scholarly journals Improvement of Rat Survival and Liver Mitochondrial Function in Biliary Obstruction After Treatment With Sodium Thiosulfate

HPB Surgery ◽  
1995 ◽  
Vol 8 (4) ◽  
pp. 249-252
Author(s):  
B. Myslovaty ◽  
S. Kyzer ◽  
H. Levinsky ◽  
C. Chaimoff
Keyword(s):  
Survival Rate ◽  
Liver Function ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Biliary Obstruction ◽  
Sodium Thiosulfate ◽  
Sodium Thiosulphate ◽  
Respiratory Capacity ◽  
Effect Of Treatment

The exact cause of liver failure occurring after long standing biliary obstruction is not known. Impairment of hepatic mitochondrial respiration was postulated in some studies. Sodium thiosulphate (STS) is known to have a protective effect on liver function during administration of hepatotoxic chemotherapy. In the present experimental study the effect of treatment with STS in the presence of obstructive jaundice was studied by determination of the survival rate of rats subjected to biliary obstruction and by polarographic determination of the hepatic mitochondrial function. Treatment with STS was found to result in a significant improvement in rats' survival rate (p < 0.05). Polarography demonstrated significant preservation of mitochondrial respiratory capacity after treatment with STS. The results of the present study show that the deterioration in liver function in the presence of biliary obstruction is probably caused by impairment of mitochondrial respiration. This may be preserved by treatment with STS. The exact explanation of its effect is not yet clear.

scholarly journals Determination of the effectiveness of microbiological preparations and bioavailable nutrients while growing a vegetative apple rootstock

2021 ◽  
Vol 34 ◽  
pp. 05007
Author(s):  
Tatiana Prichko ◽  
Vladimir Mager ◽  
Roman Oplachko
Keyword(s):  
Amino Acids ◽  
Survival Rate ◽  
Soil Microorganisms ◽  
Natural Soil ◽  
Apple Rootstock ◽  
Biometric Parameters ◽  
Protein Amino Acids ◽  
Effect Of Treatment ◽  
The Impact

This article presents the results of a study of the effect of treatment of the root system of the M9 stock with the microbiological preparation Agrinos 1, which is a consortium of natural soil microorganisms - more than 80 strains from 10 families in combination with the preparation Agrinos 2, containing a complex of bioavailable nutrients (macro-, microelements, protein, amino acids, chitin, chitosan) in order to activate metabolic processes, reduce the impact of stress on the plant. The effect of biological products on the survival rate of the stock in the nursery, an increase in the yield and standardization of offshoots, and an improvement in their biometric parameters was established.

scholarly journals Satellite cell-derived extracellular vesicles reverse peroxide-induced mitochondrial dysfunction in myotubes

2020 ◽  
Author(s):  
Kyle T. Shuler ◽  
Brittany E. Wilson ◽  
Eric R. Muñoz ◽  
Andrew D. Mitchell ◽  
Joshua T. Selsby ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Extracellular Vesicles ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Untreated Control ◽  
Recovery Period ◽  
Fluorescent Microscopy ◽  
C2c12 Myotubes ◽  
Control Group ◽  
Respiratory Capacity

ABSTRACTSatellite cells (SCs) are muscle-specific stem cells that have a central role in muscle remodeling. Despite their therapeutic potential, SC-based therapies have been met with numerous logistical challenges, limiting their ability to effectively treat systemic muscle diseases, such as Duchenne muscular dystrophy (DMD). Delivery of SC-derived extracellular vesicles (SC-EVs) may unlock the potential offered by SCs and overcome their numerous limitations.PurposeThe purpose of this investigation was to determine the extent to which SC-EVs could restore mitochondrial function in cultured myotubes following oxidative injury.MethodsSC-EVs were isolated from cultured SCs from C57 mice and quantified using nanoparticle tracking analysis (NTA). C2C12 myotubes were cultured and divided into four treatment groups: untreated control, treated for 24 h with SC-EV, 24 h exposure to 50 μM H2O2 followed by a 24 h recovery period with no treatment, or 24 h exposure to 50 μM H2O2 followed by a 24 h treatment with SC-EV. Inter-group differences in mitochondrial function were assessed via one-way ANOVA with Tukey post hoc analysis (p<0.05).ResultsGiven the seeding density used, we calculated that each SC releases approximately 2.35 × 105 ± 3.10 × 104 EVs per 24 h. Further, using fluorescent microscopy, we verified SC-EVs deliver cargo into myotubes, some of which was localized to the mitochondria. H2O2 exposure resulted in a 42% decline in peak mitochondrial respiration (p=0.0243) as well as a 46% reduction in spare respiratory capacity (p=0.0185) relative to the untreated control group. Subsequent treatment with SC-EVs (3.12×108 SC-EV; 24 h) following H2O2 exposure restored 76% of peak mitochondrial respiration (p=0.0187) and 84% of spare respiratory capacity in the damaged myotubes (p=0.0198). SC-EVs did not affect mitochondrial function in the undamaged myotubes.ConclusionCollectively, these data demonstrate SC-EVs may represent a novel therapeutic approach for treatment of myopathies associated with mitochondrial dysfunction.

Impaired mitochondrial function in chronically ischemic human heart

2013 ◽  
Vol 304 (11) ◽  
pp. H1407-H1414 ◽  
Author(s):  
Nis Stride ◽  
Steen Larsen ◽  
Martin Hey-Mogensen ◽  
Christina N. Hansen ◽  
Clara Prats ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Human Heart ◽  
Ex Vivo ◽  
Ischemic Myocardium ◽  
Acute Ischemia ◽  
Ros Production ◽  
Respiratory Capacity ◽  
Mitochondrial Respiratory

Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitochondrial damage, hereby reinforcing a vicious circle. Ischemic preconditioning has been proven protective in acute ischemia, but the subject of chronic ischemic preconditioning has not been explored in humans. We hypothesized that mitochondrial respiratory capacity would be diminished in chronic ischemic regions of human myocardium but that these mitochondria would be more resistant to ex vivo ischemia and, second, that ROS generation would be higher in ischemic myocardium. The aim of this study was to test mitochondrial respiratory capacity during hyperoxia and hypoxia, to investigate ROS production, and finally to assess myocardial antioxidant levels. Mitochondrial respiration in biopsies from ischemic and nonischemic regions from the left ventricle of the same heart was compared in nine human subjects. Maximal oxidative phosphorylation capacity in fresh muscle fibers was lower in ischemic compared with nonischemic myocardium ( P < 0.05), but the degree of coupling (respiratory control ratio) did not differ ( P > 0.05). The presence of ex vivo hypoxia did not reveal any chronic ischemic preconditioning of the ischemic myocardial regions ( P > 0.05). ROS production was higher in ischemic myocardium ( P < 0.05), and the levels of antioxidant protein expression was lower. Diminished mitochondrial respiration capacity and excessive ROS production demonstrate an impaired mitochondrial function in ischemic human heart muscle. No chronic ischemic preconditioning effect was found.

scholarly journals Atorvastatin impairs liver mitochondrial function in obese Göttingen Minipigs but heart and skeletal muscle are not affected

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liselotte Bruun Christiansen ◽  
Tine Lovsø Dohlmann ◽  
Trine Pagh Ludvigsen ◽  
Ewa Parfieniuk ◽  
Michal Ciborowski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Obese Group ◽  
Control Group ◽  
Dependent Manner ◽  
Respiratory Capacity ◽  
Protein Carbonyl Content ◽  
Functional Changes ◽  
Mitochondrial Respiratory

AbstractStatins lower the risk of cardiovascular events but have been associated with mitochondrial functional changes in a tissue-dependent manner. We investigated tissue-specific modifications of mitochondrial function in liver, heart and skeletal muscle mediated by chronic statin therapy in a Göttingen Minipig model. We hypothesized that statins enhance the mitochondrial function in heart but impair skeletal muscle and liver mitochondria. Mitochondrial respiratory capacities, citrate synthase activity, coenzyme Q10 concentrations and protein carbonyl content (PCC) were analyzed in samples of liver, heart and skeletal muscle from three groups of Göttingen Minipigs: a lean control group (CON, n = 6), an obese group (HFD, n = 7) and an obese group treated with atorvastatin for 28 weeks (HFD + ATO, n = 7). Atorvastatin concentrations were analyzed in each of the three tissues and in plasma from the Göttingen Minipigs. In treated minipigs, atorvastatin was detected in the liver and in plasma. A significant reduction in complex I + II-supported mitochondrial respiratory capacity was seen in liver of HFD + ATO compared to HFD (P = 0.022). Opposite directed but insignificant modifications of mitochondrial respiratory capacity were seen in heart versus skeletal muscle in HFD + ATO compared to the HFD group. In heart muscle, the HFD + ATO had significantly higher PCC compared to the HFD group (P = 0.0323). In the HFD group relative to CON, liver mitochondrial respiration decreased whereas in skeletal muscle, respiration increased but these changes were insignificant when normalizing for mitochondrial content. Oral atorvastatin treatment in Göttingen Minipigs is associated with a reduced mitochondrial respiratory capacity in the liver that may be linked to increased content of atorvastatin in this organ.

STUDIES ON FOLIC ACID IN INFANCY

PEDIATRICS ◽  
1964 ◽  
Vol 33 (5) ◽  
pp. 694-699
Author(s):  
Yehuda Matoth ◽  
Rina Zamir ◽  
Shulamith Bar-Shani ◽  
Nathan Grossowicz
Keyword(s):  
Bone Marrow ◽  
Folic Acid ◽  
Folinic Acid ◽  
Whole Blood ◽  
Blood Picture ◽  
Normal Range ◽  
Acid Status ◽  
Effect Of Treatment ◽  
Low Levels

Folic acid was assayed microbiologically in whole blood in a group of infants hospitalized for diarrhea, various infections, and malnutrition. Folic acid activity was decreased in the majority of cases. In some of the infants very low levels were observed. The value of the determination of folic acid in whole blood as a sensitive index of the folic acid status of an individual was confirmed by parallel observations on bone marrow morphology and the level of folic acid in serum. Folinic acid levels were within the normal range in most cases. Low folinic acid levels were common only when folic acid was extremely low. Many patients with low folic acid levels were not anemic, or mildly anemic. In the anemic patients a hypochromic microcytic blood picture was the rule. The effect of treatment with folic acid on the general condition of the patients was more striking than the hematological response.

EXPRESS METHOD FOR DETERMINING OF IODINE NUMBER IN FATS AND OILS

2019 ◽  
Author(s):  
В.И. МАРТОВЩУК ◽  
Е.В. МАРТОВЩУК ◽  
А.А. ЛОБАНОВ ◽  
И.В. РЫБАНЧУК ◽  
Ю.Ш. ЮСУПОВА
Keyword(s):  
Iodine Number ◽  
Rapid Determination ◽  
Sodium Thiosulfate ◽  
Fats And Oils ◽  
Alcoholic Solution ◽  
Test Substance ◽  
Blue Color ◽  
Express Method ◽  
Excess Iodine

Разработан экспресс-метод определения йодного числа в жирах и маслах, исключающий применение агрессивных и токсичных реагентов и значительно сокращающий длительность измерения. Разработанный метод позволяет определить показатель степени непредельности жиров и масел, жиросодержащих пищевых продуктов. Методика предусматривает предварительную обработку масел в МХА. Затем навеску исследуемого вещества от 0,03 до 0,05 г, взятую с точностью до ± 0,0002 г, помещают в сухую коническую колбу с притертой пробкой. В колбу вносят 10 см3спирто-эфирной смеси (1 : 1), тщательно перемешивают. Затем к навеске добавляют 30 см3 спиртового раствора йода концентрацией 0,1 моль/дм3, перемешивают. Приливают 100 см3 дистиллированной воды. Колбу закрывают пробкой, встряхивают и выдерживают в темноте 20 мин. Избыточный йод оттитровывают раствором тиосульфата натрия концентрацией 0,1 моль/дм3. Перед окончанием титрования, когда раствор приобретет соломенно-желтый цвет, добавляют 1 см31%-го раствора крахмала и титруют до исчезновения синей окраски. Относительная погрешность определения йодного числа по разработанной методике невелика – от 0,141 до 0,149% при надежности 0,95. Разработанный метод рекомендован для оперативного определения йодных чисел масел и жиров в производственных и лабораторных условиях. Оперативность метода позволяет быстро вносить изменения в технологические процессы и обеспечивать стабильность производства и качества продукции. The express method of determination of iodine number in fats and oils, excluding the use of aggressive and toxic reagents and significantly reducing the duration of measurement, has been developed. The developed method allows define degree of unsaturated of the fats and oils containing fat of products. The technique involves the pretreatment of oils in a techno-chemical activator. Then the sample of the test substance from 0,03 to 0,05 g, taken with an accuracy of ± 0,0002 g, is placed in a dry conical flask with a ground glass stopper. In the flask make 10 cm3alcohol-ether mixture (1 : 1), mix sample thoroughly. Then add 30 cm3of an alcoholic solution of iodine with a concentration of 0,1 mol/dm3to the sample, mix. Then, pour 100 cm3of the distilled water. The flask is closed with a stopper, shaken and kept in the dark for 20 min. Excess iodine is titrated with a solution of sodium thiosulfate concentration of 0,1 mol/dm3. Before the end of titration, when the solution becomes straw yellow, add 1 cm3 of 1% starch solution and titrate until the blue color disappears. The relative error in the determination of the iodine number by the developed method is small – from 0,141 to 0,149% with a reliability of 0,95; that allows us to recommend the developed method for the rapid determination of iodine numbers of oils and fats in production and laboratory conditions. The efficiency of the method allows you to quickly make changes in technological processes and ensure the stability of production and product quality.

Abstract 131: Anti-inflammatory and Mitochondrial Effects of Butyrate in Shr Astrocytes in vitro

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Tao Yang ◽  
Ty Redler ◽  
Carla G Bueno Silva ◽  
Rebeca Arocha ◽  
Jordan Schmidt ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Rna Isolation ◽  
Inflammatory Factors ◽  
Pcr Analysis ◽  
Sprague Dawley ◽  
Beneficial Effects ◽  
Sd Rats ◽  
Anti Inflammatory

Emerging evidence demonstrates a significant link between gut dysbiosis and hypertension (HTN). Butyrate is one of the major fermented end-products of gut microbiota that reportedly produces beneficial effects on the immune system and metabolism. A contraction in butyrate-producing bacteria in the gut of spontaneously hypertensive rats (SHR) suggests that reduced butyrate may be associated with HTN. Considering its role in mitochondrial metabolism, we proposed that the positive anti-inflammatory effects of butyrate may be mediated via improvement in mitochondrial function in astrocytes. Methods: Sprague Dawley (SD) and SHR primary astrocytes from two-day old pups were cultured in DMEM, supplemented with 10% FBS and 1% pen/strep, for 14 days, prior to treatment with butyrate (0-1mM) for 4 hours. Cells were then subjected to the Seahorse XFe24 Extracellular Flux Analyzer to evaluate mitochondrial function following butyrate treatment. Additional samples were collected for total RNA isolation for real time PCR analysis of inflammatory factors and transcripts related to mitochondrial function and stress. Results: Butyrate significantly increased both basal and maximal mitochondrial respiration (by 3-4 fold, P<0.001) and elevated proton leak (by 4 fold, P<0.01) in astrocytes from SD rats but not SHR. Furthermore, we observed a trend for an increase in both ATP-linked and non-mitochondrial respiration in SD astrocytes compared to SHR (by 2-3 fold, P=0.07). This was associated with a significant reduction in relative expression levels in catalase (by 50%, P<0.05) and a trend in reduction in Sod1 and Sod2 (by 25%-50%, P=0.1) in astrocytes harvested from SD rats but not the SHR. Conversely, butyrate significantly lowered expression of pro-inflammatory Ccl2 (by 33%, P<0.05) and Tlr4 (by 48%, P <0.05) in astrocytes of SHR, but not SD rats. Conclusion: Butyrate modulated mitochondrial bioenergetics in SD but not the SHR, suggesting that the mitochondria of astrocytes may be less sensitive to the effects of butyrate in HTN. In addition, butyrate reduced inflammatory mediators in the SHR, but had no effect in the SD rat astrocytes. Thus, central anti-inflammatory effects of butyrate may be mediated via a mitochondria-independent mechanism.

scholarly journals Effect of hyperbaric oxygen therapy on liver function during intermittent ischemia

2013 ◽  
Vol 28 (suppl 1) ◽  
pp. 61-65 ◽  
Author(s):  
Leticia Botigeli Baldim ◽  
Ricardo Nejo Jr ◽  
Maria Eliza Jordani Souza ◽  
Maria Cecília Jordani Gomes ◽  
Maria Aparecida Neves Cardoso Picinato ◽  
...  
Keyword(s):  
Liver Function ◽  
Hyperbaric Oxygen ◽  
Mitochondrial Function ◽  
Hyperbaric Oxygen Therapy ◽  
Aspartate Aminotransferase ◽  
Alanine Aminotransferase ◽  
Oxygen Therapy ◽  
Respiratory Control ◽  
Respiratory Control Ratio ◽  
Hepatic Pedicle

PURPOSE: To analyze the effects of hyperbaric oxygen therapy on liver function in rats previously subjected to ischemia and reperfusion. METHODS: A randomly distribution of 23 Wistar rats was conducted into three groups: SHAM, animals subjected to surgical stress without restricting blood flow by clamping the hepatic pedicle, IR, rats underwent hepatic vascular occlusion intermittently for two complete cycles of 15 minutes of ischemia followed by 5 min of reperfusion, IR / HBO, rats underwent hepatic pedicle clamping and thereafter exposed to hyperbaric oxygen pressure of 2 absolute atmospheres for 60 minutes. We evaluated liver function through mitochondrial function, determined by the stages 3 and 4 of respiration, respiratory control ratio (RCR) and mitochondrial permeability transition (Swelling). Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also quantified . We analyzed the results using the Mann-Whitney test and were considered significant all results with p <0.05. RESULTS: There were significant differences between the results of stage 3 in SHAM vs IR group ; of the stage 4 in the groups IR vs SHAM and SHAM vs IR /HBO; of the Respiratory Control Ratio (RCR) in the group IR vs IR / HBO ; of alanine aminotransferase in the groups IR vs SHAM , SHAM vs IR/HBO and IR vs IR / HBO; aspartate aminotransferase in the groups SHAM vs IR and SHAM vs IR / HBO. CONCLUSION: The whole analysis of the mitochondiral function indicators permits us to conclude that the hyperbaric oxygen therapy acted as a protective agent of the mitochondrial function, minimizing the ischemia-reperfusion injury of the hepatic parenchyma.

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