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BackgroundAn ongoing important need exists to rapidly develop novel therapeutics for COVID-19 that will retain antiviral efficacy in the setting of rapidly evolving SARS-CoV-2 variants and potential future development of resistance of SARS-COV-2 to remdesivir and protease inhibitors. To date, there is no FDA-approved treatment for post-exposure prophylaxis against SAR-CoV-2. We have shown that the mitochondrial antioxidant mitoquinone/mitoquinol mesylate (Mito-MES), a dietary supplement, has antiviral activity against SARS-CoV-2 in vitro and in SARS-CoV-2 infected K18-hACE2 mice.MethodsIn this exploratory, pragmatic open label clinical trial (ClinicalTrials.gov identifier NCT05381454), we studied whether Mito-MES is an effective post-exposure prophylaxis treatment in people who had high-grade unmasked exposures to SARS-CoV-2 within 5 days prior to study entry. Participants were enrolled in real-world setting in Los Angeles, United States between May 1 and December 1, 2022 and were assigned to either mito-MES 20 mg daily for 14 days (n = 40) or no mito-MES (controls) (n = 40). The primary endpoint was development of SARS-CoV-2 infection based on 4 COVID-19 diagnostic tests [rapid antigen tests (RATs) or PCR] performed during the study period (14 days post exposure).FindingsOut of 40 (23 females; 57.5%) study participants who took Mito-MES, 12 (30%) developed SARS-CoV-2 infection compared to 30 of the 40 controls (75%) (difference -45.0%, 95% confidence intervals (CI): -64.5%, -25.5%). Out of 40 (19 females; 47.5%) study participants in the control group, 30 (75.0%) had at least one positive COVID-19 diagnostic test and 23 (57.5%) were symptomatic. With regards to key secondary outcomes, among symptomatic SARS-CoV-2 infections, the median duration of viral symptoms was lower in the Mito-MES group (median 3.0, 95% CI 2.75, 3.25) compared to the control group (median 5.0, 95% CI 4.0, 7.0). None of the study participants was hospitalized or required oxygen therapy. Mito-MES was well tolerated and no serious side effect was reported in any study participant.InterpretationThis work describes antiviral activity of mito-MES in humans. Mito-MES was well tolerated in our study population and attenuated transmission of SARS-CoV-2 infection. Given established safety of Mito-MES in humans, our results suggest that randomized control clinical trials of Mito-MES as post-exposure prophylaxis against SARS-CoV-2 infection are warranted.FundingThis work was supported in part by National Institutes of Health grant R01AG059501 (TK), National Institutes of Health grant R01AG059502 04S1 (TK), NIH/National Center for Advancing Translational Sciences (NCATS) UCLA CTSI Grant Number UL1TR001881 and California HIV/AIDS Research Program grant OS17-LA-002 (TK).

Coenzyme Q (CoQ) is essential for mitochondrial respiration and required for thermogenic activity in brown adipose tissues (BAT). CoQ deficiency leads to a wide range of pathological manifestations, but mechanistic consequences of CoQ deficiency in specific tissues, such as BAT, remain poorly understood. Here, we show that pharmacological or genetic CoQ deficiency in BAT leads to stress signals causing accumulation of cytosolic mitochondrial RNAs and activation of the eIF2α kinase PKR, resulting in activation of the integrated stress response (ISR) with suppression of UCP1 but induction of FGF21 expression. Strikingly, despite diminished UCP1 levels, BAT CoQ deficiency displays increased whole-body metabolic rates at room temperature and thermoneutrality resulting in decreased weight gain on high-fat diets (HFD). In line with enhanced metabolic rates, BAT and inguinal white adipose tissue (iWAT) interorgan crosstalk caused increased browning of iWAT in BAT-specific CoQ deficient animals. This mitohormesis-like effect depends on the ATF4-FGF21 axis and BAT-secreted FGF21, revealing an unexpected role for CoQ in the modulation of whole-body energy expenditure with wide-ranging implications for primary and secondary CoQ deficiencies.

Purpose of Review: Currently, the preventive and treatment strategies for metabolic disorders are not fully effective, and many limitations remain with these tools. Coenzyme Q10 (CoQ10) is a new promising antioxidant and anti-inflammatory option that can target the mechanisms involved in the progression of metabolic disorders. The purpose of this study was to assess and summarize the implication of CoQ10 in diabetes, hyperlipidemia, and kidney disease. Recent Findings: Emerging evidence indicated that CoQ10 is effective for familial hypercholesterolemia, familial combined hyperlipidemia, hypercholesterolemia-induced atherosclerosis and cardiac damage, hypercholesterolemia-induced Alzheimer's-like disease, Type 2 diabetes mellitus, diabetic nephropathy, and metabolic-associated liver disease. Summary: CoQ10 could be a novel agent for the treatment of metabolic disorders including diabetes and its complications, several forms of hyperlipidemia, and metabolic-associated liver disease. [ABSTRACT FROM AUTHOR]

Oxygen is essential for aerobic life on earth but it is also the origin of harmful reactive oxygen species (ROS). Ubiquinone is par excellence the endogenous cellular antioxidant, but a very hydrophobic one. Because of that, other molecules have been envisaged, such as idebenone (IDE) and mitoquinone (MTQ), molecules having the same redox active benzoquinone moiety but higher solubility. We have used molecular dynamics to determine the location and interaction of these molecules, both in their oxidized and reduced forms, with membrane lipids in a membrane similar to that of the mitochondria. Both IDE and reduced IDE (IDOL) are situated near the membrane interface, whereas both MTQ and reduced MTQ (MTQOL) locate in a position adjacent to the phospholipid hydrocarbon chains. The quinone moieties of both ubiquinone 10 (UQ10) and reduced UQ10 (UQOL10) in contraposition to the same moieties of IDE, IDOL, MTQ and MTQOL, located near the membrane interphase, whereas the isoprenoid chains remained at the middle of the hydrocarbon chains. These molecules do not aggregate and their functional quinone moieties are located in the membrane at different depths but near the hydrophobic phospholipid chains whereby protecting them from ROS harmful effects. [Display omitted] • We simulate molecular dynamics of the location and interaction of idebenone, mitoquinone and ubiquinone 10, in both their oxidized and reduced form, in a membrane. • Idebenone and reduced idebenone are near the membrane interface, whereas mitoquinone and reduced mitoquinone locate adjacent to the phospholipid hydrocarbon chains. • The quinone moieties of idebenone and mitoquinone, in their both forms, locate at the middle of the palisade structure of the membrane, whereas their isoprenoid chains remain near the phospholipid interphase. • The quinone moieties of ubiquinone 10, in its both forms, are near the phospholipid interphase whereas the isoprenoid chains remained at the middle of the hydrocarbon chains. [ABSTRACT FROM AUTHOR]

In all resolved structures of complex I, there exists a tunnel-like Q-chamber for ubiquinone binding and reduction. The entrance to the Q-chamber in ND1 subunit forms a narrow bottleneck, which is rather tight and requires thermal conformational changes for ubiquinone to get in and out of the binding chamber. The substitution of alanine with threonine at the bottleneck (AlaThr MUT), associated with 3460/ND1 mtDNA mutation in human complex I, is implicated in Leber's Hereditary Optic Neuropathy (LHON). Here, we show the AlaThr MUT further narrows the Q-chamber entrance cross-section area by almost 30%, increasing the activation free energy barrier of quinone passage by approximately 5 kJ mol-1. This severely disrupts quinone binding and reduction as quinone passage through the bottleneck is slowed down almost tenfold. Our estimate of the increase in free energy barrier is entirely due to the bottleneck narrowing, leading to a reduction of the transition state entropy between WT and MUT, and thus more difficult quinone passage. Additionally, we investigate details of possible water exchange between the Q-chamber and membrane. We find water exchange is dynamic in WT but may be severely slowed in MUT. We propose that LHON symptoms caused by 3460/ND1 mtDNA mutation are due to slowed quinone binding. This leads to an increased production of reactive oxidative species due to upstream electron backup at the FMN site of complex I, thus resulting in a mt bioenergetic defect.

PurposeTo describe a case of primary coenzyme Q10 deficiency in a child manifesting as early-onset renal failure, retinal dystrophy, and optic atrophy leading to progressive vision loss.MethodsClinical presentation and workup including visual fields, electroretinogram, and optical coherence tomography are presented. Genetic testing was performed.ResultsAn eight-year-old female with nephropathy requiring renal transplantation subsequently developed progressive cone-rod dystrophy and optic atrophy. The patient had negative results on a targeted next-generation sequencing retinal dystrophy panel but whole-exome sequencing revealed two variants in COQ2 (likely biallelic), consistent with a diagnosis of primary coenzyme Q10 deficiency.ConclusionsPrimary coenzyme Q10 deficiency is a rare disorder with variable systemic and ocular findings; there is also genetic heterogeneity. Genetic testing aids in the diagnosis of this condition, and variants in the COQ2 and PDSS1 genes appear to have the strongest association with ocular manifestations. Oral supplementation of coenzyme Q10 may slow progression of disease. This case highlights the utility of whole-exome sequencing in the diagnosis of a rare syndromic form of ocular disease and reports a novel phenotypic association for this condition.

Tissue resident memory CD8+ T (TRM) cells offer rapid and long-term protection at sites of reinfection1. Tumour-infiltrating lymphocytes with characteristics of TRM cells maintain enhanced effector functions, predict responses to immunotherapy and accompany better prognoses2,3. Thus, an improved understanding of the metabolic strategies that enable tissue residency by T cells could inform new approaches to empower immune responses in tissues and solid tumours. Here, to systematically define the basis for the metabolic reprogramming supporting TRM cell differentiation, survival and function, we leveraged in vivo functional genomics, untargeted metabolomics and transcriptomics of virus-specific memory CD8+ T cell populations. We found that memory CD8+ T cells deployed a range of adaptations to tissue residency, including reliance on non-steroidal products of the mevalonate-cholesterol pathway, such as coenzyme Q, driven by increased activity of the transcription factor SREBP2. This metabolic adaptation was most pronounced in the small intestine, where TRM cells interface with dietary cholesterol and maintain a heightened state of activation4, and was shared by functional tumour-infiltrating lymphocytes in diverse tumour types in mice and humans. Enforcing synthesis of coenzyme Q through deletion of Fdft1 or overexpression of PDSS2 promoted mitochondrial respiration, memory T cell formation following viral infection and enhanced antitumour immunity. In sum, through a systematic exploration of TRM cell metabolism, we reveal how these programs can be leveraged to fuel memory CD8+ T cell formation in the context of acute infections and enhance antitumour immunity.

Main conclusion: The contribution of p-coumarate β-oxidation and kaempferol cleavage to the pools of glycosylated, free and cell wall-bound 4-hydroxybenzoate is organ-dependent in Arabidopsis. 4-Hydroxybenzoate (4-HB) is a vital precursor for a number of plant primary and specialized metabolites, as well as for the assembly of the plant cell wall. In Arabidopsis, it is known that 4-HB is derived independently from phenylalanine and tyrosine, and that the metabolism of phenylalanine into 4-HB proceeds via at least two biosynthetic routes: the β-oxidation of p-coumarate and the peroxidative cleavage of kaempferol. The precise contribution of these precursors and branches to 4-HB production, however, is not known. Here, we combined isotopic feeding assays, reverse genetics, and quantification of soluble (i.e., free and glycosylated) and cell wall-bound 4-HB to determine the respective contributions of phenylalanine, tyrosine, β-oxidation of p-coumarate, and peroxidative cleavage of kaempferol to 4-HB biosynthesis in Arabidopsis tissues. Over 90% of 4-HB was found to originate from phenylalanine in both leaves and roots. Soluble 4-HB level varied significantly between organs, while the proportion of cell wall-bound 4-HB was relatively constant. In leaves and flowers, glycosylated and cell wall-bound 4-HB were the most and least abundant forms, respectively. Flowers displayed the highest specific content of 4-HB, while free 4-HB was not detected in roots. Although p-coumarate β-oxidation and kaempferol catabolism were found to both contribute to the supply of 4-HB in all tissues, the proportion of kaempferol-derived 4-HB was higher in roots than in leaves and flowers. Within the β-oxidative branch, p-coumaroyl-CoA ligase 4-CL8 (At5g38120) bore a preponderant role in the production of soluble and cell wall-bound 4-HB in leaves, while p-coumaroyl-CoA ligase At4g19010 appeared to control the biosynthesis of soluble 4-HB in flowers. Furthermore, analysis of a series of Arabidopsis T-DNA mutants corresponding to the three major UDP-glucosyltransferases known to act on 4-HB in vitro (UGT75B1, UGT89B1, and UGT71B1) showed that none of these enzymes appeared in fact to have a significant role in the glycosylation of 4-HB in vivo. [ABSTRACT FROM AUTHOR]

Background. The purpose of this study was to investigate urinary uromodulin (uUMOD) excretion, reactivity of the autonomic nervous system and impaired renal blood circulation in patients with predialysis chronic kidney disease (CKD), the effect of antioxidant therapy on these parameters. Materials and me­thods. Ninety-one patients with CKD stage 1–5 whose ave­rage age was 47.00 ± 12.12 years took part in the ROLUNT (UROmoduLin UbiquinoNe GlutaThione) study. Thirty (32.97 %) men and 61 (67.03 %) women were divided into two groups, which were representative in terms of age and gender composition: group 1 (n = 46) — patients with CKD stage 1–5 who had a Charlson comorbidity index ≤ 2, group 2 (n = 45) — patients with CKD stage 1–5 who had a Charlson comorbidity index ≥ 3. Both groups were divided into subgroups A and B. Subgroups A included patients with impaired vegetative status, subgroups B — those without impaired vegetative status. The first A and second B subgroups took glutathione 100 mg twice a day with food for 3 months, the first B and se­cond A subgroups took ubiquinone 100 mg once a day with food for 3 months. Results. The results of the paired t-test showed that there is a significant difference between the indicators at baseline and at the end of the study. The Pearson correlation results showed that in the group 1 (subgroup A), there is a significant average positive relationship between uUMOD and estimated glomerular filtration rate (r(21) = 0.418, p = 0.047); in the group 1 (subgroup B), there is a significant large positive relationship between uUMOD and Hb indicators (r(21) = 0.513, p = 0.012); a significant very small negative relationship between uUMOD and albumin-creatinine ratio (r(21) = 0.441, p = 0.035); in the group 2 (subgroup A), there is a significant very small negative relationship between uUMOD indicators and Kérdö index (r(20) = 0.427, p = 0.048); in the group 2 (subgroup B), there is a significant very small negative relationship between the uUMOD indicators and Yu.M. Chernov’s questionnaire (r(21) = 0.421, p = 0.045). Conclusions. Antioxidant therapy with glutathione and ubiquinone significantly affects the examination parameters in patients with CKD. Considering the safety and effectiveness of antioxidant therapy, we suggest including it in the treatment protocols for patients with CKD. Further research is re­commended to develop a standard protocol.

Mitochondrial NADH–ubiquinone oxidoreductase (complex I) couples electron transfer from NADH to ubiquinone with proton translocation in its membrane part. Structural studies have identified a long (~ 30 Å), narrow, tunnel‐like cavity within the enzyme, through which ubiquinone may access a deep reaction site. Although various inhibitors are considered to block the ubiquinone reduction by occupying the tunnel's interior, this view is still debatable. We synthesized a phosphatidylcholine‐quinazoline hybrid compound (PC‐Qz1), in which a quinazoline‐type toxophore was attached to the sn‐2 acyl chain to prevent it from entering the tunnel. However, PC‐Qz1 inhibited complex I and suppressed photoaffinity labeling by another quinazoline derivative, [125I]AzQ. This study provides further experimental evidence that is difficult to reconcile with the canonical ubiquinone‐accessing tunnel model. [ABSTRACT FROM AUTHOR]

Researchers have studied the effects of exercise on serum methyl-arginine and vitamin D metabolites; however, the effects of exercise combined with antioxidants are not well documented. Since oxidative stress affects the metabolism of vitamin D and methyl-arginine, we hypothesised that the antioxidant coenzyme Q10 (CoQ10) might modulate exercise-induced changes. A group of twenty-eight healthy men participated in this study and were divided into two groups: an experimental group and a control group. The exercise test was performed until exhaustion, with gradually increasing intensity, before and after the 21-day CoQ10 supplementation. Blood samples were collected before, immediately after, and 3 and 24 h after exercise. CoQ10, vitamin D metabolites, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine, methylarginine, dimethylamine, arginine, citrulline, and ornithine were analysed in serum samples. CoQ10 supplementation caused a 2.76-fold increase in the concentration of serum CoQ10. Conversely, the 25(OH)D3 concentration increased after exercise only in the placebo group. ADMA increased after exercise before supplementation, but a decrease was observed in the CoQ10 supplementation group 24 h after exercise. In conclusion, our data indicate that CoQ10 supplementation modifies the effects of exercise on vitamin D and methyl-arginine metabolism, suggesting its beneficial effects. These findings contribute to the understanding of how antioxidants like CoQ10 can modulate biochemical responses to exercise, potentially offering new insights for enhancing athletic performance and recovery. [ABSTRACT FROM AUTHOR]

Coenzyme Q10 (CoQ10) plays a key role in many aspects of cellular metabolism. For CoQ10 to function normally, continual interconversion between its oxidised (ubiquinone) and reduced (ubiquinol) forms is required. Given the central importance of this ubiquinone–ubiquinol redox cycle, this article reviews what is currently known about this process and the implications for clinical practice. In mitochondria, ubiquinone is reduced to ubiquinol by Complex I or II, Complex III (the Q cycle) re-oxidises ubiquinol to ubiquinone, and extra-mitochondrial oxidoreductase enzymes participate in the ubiquinone–ubiquinol redox cycle. In clinical terms, the outcome of deficiencies in various components associated with the ubiquinone–ubiquinol redox cycle is reviewed, with a particular focus on the potential clinical benefits of CoQ10 and selenium co-supplementation. [ABSTRACT FROM AUTHOR]

Abstract Background Hepatorenal syndrome is a life-threatening medical complication of liver cirrhosis. Hepatic cirrhosis is commonly accompanied by rapid failure of renal functions. Thioacetamide (TAA) is a potent hepatotoxin and a class 2-type carcinogen. Ubiquinone (Coq10) and lactoferrin (LF) are potent antioxidants with antifibrotic and antiinflammatory effects. However, whether Coq10 and LF reduce the hepatorenal injury induced by TAA remains unclear. Here, we investigated the potential protective effect of both/or Coq10 and LF in ameliorating TAA-induced hepatorenal injury and the role of WNT4 gene expression in detecting TAA-induced renal injury in rats. Seventy healthy and mature male Sprague Dawley rats, weighting (200 g ± 20 g) and aging (4–6) weeks were randomly divided into seven groups (n = 10): control, Coq10, LF, TAA, TAA + Coq10, TAA + LF, and TAA + Coq10 + LF. The hepatorenal injury was induced through intraperitoneal (i.p.) injection of TAA (150 mg/kg/twice/weekly) for nine weeks. Coq10 (10 mg/kg/day) and LF (200 mg/kg/day) were orally administered for nine weeks. Results TAA induced marked hepatorenal damage, evident by the significant increase in the alanine aminotransferase (ALT), aspartate transaminase (AST), serum creatinine (SCr) activities, and the blood urea nitrogen (BUN) level. Besides, the significant increases in concentrations of malondialdehyde (MDA) and nitric oxide (NOx) together with significant decreases in the activities of catalase (CAT) and superoxide dismutase (SOD). The histopathological analysis of the TAA group showed obvious fibrosis, steatosis, and inflammation of the hepatic parenchyma as well as severe glomerular and tubular damage of the renal parenchyma. In addition, TAA induced marked ultrastructural alterations and up-regulation in the expression of the WNT4 gene in the kidney. Meanwhile, the biochemical, histopathological, and ultrastructural alterations were significantly decreased with significant down-regulation in the expression of WNT4 in the groups exposed to TAA and treated with Coq10 and LF. Conclusion Our data suggested that Coq10 and LF could have protective effects on TAA hepatorenal damage, through improving the hepatic and renal functions, reduction of oxidative stress, structural and ultrastructural alterations, besides down-regulation in the expression of WNT4.

Background: Hepatorenal syndrome is a life-threatening medical complication of liver cirrhosis. Hepatic cirrhosis is commonly accompanied by rapid failure of renal functions. Thioacetamide (TAA) is a potent hepatotoxin and a class 2-type carcinogen. Ubiquinone (Coq10) and lactoferrin (LF) are potent antioxidants with antifibrotic and antiinflammatory effects. However, whether Coq10 and LF reduce the hepatorenal injury induced by TAA remains unclear. Here, we investigated the potential protective effect of both/or Coq10 and LF in ameliorating TAA-induced hepatorenal injury and the role of WNT4 gene expression in detecting TAA-induced renal injury in rats. Seventy healthy and mature male Sprague Dawley rats, weighting (200 g ± 20 g) and aging (4–6) weeks were randomly divided into seven groups (n = 10): control, Coq10, LF, TAA, TAA + Coq10, TAA + LF, and TAA + Coq10 + LF. The hepatorenal injury was induced through intraperitoneal (i.p.) injection of TAA (150 mg/kg/twice/weekly) for nine weeks. Coq10 (10 mg/kg/day) and LF (200 mg/kg/day) were orally administered for nine weeks. Results: TAA induced marked hepatorenal damage, evident by the significant increase in the alanine aminotransferase (ALT), aspartate transaminase (AST), serum creatinine (SCr) activities, and the blood urea nitrogen (BUN) level. Besides, the significant increases in concentrations of malondialdehyde (MDA) and nitric oxide (NOx) together with significant decreases in the activities of catalase (CAT) and superoxide dismutase (SOD). The histopathological analysis of the TAA group showed obvious fibrosis, steatosis, and inflammation of the hepatic parenchyma as well as severe glomerular and tubular damage of the renal parenchyma. In addition, TAA induced marked ultrastructural alterations and up-regulation in the expression of the WNT4 gene in the kidney. Meanwhile, the biochemical, histopathological, and ultrastructural alterations were significantly decreased with significant down-regulation in the expression of WNT4 in the groups exposed to TAA and treated with Coq10 and LF. Conclusion: Our data suggested that Coq10 and LF could have protective effects on TAA hepatorenal damage, through improving the hepatic and renal functions, reduction of oxidative stress, structural and ultrastructural alterations, besides down-regulation in the expression of WNT4. [ABSTRACT FROM AUTHOR]

To date, there have been no review articles specifically relating to the general efficacy and safety of coenzyme Q10 (CoQ10) supplementation in younger subjects. In this article, we therefore reviewed the efficacy and safety of CoQ10 supplementation in neonates (less than 1 month of age), infants (up to 1 year of age) and children (up to 12 years of age). As there is no rationale for the supplementation of CoQ10 in normal younger subjects (as there is in otherwise healthy older subjects), all of the articles in the medical literature reviewed in the present article therefore refer to the supplementation of CoQ10 in younger subjects with a variety of clinical disorders; these include primary CoQ10 deficiency, acyl CoA dehydrogenase deficiency, Duchenne muscular dystrophy, migraine, Down syndrome, ADHD, idiopathic cardiomyopathy and Friedreich's ataxia. [ABSTRACT FROM AUTHOR]

The coenzyme ubiquinone-10 (CoQ10) is not only an important part of the electron transport chain of the mitochondrial inner membrane but also has complex biological functions beyond mitochondrial respiration. It is a natural nutrient that is not only produced by the body but is also found in foods, such as meat, eggs, fish, and vegetable oils. Because some types of cancer reduce CoQ10 blood levels, the use of CoQ10 supplements is recommended for the treatment of cancer patients. The anti-cancer effects of CoQ10 supplementation have been reported in several cancers, including colon and breast cancer. CoQ10 scavenges free radicals to reduce oxidative stress and minimize tissue damage. CoQ10 protects the body from damage caused by chemotherapy drugs by reducing the production of inflammatory cytokines and other inflammatory factors. Recent studies suggest that CoQ10 may be a supplement to pharmacotherapy for hepatocellular carcinoma. This article examines the effects of CoQ10 in hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]

Background. The purpose of this study was to investigate urinary uromodulin (uUMOD) excretion, reactivity of the autonomic nervous system and impaired renal blood circulation in patients with predialysis chronic kidney disease (CKD), the effect of antioxidant therapy on these parameters. Materials and methods. Ninety-one patients with CKD stage 1–5 whose average age was 47.00 ± 12.12 years took part in the ROLUNT (UROmoduLin UbiquinoNe GlutaThione) study. Thirty (32.97 %) men and 61 (67.03 %) women were divided into two groups, which were representative in terms of age and gender composition: group 1 (n = 46) — patients with CKD stage 1–5 who had a Charlson comorbidity index ≤ 2, group 2 (n = 45) — patients with CKD stage 1–5 who had a Charlson comorbidity index ≥ 3. Both groups were divided into subgroups A and B. Subgroups A included patients with impaired vegetative status, subgroups B — those without impaired vegetative status. The first A and second B subgroups took glutathione 100 mg twice a day with food for 3 months, the first B and second A subgroups took ubiquinone 100 mg once a day with food for 3 months. Results. The results of the paired t-test showed that there is a significant difference between the indicators at baseline and at the end of the study. The Pearson correlation results showed that in the group 1 (subgroup A), there is a significant average positive relationship between uUMOD and estimated glomerular filtration rate (r(21) = 0.418, p = 0.047); in the group 1 (subgroup B), there is a significant large positive relationship between uUMOD and Hb indicators (r(21) = 0.513, p = 0.012); a significant very small negative relationship between uUMOD and albumin-creatinine ratio (r(21) = 0.441, p = 0.035); in the group 2 (subgroup A), there is a significant very small negative relationship between uUMOD indicators and Kérdö index (r(20) = 0.427, p = 0.048); in the group 2 (subgroup B), there is a significant very small negative relationship between the uUMOD indicators and Yu.M. Chernov’s questionnaire (r(21) = 0.421, p = 0.045). Conclusions. Antioxidant therapy with glutathione and ubiquinone significantly affects the examination parameters in patients with CKD. Considering the safety and effectiveness of antioxidant therapy, we suggest including it in the treatment protocols for patients with CKD. Further research is recommended to develop a standard protocol. [ABSTRACT FROM AUTHOR]