Hyphobacterium marinum sp. nov. and Hyphobacterium lacteum sp. nov., isolated from marine sediment.

Two bacterial strains, Y60-23T and HN-65T, were isolated from marine sediment samples collected from Xiaoshi Island, Weihai, and Dongzhai Harbour, Haikou, PR China, respectively. Based on the 16S rRNA gene sequences, strain Y60-23T exhibited 96.0% similarity to its most related type strain Hyphobacterium vulgare KCTC 52487T, while strain HN-65T exhibited 97.3% similarity to its most related type strain Hyphobacterium indicum 2ED5T. The 16S rRNA gene sequence similarity between the two strains was 95.8%. Phylogenetic analysis based on 16S rRNA gene sequences showed that strains Y60-23T and HN-65T belonged to the genus Hyphobacterium. Cells of strains Y60-23T and HN-65T were rod-shaped, Gram-stain-negative, aerobic, non-motile, prosthecate and multiplied by binary fission. The major cellular fatty acids (>10.0%) of strain Y60-23T were C18 : 1 ω7c and C17 : 0, while those of strain HN-65T were iso-C17 : 1 ω9c, iso-C17 : 0 and C18 : 1 ω7c. The major respiratory quinone in both strains was ubiquinone-10 (Q-10) and the major polar lipids were monoglycosyl diglyceride, sulfoquinovosyl diacylglycerol and glucuronopyranosyl diglyceride. The genomic DNA G+C contents of strains Y60-23T and HN-65T were 63.9 and 60.7 mol%, respectively. The average nucleotide identity value between the two strains was 72.1% and the DNA-DNA hybridization value was 18.4%, clearly distinguishing them from each other. According to the results of the phenotypic, chemotaxonomic, phylogenetic and genomic analyses, the two strains represented two novel species within the genus Hyphobacterium, for which the names Hyphobacterium marinum sp. nov. and Hyphobacterium lacteum sp. nov. were proposed with the type strains Y60-23T (=MCCC 1H01433T=KCTC 8172T) and HN-65T (=MCCC 1H01434T=KCTC 8169T), respectively.

Streptomyces castrisilvae sp. nov. and Streptomyces glycanivorans sp. nov., novel soil streptomycetes metabolizing mutan and alternan.

Six bacterial strains, Mut1T, Mut2, Alt1, Alt2, Alt3T, and Alt4, were isolated from soil samples collected in parks in Gothenburg, Sweden, based on their ability to utilize the insoluble polysaccharides α-1,3-glucan (mutan; Mut strains) or the mixed-linkage α-1,3/α-1,6-glucan (alternan; Alt strains). Analysis of 16S rRNA gene sequences identified all strains as members of the genus Streptomyces. The genomes of the strains were sequenced and subsequent phylogenetic analyses identified Mut2 as a strain of Streptomyces laculatispora and Alt1, Alt2 and Alt4 as strains of Streptomyces poriferorum, while Mut1T and Alt3T were most closely related to the type strains Streptomyces drozdowiczii NBRC 101007T and Streptomyces atroolivaceus NRRL ISP-5137T, respectively. Comprehensive genomic and biochemical characterizations were conducted, highlighting typical features of Streptomyces, such as large genomes (8.0-9.6 Mb) with high G+C content (70.5-72.0%). All six strains also encode a wide repertoire of putative carbohydrate-active enzymes, indicating a capability to utilize various complex polysaccharides as carbon sources such as starch, mutan, and cellulose, which was confirmed experimentally. Based on phylogenetic and phenotypic characterization, our study suggests that strains Mut1T and Alt3T represent novel species in the genus Streptomyces for which the names Streptomyces castrisilvae sp. nov. and Streptomyces glycanivorans sp. nov. are proposed, with strains Mut1T (=DSM 117248T=CCUG 77596T) and Alt3T (=DSM 117252T=CCUG 77600T) representing the respective type strains.

Therapeutic roles of coenzyme Q10 in peripheral nerve injury-induced neurosensory disturbances: Mechanistic insights from injury to recovery.

Peripheral nerve injuries (PNIs) are prevalent conditions mainly resulting from systemic causes, including autoimmune diseases and diabetes mellitus, or local causes, for example, chemical injury and perioperative nerve injury, which can cause a varying level of neurosensory disturbances (NSDs). Coenzyme Q10 (CoQ10) is an essential regulator of mitochondrial respiration and oxidative metabolism. Here, we review the pathophysiology of NSDs caused by PNIs, the current understanding of CoQ10's bioactivities, and its potential therapeutic roles in nerve regeneration, based on evidence from experimental and clinical studies involving CoQ10 supplementation. In summary, CoQ10 supplementation shows promise as a neuroprotective agent, potentially enhancing treatment efficacy for NSDs by reducing oxidative stress and inflammation. Future studies should focus on well-designed clinical trials with large sample sizes, using CoQ10 formulations with proven bioavailability and varying treatment duration, to further elucidate its neuroprotective effects and to optimize nerve regeneration in PNIs-induced NSDs.

Paracraurococcus lichenis sp. nov., isolated from lichen in Thailand.

A novel bacterium, designated as strain LOR1-02T and isolated from a lichen sample collected from Kham Riang Subdistrict, Kantharawichai District, Maha Sarakham Province, Thailand, underwent thorough investigation utilizing a polyphasic taxonomic approach. Strain LOR1-02T demonstrated growth within a temperature range of 20-42 °C (optimal at 30 °C), pH range of 5.0-7.5 (optimal at pH 7.0), and tolerance to 4.0% (w/v) NaCl. Phylogenetic analysis revealed its close relation to Paracraurococcus ruber JCM 9931T, with a 16S rRNA gene sequence similarity of 97.16%, placing it within the genus Paracraurococcus. The approximate genome size of strain LOR1-02T was determined to be 8.6 Mb, with a G + C content of 70.9 mol%. Additionally, ANIb, ANIm, and AAI values between the whole genomes of strain LOR1-02T and type strains were calculated as 82.6-83.4%, 86.1-86.8%, and 81.4-82.2%, respectively, while the dDDH value was determined to be 26.3-28.5% (C.I. 24.0-31.0%). The predominant fatty acids detected were C18:1ω7c and/or C18:1ω6c, C16:0, and C18:12OH. The major ubiquinone identified was Q-10, and the polar lipids included phosphatidylglycerol, phosphatidylethanolamine, phosphatidylcholine, diphosphatidylglycerol, along with unidentified phosphoaminolipid, lipids, and an amino lipid. Based on comprehensive phenotypic, chemotaxonomic, and genotypic characterization, it is concluded that strain LOR1-02T represents a novel species within the genus Paracraurococcus, for which the name Paracraurococcus lichenis sp. nov. is proposed. The type strain designation is LOR1-02T (= JCM 33121T = NBRC 112776T = TISTR 2503T).

NQO1 promotes osteogenesis and suppresses angiogenesis in DPSCs via MAPK pathway modulation.

BACKGROUND: Influence on stem cells' angiogenesis and osteogenesis of NAD(P)H Quinone Dehydrogenase 1(NQO1) has been established, but its impact on dental pulp stem cells (DPSCs) is unexplored. An important strategy for the treatment of arteriosclerosis is to inhibit calcium deposition and to promote vascular repair and angiogenesis. This study investigated the function and mechanism of NQO1 on angiogenesis and osteogenesis of DPSCs, so as to provide a new ideal for the treatment of arteriosclerosis. METHODS: Co-culture of human DPSCs and human umbilical vein endothelial cells (HUVECs) was used to detect the angiogenesis ability. Alkaline phosphatase (ALP) activity, alizarin red staining (ARS), and transplantation of HA/tricalcium phosphate with DPSCs were used to detect osteogenesis. RESULTS: NQO1 suppressed in vitro tubule formation, migration, chemotaxis, and in vivo angiogenesis, as evidenced by reduced CD31 expression. It also enhanced ALP activity, ARS, DSPP expression and osteogenesis and boosted mitochondrial function in DPSCs. CoQ10, an electron transport chain activator, counteracted the effects of NQO1 knockdown on these processes. Additionally, NQO1 downregulated MAPK signaling, which was reversed by CoQ10 supplementation in DPSCs-NQO1sh. CONCLUSIONS: NQO1 inhibited angiogenesis and promoted the osteogenesis of DPSCs by suppressing MAPK signaling pathways and enhancing mitochondrial respiration.

Cancer cell stiffening via CoQ10 and UBIAD1 regulates ECM signaling and ferroptosis in breast cancer.

CoQ10 (Coenzyme Q10) is an essential fat-soluble metabolite that plays a key role in cellular metabolism. A less-known function of CoQ10 is whether it may act as a plasma membrane-stabilizing agent and whether this property can affect cancer development and progression. Here, we show that CoQ10 and its biosynthetic enzyme UBIAD1 play a critical role in plasmamembrane mechanical properties that are of interest for breast cancer (BC) progression and treatment. CoQ10 and UBIAD1 increase membrane fluidity leading to increased cell stiffness in BC. Furthermore, CoQ10 and UBIAD1 states impair ECM (extracellular matrix)-mediated oncogenic signaling and reduce ferroptosis resistance in BC settings. Analyses on human patients and mouse models reveal that UBIAD1 loss is associated with BC development and progression and UBIAD1 expression in BC limits CTCs (circulating tumor cells) survival and lung metastasis formation. Overall, this study reveals that CoQ10 and UBIAD1 can be further investigated to develop therapeutic interventions to treat BC patients with poor prognosis.

Effects of alfa lipoic acid and coenzyme Q10 treatment on AFB1-induced oxidative, inflammatory, and DNA damages in rats.

Food contamination with Aflatoxin B1 (AFB1) is a worldwide concern that adversely affects animal and human health. The study aimed to evaluate the protective effect of alpha lipoic acid (ALA) and/or co-enzyme Q10 (CQ10) against the harmful effects of AFB1 on the liver and kidneys. Fifty-six mature male Wistar Albino rats (180-200 g) were divided into seven groups, each with eight rats: (1) saline was given as a control, (2) ALA (100 mg/kg bw/day) was given by stomach gavage for fifteen days, and (3) CQ10 (10 mg/kg bw/day) was given by stomach gavage for fifteen days. Group (4) orally given AFB1 (2.5 mg/kg bw) on days 12th and 14th, (5) received AFB1 and ALA, (6) received AFB1 and CQ10, and (7) received AFB1, ALA, and CQ10, as previously described in the ALA, CQ10, and AFB1 groups. After the exposure to AFB1, a significant increase in liver markers (AST, ALT, ALP, and LDH) and renal function tests (BUN and creatinine) was observed compared with the control. ALA and/or CQ10 significantly reduced enzymes of liver and renal functions, as compared with AFB1. AFB1 exposure threw off the balance between oxidants and antioxidants. Still, ALA and/or CQ10 made oxidative stress (MDA, NO, and 8-OHdG) much lower and antioxidant activities (GSH, GSH-Px, SOD, and CAT) much higher. When we used the two together, the activities matched the control levels. Interestingly, this study shows that ALA and CQ10 significantly lowered IL-1ß, IL-6, and TNF-α levels compared to the control values when used together after AFB1 exposure caused robust inflammation. Some CQ10 treatment parameters significantly outperformed those of ALA. ALA and CQ10 together worked better than either one alone to protect against AFB1-induced toxicity in the hepatic and renal parenchyma in terms of reducing inflammation, preventing DNA damage, and fighting free radicals.

Identification of genes supporting cold resistance of mammalian cells: lessons from a hibernator.

Susceptibility of human cells to cold stress restricts the use of therapeutic hypothermia and long-term preservation of organs at low temperatures. In contrast, cells of mammalian hibernators possess remarkable cold resistance, but little is known about the molecular mechanisms underlying this phenomenon. In this study, we conducted a gain-of-function screening of genes that confer cold resistance to cold-vulnerable human cells using a cDNA library constructed from the Syrian hamster, a mammalian hibernator, and identified Gpx4 as a potent suppressor of cold-induced cell death. Additionally, genetic deletion of or pharmacological inhibition of Gpx4 revealed that Gpx4 is necessary for suppressing lipid peroxidation specifically under cold in hamster cell lines. Genetic disruption of other ferroptosis-suppressing pathways, namely biopterin synthesis and mitochondrial or plasma membrane CoQ reduction pathways, also accelerated cold-induced cell death under Gpx4 dysfunction. Collectively, ferroptosis-suppressing pathways protect the cells of a mammalian hibernator from cold-induced cell death and the augmentation of these pathways renders cold resistance to cells of non-hibernators, including humans.

Dongia sedimenti sp. nov., isolated from river sediment.

A Gram-stain-negative, non-spore-forming and strictly aerobic bacterial strain, designated R-7T, was isolated from river sediment in Wuxi, Jiangsu, PR China. Cells (1.6-3.8 µm long and 0.6-0.8 µm wide) were slightly curved to straight rods and motile by means of a polar flagellum. The strain grew optimally on Reasoner's 2A medium at 30 °C, pH 7.0 and with 1.0% (w/v) NaCl. Strain R-7T exhibited closest 16S rRNA gene sequence similarities to Dongia mobilis CGMCC 1.7660T (95.4%), D. rigui 04SU4-PT (94.6%) and D. soli D78T (93.8%). The phylogenetic trees based on genomic and 16S rRNA gene sequences showed that strain R-7T was clustered in the genus Dongia. The obtained average nucleotide identity and digital DNA-DNA hybridization values between R-7T and the three type strains of the genus Dongia were 73.4, 72.8 and 72.4% and 19.5, 19.0 and 18.7%, respectively. The major respiratory quinone was Q-10. The major polar lipids were phosphatidylethanolamine, phosphatidylglycerol, three unidentified aminolipids, two unidentified aminophospholipids and nine unidentified polar lipids. The major cellular fatty acids (>5% of the total) were cyclo-C19 : 0 ω8c, C16 : 0 and C16 : 0 2-OH. The DNA G+C content was 65.5 mol%. On the basis of the evidence presented in this study, strain R-7T represents a novel species of the genus Dongia, for which the name Dongia sedimenti sp. nov. is proposed, with strain R-7T (=KCTC 8082T=MCCC 1K08805T) as the type strain.

Microbulbifer spongiae sp. nov., isolated from marine sponge Diacarnus erythraeanus.

A novel bacterium, designated as MI-GT, was isolated from marine sponge Diacarnus erythraeanus. Cells of strain MI-GT are Gram-stain-negative, aerobic, and rod or coccoid-ovoid in shape. MI-GT is able to grow at 10-40 °C (optimum, 28 °C), with 1.0-8.0% (w/v) NaCl (optimum, 4.0%), and at pH 5.5-9.0 (optimum, pH 8.0). The 16S rRNA gene sequence of strain MI-GT shows 98.35, 97.32 and 97.25% similarity to those of Microbulbifer variabilis Ni-2088T, Microbulbifer maritimus TF-17T and Microbulbifer echini AM134T, respectively. Phylogenetic analysis also exhibits that strain MI-GT falls within a clade comprising members of the genus Microbulbifer (class Gammaproteobacteria). The genome size of strain MI-GT is 4478124 bp with a G+C content of 54.51 mol%. The average nucleotide identity (ANI) and digital DNA-DNA hybridization (dDDH) values between strain MI-GT and other type strains are 71.61-76.44% (ANIb), 83.27-84.36% (ANIm) and 13.4-18.7% (dDDH), respectively. These values are significantly lower than the recommended threshold values for bacterial species delineation. Percentage of conserved proteins and average amino acid identity values among the genomes of strain MI-GT and other closely related species are 52.04-59.13% and 67.47-77.21%, respectively. The major cellular fatty acids of MI-GT are composed of summed feature 8 (C18 : 1 ω7c or C18 : 1 ω6c), iso-C11 : 0 3-OH, iso-C15 : 0, C16 : 0, and summed feature 9 (C17 : 1 iso ω9c or C16 : 0 10-methyl). The polar lipids of MI-GT mainly consist of phosphatidylethanolamine, phosphatidylglycerol, aminolipid, and two glycolipids. The major respiratory quinone is Q-8. Based on differential phenotypic and phylogenetic data, strain MI-GT is considered to represent a novel species of genus Microbulbifer, for which the name Microbulbifer spongiae sp. nov. is proposed. The type strain is MI-GT (=MCCC 1K07826T=KCTC 8081T).

The Scavenging Activity of Coenzyme Q10 Plus a Nutritional Complex on Human Retinal Pigment Epithelial Cells.

Age-related macular degeneration (AMD) and diabetic retinopathy (DR) are common retinal diseases responsible for most blindness in working-age and elderly populations. Oxidative stress and mitochondrial dysfunction play roles in these pathogenesis, and new therapies counteracting these contributors could be of great interest. Some molecules, like coenzyme Q10 (CoQ10), are considered beneficial to maintain mitochondrial homeostasis and contribute to the prevention of cellular apoptosis. We investigated the impact of adding CoQ10 (Q) to a nutritional antioxidant complex (Nutrof Total®; N) on the mitochondrial status and apoptosis in an in vitro hydrogen peroxide (H2O2)-induced oxidative stress model in human retinal pigment epithelium (RPE) cells. H2O2 significantly increased 8-OHdG levels (p < 0.05), caspase-3 (p < 0.0001) and TUNEL intensity (p < 0.01), and RANTES (p < 0.05), caspase-1 (p < 0.05), superoxide (p < 0.05), and DRP-1 (p < 0.05) levels, and also decreased IL1ß, SOD2, and CAT gene expression (p < 0.05) vs. control. Remarkably, Q showed a significant recovery in IL1ß gene expression, TUNEL, TNFα, caspase-1, and JC-1 (p < 0.05) vs. H2O2, and NQ showed a synergist effect in caspase-3 (p < 0.01), TUNEL (p < 0.0001), mtDNA, and DRP-1 (p < 0.05). Our results showed that CoQ10 supplementation is effective in restoring/preventing apoptosis and mitochondrial stress-related damage, suggesting that it could be a valid strategy in degenerative processes such as AMD or DR.

Gilvimarinus gilvus sp. nov. and Gilvimarinus algae sp. nov., isolated from kelp seedlings.

Two novel rod-shaped, strictly aerobic, non-motile and Gram-stain-negative bacterial strains, designated SDUM040013T and SDUM040014T, were isolated from kelp seedlings in Weihai, PR China. Cells of strain SDUM040013T were 0.3-0.4 µm wide and 0.8-1.8 µm long, catalase-positive and oxidase-positive. Growth of SDUM040013T was observed at 0-37 °C (optimum, 28-30 °C) and pH 5.5-9 (optimum, pH 8.0) and in the presence of 1-8 % (w/v) NaCl (optimum, 2 %). The DNA G+C content of strain SDUM040013T was 50.5 %. Strain SDUM040013T showed the highest 16S rRNA gene sequence similarity (97.1 %) to Gilvimarinus chinensis. Cells of strain SDUM040014T were 0.4-0.5 µm wide and 1.0-1.4 µm long, catalase-positive and oxidase-positive. Growth of SDUM040014T was observed at 4-40 °C (optimum, 28-30 °C) and pH 5.5-9 (optimum, pH 8.5) and in the presence of 0-8 % (w/v) NaCl (optimum, 2 %). The DNA G+C content of strain SDUM040014T was 56.5 %. Strain SDUM040014T showed the highest 16S rRNA gene sequence similarity (96.2%) to Gilvimarinus polysaccharolyticus. The isoprenoid quinone of both strains was Q-8 and the predominant fatty acids were summed feature 3 (C16 : 1 ω7c and/or C16 : 1 ω6c), summed feature 8 (C18 : 1 ω7c) and C16 : 0. Diphosphatidylglycerol, phosphatidylglycerol and phosphatidylethanolamine were the major polar lipids. Given these phenotypic and chemotaxonomic properties, as well as phylogenetic data, strains SDUM040013T and SDUM040014T were considered to represent two novel species of the genus Gilvimarinus, for which the names Gilvimarinus gilvus sp. nov. and Gilvimarinus algae sp. nov. are proposed. The type strains are SDUM040013T (=KCTC 8123T=MCCC 1H01413T) and SDUM040014T (=KCTC 8124T=MCCC 1H01414T), respectively.

Effect of Mitoquinone on sperm quality of cryopreserved stallion semen.

This study aimed to investigate the effect of mitochondria-targeted antioxidants (Mitoquinone, MitoQ) on the quality of frozen-thawed stallion semen. Semen samples collected from three fertile stallions aged 10 - 13 years, were filtered, centrifuged in a skimmed milk-based extender, and diluted to a final concentration of 50 × 106 sperm/mL in freezing medium. Diluted semen was divided into five experimental groups supplemented with MitoQ at concentrations of 0 (control), 25, 50, 100, and 200 nM and then subjected to freezing after cooling and equilibration. After thawing, semen was evaluated for motility and kinetics at different time points. Sperm viability, plasma membrane, acrosome, DNA integrity, mitochondrial membrane potential, apoptosis, and intracellular reactive oxygen species (ROS) concentrations were evaluated. The results revealed that MitoQ at concentrations of 25, 50, and 100 nM improved (P< 0.01) the total sperm motility after 30 minutes of incubation. In addition, 25 nM MitoQ improved the sperm amplitude of lateral head displacement values (P< 0.01) after 30 minutes of incubation. Conversely, negative effects on sperm motility, kinetics, and viability were observed with the highest tested concentration of MitoQ (200 nM). The various concentrations of MitoQ did not affect the plasma membrane, acrosome, and DNA integrity, or the mitochondrial membrane potential and intracellular ROS concentrations. In conclusion, supplementation of MitoQ during cryopreservation, had a mild positive effect on sperm motility and kinetics especially at a concentration of 25 nM, while the highest concentration (200nM) has a detrimental effect on motility and viability parameters of frozen-thawed stallion sperm.

The Role of Antioxidants in the Therapy of Cardiovascular Diseases-A Literature Review.

Antioxidants are endogenous and exogenous substances with the ability to inhibit oxidation processes by interacting with reactive oxygen species (ROS). ROS, in turn, are small, highly reactive substances capable of oxidizing a wide range of molecules in the human body, including nucleic acids, proteins, lipids, carbohydrates, and even small inorganic compounds. The overproduction of ROS leads to oxidative stress, which constitutes a significant factor contributing to the development of disease, not only markedly diminishing the quality of life but also representing the most common cause of death in developed countries, namely, cardiovascular disease (CVD). The aim of this review is to demonstrate the effect of selected antioxidants, such as coenzyme Q10 (CoQ10), flavonoids, carotenoids, and resveratrol, as well as to introduce new antioxidant therapies utilizing miRNA and nanoparticles, in reducing the incidence and progression of CVD. In addition, new antioxidant therapies in the context of the aforementioned diseases will be considered. This review emphasizes the pleiotropic effects and benefits stemming from the presence of the mentioned substances in the organism, leading to an overall reduction in cardiovascular risk, including coronary heart disease, dyslipidaemia, hypertension, atherosclerosis, and myocardial hypertrophy.

Description of Pseudomarimonas salicorniae sp. nov., Isolated from Salicornia herbacea L. in the Tidal Flat of the Yellow Sea.

A Gram-stain-negative, strictly aerobic, non-motile, rod-shaped, designated strain CAU 1642 T, was isolated from a Salicornia herbacea collected from a tidal flat in the Yellow Sea. Strain CAU 1642 T grew optimally at pH 8.0 and 30 °C. The highest 16S rRNA gene sequence similarity was 97.25%, with Pseudomarinomonas arenosa CAU 1598 T, and phylogenetic analysis indicated that strain CAU 1642 T belongs to the genus Pseudomarinomonas. The major cellular fatty acids were iso-C15:0, iso-C16:0, and summed feature 9 (iso-C17:1ω9c and/or 10-methyl C16:0). Ubiquinone-8 was the major respiratory quinone. The draft genome of strain CAU 1642 T was 4.5 Mb, with 68.7 mol% of G + C content. The phylogenetic, phenotypic, and chemotaxonomic analysis data reveal strain CAU 1642 T to be of a novel genus in the family Lysobacteraceae, with the proposed name Pseudomarinomonas salicorniae sp. nov. with type strain CAU 1642 T (= KCTC 92084 T = MCCC 1K07085T).

Oxygen-Binding Sites of Enriched Gold Nanoclusters for Capturing Mitochondrial Reverse Electrons.

Reverse electron transfer (RET), an abnormal backward flow of electrons from complexes III/IV to II/I of mitochondria, causes the overproduction of a reduced-type CoQ to boost downstream production of mitochondrial superoxide anions that leads to ischemia-reperfusion injury (IRI) to organs. Herein, we studied low-coordinated gold nanoclusters (AuNCs) with abundant oxygen-binding sites to form an electron-demanding trapper that allowed rapid capture of electrons to compensate for the CoQ/CoQH2 imbalance during RET. The AuNCs were composed of only eight gold atoms that formed a Cs-symmetrical configuration with all gold atoms exposed on the edge site. The geometry and atomic configuration enhance oxygen intercalation to attain a d-band electron deficiency in frontier orbitals, forming an unusually high oxidation state for rapid mitochondrial reverse electron capture under a transient imbalance of CoQ/CoQH2 redox cycles. Using hepatic IRI cells/animals, we corroborated that the CoQ-like AuNCs prevent inflammation and liver damage from IRI via recovery of the mitochondrial function.

MitoQ relieves mitochondrial dysfunction in UVA and cigarette smoke-induced Fuchs endothelial corneal dystrophy.

Fuchs endothelial corneal dystrophy (FECD), a degenerative corneal condition, is characterized by the droplet-like accumulation of the extracellular matrix, known as guttae and progressive loss of corneal endothelial cells ultimately leading to visual distortion and glare. FECD can be influenced by environmental stressors and genetic conditions. However, the role of mitochondrial dysfunction for advancing FECD pathogenesis is not yet fully studied. Therefore, in the present study we sought to determine whether a combination of environmental stressors (ultraviolet-A (UVA) light and cigarette smoke condensate (CSC)) can induce mitochondrial dysfunction leading to FECD. We also investigated if MitoQ, a water-soluble antioxidant, can target mitochondrial dysfunction induced by UVA and CSC in human corneal endothelial cells mitigating FECD pathogenesis. We modeled the FECD by increasing exogenous oxidative stress with CSC (0.2%), UVA (25J/cm2) and a combination of UVA + CSC and performed a temporal analysis of their cellular and mitochondrial effects on HCEnC-21T immortalized cells in vitro before and after MitoQ (0.05 µM) treatment. Interestingly, we observed that a combination of UVA + CSC exposure increased mitochondrial ROS and fragmentation leading to a lower mitochondrial membrane potential and increased levels of cytochrome c release leading to apoptosis and cell death. MitoQ intervention successfully mitigated these effects and restored cell viability. The UVA + CSC model could be used to study stress induced mitochondrial dysfunction. Additionally, MitoQ can serve as a viable antioxidant in attenuating mitochondrial dysfunction, underscoring its potential as a molecular-focused treatment approach to combat FECD pathogenesis.