Mitochondrial genome variability and metabolic alterations reveal new biomarkers of resistance in testicular germ cell tumors.

Mutations in the mitochondrial (mt) genome contribute to metabolic dysfunction and their accumulation relates to disease progression and resistance development in cancer cells. This study explores the mutational status of the mt genome of cisplatin-resistant -sensitive testicular germ cell tumor (TGCT) cells and explores its association with their respiration parameters, expression of respiratory genes, and preferences for metabolic pathways to reveal new markers of therapy resistance in TGCTs. Using Illumina sequencing with Twist Enrichment Panel, the mutations of mt genomes of sensitive 2102EP, H12.

Platelet Mitochondrial Function and Endogenous Coenzyme Q Levels Could Be Used as Markers of Mitochondrial Health in Infertile Men: A Pilot Study.

Fertility disorders are a worldwide problem affecting 8-12% of the population, with the male factor substantially contributing to about 40-50% of all infertility cases. Mitochondria, crucial organelles for cellular viability, play a pivotal role in the processes of spermatogenesis and significantly affect sperm quality and their fertilizing ability. Mitochondrial oxidative phosphorylation (OXPHOS) dysfunction, reduced energy supply for sperm, reduced endogenous coenzyme Q (CoQ) levels, and oxidative stress are among the main factors that contribute to male infertility.

Perspective targeted diagnosis and therapy of mitochondrial bioenergetics across different diagnoses.

Important metabolic variables that lead to the development of many diseases, including "mitochondrial diseases," include increased oxidative stress and mitochondrial malfunction. Given that the clinical picture and metabolic alterations in individuals suspected of having mitochondrial illnesses lack distinct characteristics, the development of sensitive and specific diagnostic techniques to detect alterations in mitochondrial bioenergetics is imperative. High-resolution respirometry (HRR), is a minimally invasive technique that enables the analysis of mitochondrial function in platelets taken from peripheral blood.

Astaxanthin, Compared to Other Carotenoids, Increases the Efficacy of Methotrexate in Rat Adjuvant Arthritis.

This in vivo study performed in rat adjuvant arthritis aims to advance the understanding of astaxanthin's therapeutic properties for the possible treatment of rheumatoid arthritis (RA) in monotherapy and along with the standard RA treatment, methotrexate (MTX), in combination therapy. The main goal was to elucidate astaxanthin's full therapeutic potential, evaluate its dose dependency, and compare its effects in monotherapy with other carotenoids such as β-carotene and β-cryptoxanthin (KXAN). Moreover, potential differences in therapeutic activity caused by using different sources of astaxanthin, synthetic (ASYN) versus isolated from (ASTAP), were evaluated using one-way ANOVA (Tukey-Kramer post hoc test).

The Effect of Adjuvant Therapy with Molecular Hydrogen on Endogenous Coenzyme Q Levels and Platelet Mitochondrial Bioenergetics in Patients with Non-Alcoholic Fatty Liver Disease.

Molecular hydrogen (H) has been recognized as a novel medical gas with antioxidant and anti-inflammatory effects. Non-alcoholic fatty liver disease (NAFLD) is a liver pathology with increased fat accumulation in liver tissue caused by factors other than alcohol consumption. Platelet mitochondrial function is considered to reflect systemic mitochondrial health.

Effect of Vaccination on Platelet Mitochondrial Bioenergy Function of Patients with Post-Acute COVID-19.

Background: Mitochondrial dysfunction and redox cellular imbalance indicate crucial function in COVID-19 pathogenesis. Since 11 March 2020, a global pandemic, health crisis and economic disruption has been caused by SARS-CoV-2 virus. Vaccination is considered one of the most effective strategies for preventing viral infection.

Benefit of mountain spa rehabilitation and ubiquinol treatment in patients with post-COVID-19 syndrome.

Background: SARS-CoV-2 infection is associated with inflammation, decrease in antioxidants and oxidative damage. We aimed to investigate whether ubiquinol, reduced form of coenzyme Q10 (CoQ10), with mountain spa rehabilitation (MR) will contribute to recovering of patients with post-COVID-19 syndrome.

Methods: The study included 36 patients on MR lasting 16-18 days.

Reduced platelet mitochondrial respiration and oxidative phosphorylation in patients with post COVID-19 syndrome are regenerated after spa rehabilitation and targeted ubiquinol therapy.

European Association of Spa Rehabilitation recommend spa rehabilitation for patients with post COVID-19 syndrome (post C-19). We studied effects of special mountain spa rehabilitation program and its combination with ubiquinol (reduced form of coenzyme Q-CoQ) supplementation on pulmonary function, clinical symptoms, endogenous CoQ levels, and platelet mitochondrial bioenergetics of patients with post C-19. 36 patients with post C-19 enrolled for rehabilitation in mountain spa resort and 15 healthy volunteers representing the control group were included in this study.

Biological Effects of Hydrogen Water on Subjects with NAFLD: A Randomized, Placebo-Controlled Trial.

Non-alcoholic fatty liver disease (NAFLD) is a liver pathology affecting around 25% of the population worldwide. Excess oxidative stress, inflammation and aberrant cellular signaling can lead to this hepatic dysfunction and eventual carcinoma. Molecular hydrogen has been recognized for its selective antioxidant properties and ability to attenuate inflammation and regulate cellular function.

Mountain spa rehabilitation improved health of patients with post-COVID-19 syndrome: pilot study.

European Association of Spa Rehabilitation (ESPA) recommends spa rehabilitation for patients with post-COVID-19 syndrome. We tested the hypothesis that a high-altitude environment with clean air and targeted spa rehabilitation (MR - mountain spa rehabilitation) can contribute to the improving platelet mitochondrial bioenergetics, to accelerating patient health and to the reducing socioeconomic problems. Fifteen healthy volunteers and fourteen patients with post-COVID-19 syndrome were included in the study.

D-galactose-induced aging in rats - The effect of metformin on bioenergetics of brain, skeletal muscle and liver.

Chronic D-galactose administration induces accelerated aging in rodents. The aim of the study was to find by in vivoP MRS suitable markers of early stages of brain degeneration on this metabolic model in rats. Additionally, we studied the therapeutic effect of antidiabetic drug metformin.

Platelet Mitochondrial Bioenergetics Reprogramming in Patients with Urothelial Carcinoma.

Mitochondrial bioenergetics reprogramming is an essential response of cells to stress. Platelets, an accessible source of mitochondria, have a crucial role in cancer development; however, the platelet mitochondrial function has not been studied in urothelial carcinoma (UC) patients. A total of 15 patients with UC and 15 healthy controls were included in the study.

Platelet mitochondrial function and endogenous coenzyme Q10 levels are reduced in patients after COVID-19.

Background: After an acute treatment for coronavirus disease (COVID-19), some symptoms may persist for several weeks, for example: fatigue, headaches, muscle and joint pain, cough, loss of taste and smell, sleep and memory disturbances, depression. Many viruses manipulate mitochondrial function, but the exact mechanisms of SARS-CoV-2 virus effect remain unclear. We tested the hypothesis that SARS-CoV-2 virus may affect mitochondrial energy production and endogenous biosynthesis of coenzyme Q10 (CoQ10).

Platelet mitochondrial respiration and coenzyme Q10 could be used as new diagnostic strategy for mitochondrial dysfunction in rheumatoid diseases.

Introduction: Rheumatoid arthritis (RA) is a chronic inflammatory autoimunne disorder affecting both small and large synovial joints, leading to their destruction. Platelet biomarkers are involved in inflammation in RA patients. Increased circulating platelet counts in RA patients may contribute to platelet hyperactivity and thrombosis.

Is mitochondrial bioenergetics and coenzyme Q10 the target of a virus causing COVID-19?

COVID-19 ‒ a coronavirus disease, affected almost all countries in the world. It is a new virus disease, nobody has prior immunity to it, human population is prone to infections. In March 11 2020, WHO declared the pandemic status.

The importance of coenzyme Q10 and its ratio to cholesterol in the progress of chronic kidney diseases linked to non- -communicable diseases.

Objectives: The mortality of patients with chronic kidney diseases (CKD) increases with the decrease in glomerular filtration rate (eGFR). In the progress of CKD that is closely linked to non-communicable diseases (NCDs), the role of coenzyme Q10 (CoQ10) is not fully evaluated. We aimed to evaluate the importance of CoQ10, CoQ10/cholesterol ratio, and oxidative stress in the progress of CKD.

Platelet Mitochondrial Respiration, Endogenous Coenzyme Q and Oxidative Stress in Patients with Chronic Kidney Disease.

Unlabelled: Chronic kidney disease (CKD) is characterized by a progressive loss of renal function and a decrease of glomerular filtration rate. Reduced mitochondrial function, coenzyme Q (CoQ), and increased oxidative stress in patients with CKD contribute to the disease progression. We tested whether CoQ levels, oxidative stress and platelet mitochondrial bioenergetic function differ between groups of CKD patients.

A new insight into the molecular hydrogen effect on coenzyme Q and mitochondrial function of rats.

Mitochondria are the major source of cellular energy metabolism. In the cardiac cells, mitochondria produce by way of the oxidative phosphorylation more than 90% of the energy supply in the form of ATP, which is utilized in many ATP-dependent processes, like cycling of the contractile proteins or maintaining ion gradients. Reactive oxygen species (ROS) are by-products of cellular metabolism and their levels are controlled by intracellular antioxidant systems.

Platelet mitochondrial bioenergetic analysis in patients with nephropathies and non-communicable diseases: a new method.

Objectives: To test the hypothesis if mitochondrial bioenergetic function analyzed in circulating platelets may represent peripheral signature of mitochondrial dysfunction in nephropathy associated to non-communicable human diseases such as cardiovascular diseases, diabetes and with statins treatment.

Methods: High-resolution respirometry was used for analysis of mitochondrial bioenergetics in human platelets isolated from peripheral blood. This method is less-invasively compared to skeletal muscle biopsy.

Platelets mitochondrial function depends on CoQ10 concentration in winter, not in spring season.

Seasonal variations in temperature may influence the physiological and pathological metabolic pathways, concentrations of antioxidants, degree of oxidative stress and mitochondrial function. The aim of this study was to evaluate platelet mitochondrial function in human subjects during seasonal variations in temperature. Two groups of healthy young subjects were enroled in the study.

Association of mitochondrial iron deficiency and dysfunction with idiopathic restless legs syndrome.

Background: Restless legs syndrome is a sensorimotor neurological disorder of the limbs that impairs quality of life and disturbs sleep. However, there has been progress in understanding the disease involving the dopaminergic system as well as iron metabolism. The exact pathophysiological mechanisms of restless legs syndrome remain elusive.

Exercise Performance, Muscle Oxygen Extraction and Blood Cell Mitochondrial Respiration after Repeated-Sprint and Sprint Interval Training in Hypoxia: A Pilot Study.

This study aimed to investigate and compare the effects of repeated-sprint (RSH) and sprint interval training in hypoxia (SIH) on sea level running and cycling performance, and to elucidate potential common or divergent adaptations of muscle perfusion and -oxygenation as well as mitochondrial respiration of blood cells. Eleven team-sport athletes performed either RSH (3x5x10s, 20s and 5min recovery between repetitions and sets) or SIH (4x30s, 5min recovery) cycling training for 3weeks (3 times/week) at a simulated altitude of 2,200m. Before and three days after the training period, a Wingate and a repeated cycling sprint test (5x6s, 20s recovery) were performed with a 30min resting period between the tests.

Cardioprotection induced by remote ischemic preconditioning preserves the mitochondrial respiratory function in acute diabetic myocardium.

A 2×2 factorial design was used to evaluate possible preservation of mitochondrial functions in two cardioprotective experimental models, remote ischemic preconditioning and streptozotocin-induced diabetes mellitus, and their interaction during ischemia/reperfusion injury (I/R) of the heart. Male Wistar rats were randomly allocated into four groups: control (C), streptozotocin-induced diabetic (DM), preconditioned (RPC) and preconditioned streptozotocin-induced diabetic (DM+RPC). RPC was conducted by 3 cycles of 5-min hind-limb ischemia and 5-min reperfusion.

Neuronal marker recovery after Simvastatin treatment in dementia in the rat brain: in vivo magnetic resonance study.

The aim of study was to search for new biomarkers with a magnetic resonance technique to identify the early stages of dementia, induced by D-galactose, and evaluate Simvastatin therapy. Localized proton magnetic resonance spectroscopy measurements showed a significant decrease in the concentration of N-acetylaspartate+N-acetylaspartylglutamate and myo-inositol in the D-galactose group compared to the control group, and, conversely, an increase of N-acetylaspartate+N-acetylaspartylglutamate in the D-galactose/Simvastatin group. Using a saturation transfer experiment, with phosphorus magnetic resonance spectroscopy, we observed a significant elevation of the forward rate constant of the creatine kinase reaction in the brains of the D-galactose group compared to controls, and subsequently, a significant reduction of this reaction in the D-galactose/Simvastatin group.