BK, Gotta, M, Sinclair, DA, Mills, K, McNabb, DS, Murthy, M, Pak, SM, Laroche, T, Gasser, SM, & Guarente, L 2015, Redistribution of silencing proteins from telomeres to the nucleolus is associated with extension of life span in S. cerevisiae, Cell, 89: 381-391.
Kim, HJ, Kim, JH & Noh, S 2011, Metabolomic analysis of livers and serum from high-fat diet induced obese mice, Journal of Proteome Research, 10: 722-731.
Lan, F, Cacicedo, JM, Ruderman, N & Ido, Y 2018, SIRT1 modulation of the acetylation status, cytosolic localization, and activity of LKB1. Possible role in AMP-activated protein kinase activation, Journal of Biological Chemistry, 283: 27628-27635.
Latha, NL, Gyananath, G, Kasa, A & Zubaidha, PK 2019, Validation of sigma I receptor occupancy with antipsychotic ligands: A molecular perspective. Journal of Medicinal and Chemical Sciences, 2: 41-75.
Naderi, D, Jami, R, & Rehman, F 2021, A review of RNA motifs, identification algorithms and their function on plants, Journal of Plant Bioinformatics and Biotechnology, 1: 28-40.
Nogalska, A, Pankiewicz, A 2016, The age-related inverse relationship between ob and lipogenic enzymes genes expression in rat white adipose tissue, Experimental Gerontology, 38: 415-422.
Simonsen, A, Cumming, R C, & Brech, A 2018, Promoting basal levels of autophagy in the nervous system enhances longevity and oxidant resistance in adult Drosophila, Autophagy, 4: 176–184.
Tao, R, Wei, D, Gao, H, Liu, Y, DePinho, RA & Dong, XC 2011, Hepatic FoxOs regulate lipid metabolism via modulation of expression of the nicotinamide phosphoribosyl transferase gene. Journal of Biological Chemistry, 286: 14681-14690.
Ukwubile, C, Ikpefan, E, Bingari, M, & Tam, L 2019, Acute and subchronic toxicity profiles of Melastomastrum capitatum (Vahl) Fern. (Melastomataceae) root aqueous extract in Swiss albino mice, Progress in Chemical and Biochemical Research, 2: 74-83.
Vafaei-Nezhad, M, Ghiasi, R & Shafiei, F, 2020, Conformational Analysis of 2-halo-1, 3, 2-dioxaphosphinanes: A Density Functional Theory (DFT) Investigation. Chemical Methodologies, 4: 161-171.
Wolfson, M, & Budovsky, A 2019, The signaling hubs at the crossroad of longevity and age related disease networks, International Journal of Biochemistry & Cell Biology, 41: 516-520.
Yoshino, J, Mills, KF, Yoon, MJ, & Imai, S 2011, Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice, Cell Metabolism, 14: 528-536.