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Mitochondrial Metabolism (mitochondrial + metabolism)
Selected AbstractsMitochondrial metabolism in the rat during bladder regeneration induced by small intestinal submucosaBJU INTERNATIONAL, Issue 3 2004Rozbeh Faramarzi-Roques OBJECTIVE To assess mitochondrial metabolism of bladder tissue induced by small-intestinal submucosa (SIS), by comparing the mitochondrial enzyme metabolism in this tissue with that in normal bladder tissue and thus evaluate intracellular normality. MATERIAL AND METHODS In all, 70 rats were grouped into healthy controls (10), surgical controls with a simple bladder incision (15) and rats treated by partial cystectomy with replacement by the SIS graft (45). At 1, 3 and 6 months the rats were killed, the enzymes of mitochondrial respiratory chain complexes assayed, and the respiration of permeabilized bladder fibres assessed using polarographic analysis. RESULTS The enzyme activities of control and treated rats at 3 months were identical. The results from the polarographic analysis of respiration were also similar to that in normal tissue apart from a decrease in the number of mitochondria. Histologically, there was complete regeneration at 6 months. CONCLUSION After a phase of inflammation the bladder regenerates after a patch is placed. The new tissue has the same enzymatic and histological features as normal bladder tissue. [source] Maternal high-fat feeding primes steatohepatitis in adult mice offspring, involving mitochondrial dysfunction and altered lipogenesis gene expression,HEPATOLOGY, Issue 6 2009Kimberley D. Bruce Nonalcoholic fatty liver disease (NAFLD) describes an increasingly prevalent spectrum of liver disorders associated with obesity and metabolic syndrome. It is uncertain why steatosis occurs in some individuals, whereas nonalcoholic steatohepatitis (NASH) occurs in others. We have generated a novel mouse model to test our hypothesis: that maternal fat intake contributes to the development of NAFLD in adult offspring. Female mice were fed either a high-fat (HF) or control chow (C) diet before and during gestation and lactation. Resulting offspring were fed either a C or a HF diet after weaning, to generate four offspring groups; HF/HF, HF/C, C/HF, C/C. At 15 weeks of age, liver histology was normal in both the C/C and HF/C offspring. Kleiner scoring showed that although the C/HF offspring developed nonalcoholic fatty liver, the HF/HF offspring developed NASH. At 30 weeks, histological analysis and Kleiner scoring showed that both the HF/C and C/HF groups had NAFLD, whereas the HF/HF had a more severe form of NASH. Therefore, exposure to a HF diet in utero and during lactation contributes toward NAFLD progression. We investigated the mechanisms by which this developmental priming is mediated. At 15 weeks of age, hepatic mitochondrial electron transport chain (ETC) enzyme complex activity (I, II/III, and IV) was reduced in both groups of offspring from HF-fed mothers (HF/C and HF/HF). In addition, measurement of hepatic gene expression indicated that lipogenesis, oxidative stress, and inflammatory pathways were up-regulated in the 15-week-old HF/C and HF/HF offspring. Conclusion: Maternal fat intake contributes toward the NAFLD progression in adult offspring, which is mediated through impaired hepatic mitochondrial metabolism and up-regulated hepatic lipogenesis. (HEPATOLOGY 2009.) [source] Interactions between melatonin and nicotinamide nucleotide: NADH preservation in cells and in cell-free systems by melatoninJOURNAL OF PINEAL RESEARCH, Issue 2 2005Dun-Xian Tan Abstract:, Interactions of melatonin and nicotinamide adenine dinucleotide (NADH) have been studied in different experimental models including NADH-promoted oxyhemoglobin oxidation, vanadate-induced NADH oxidation and paraquat-induced NADH depletion in cultured PC12 cells. Our findings indicate that melatonin preserves NADH levels under oxidative stress both in cell-free systems and in cultured PC12 cells. These interactions likely involve electron donation by melatonin and reduction of the NAD radical. As a result, the NAD radical is recycled to NADH and melatonin is oxidized to N1 -acetyl- N2 -formyl-5-methoxykynuramine (AFMK). NADH is a central molecule at the crossroads between energy metabolism and the antioxidant defense system in organisms. Recycling of NADH by melatonin might improve the efficiency of NADH as an energy carrier and as an antioxidant. Interactions between melatonin and NADH may be implicated in mitochondrial metabolism. [source] Melatonin protects hepatic mitochondrial respiratory chain activity in senescence-accelerated miceJOURNAL OF PINEAL RESEARCH, Issue 3 2002Yuji Okatani Mitochondrial oxidative damage from free radicals may be a factor underlying aging, and melatonin, a powerful free radical scavenger, may participate in mitochondrial metabolism. We measured respiratory chain complex I and IV activities in liver mitochondria from a strain of senescence-accelerated prone mice (SAMP8) and a strain of senescence-accelerated resistant mice (SAMR1) at age 3, 6, and 12 months. No age-associated effects were found in either complex I and IV activities, thiobarbituric acid-reactive substances (TBARS), or glutathione peroxidase (GPx) activity in SAMR1. In contrast, SAMP8 showed significant age-associated decreases in complex I and IV activities. While no age effect was found in TBARS in SAMP8, TBARS levels in SAMP8 were significantly more abundant than in SAMR1. GPx activity in SAMP8 decreased significantly by 12 months. Daily oral melatonin administration (2 ,g/mL of drinking fluid) beginning when the mice were 7 months old significantly increased complex I and IV activity, decreased TBARS, and increased GPx activities in both SAMR1 and SAMP8 at 12 months. The implication of the findings is that melatonin may be beneficial during aging as it reduced the deteriorative oxidative changes in mitochondria and other portions of the cell associated with advanced age. [source] Role of IscS in Fe-S cluster assembly in Trypanosoma bruceiTHE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 2 2005O. SMÍD Despite the significance of proteins containing iron-sulfur cluster (Fe,S proteins), the processes of Fe,S cluster assembly and maturation of Fe,S proteins are poorly understood. However, several key proteins involved in the assembly have been identified, notably IscS, a cystein desulfurase, which provides sulfur for Fe,S cluster and IscU, a metallochaperone acting as a scaffold for cluster assembly. In this work, we studied the process of Fe,S cluster biosynthesis in Trypanosoma brucei by identifying the homologue of IscS in the T. brucei (TbIscS). To address the function of TbIscS, we inhibited its expression by means of RNA interference (RNAi). After RNAi induction, generation time of the TbIscS knock-down cell line was significantly prolonged. All types of mitochondrial ATP production in the cells were severely affected. Analysis of glucose metabolism end products determined pyruvate as major excreted metabolite of the induced cells, while the uninduced cells produced only small amount of this glycolytic end product. These data demonstrate that mitochondrial metabolism is impaired in cells with TbIscS knocked down. To test whether the observed phenomena were results of Fe,S cluster assembly disruption, we examined the Fe,S cluster-dependent activity of aconitase. This enzyme is localized in its active form in mitochondrion as well as in cytosol of T. brucei. After RNAi induction we observed the reduction of aconitase activity in both compartments (approx. 70% reduction in cytosol, approx. 30% in mitochondria). Western blots together with the EPR analysis showed that the reduction in cytosolic activity was due to impaired Fe,S cluster formation, while decrease in aconitase activity in mitochondria corresponded to the reduced level of the protein. [source] Increasing amino acid supply in pea embryos reveals specific interactions of N and C metabolism, and highlights the importance of mitochondrial metabolismTHE PLANT JOURNAL, Issue 6 2008Kathleen Weigelt Summary The application of nitrogen to legumes regulates seed metabolism and composition. We recently showed that the seed-specific overexpression of amino acid permease VfAAP1 increases amino acid supply, and the levels of N and protein in the seeds. Two consecutive field trials using Pisum sativum AAP1 lines confirmed increases in the levels of N and globulin in seed; however, compensatory changes of sucrose/starch and individual seed weight were also observed. We present a comprehensive analysis of AAP1 seeds using combinatorial transcript and metabolite profiling to monitor the effects of nitrogen supply on seed metabolism. AAP1 seeds have increased amino acids and stimulated gene expression associated with storage protein synthesis, maturation, deposition and vesicle trafficking. Transcript/metabolite changes reveal the channelling of surplus N into the transient storage pools asparagine and arginine, indicating that asparagine synthase is transcriptionally activated by high N levels and/or C limitation. Increased C-acceptor demand for amino acid synthesis, resulting from elevated levels of N in seeds, initiates sucrose mobilization and sucrose-dependent pathways via sucrose synthase, glycolysis and the TCA cycle. The AAP1 seeds display a limitation in C, which leads to the catabolism of arginine, glutamic acid and methionine to putrescine, ,-alanine and succinate. Mitochondria are involved in the coordination of C/N metabolism, with branched-chain amino acid catabolism and a ,-amino-butyric acid shunt. AAP1 seeds contain higher levels of ABA, which is possibly involved in storage-associated gene expression and the N-dependent stimulation of sucrose mobilization, indicating that a signalling network of C, N and ABA is operating during seed maturation. These results demonstrate that legume seeds have a high capacity to regulate N:C ratios, and highlight the importance of mitochondria in the control of N,C balance and amino acid homeostasis. [source] Physiological Ecology of Aquatic Overwintering in Ranid FrogsBIOLOGICAL REVIEWS, Issue 2 2008Glenn J. Tattersall Abstract In cold-temperate climates, overwintering aquatic ranid frogs must survive prolonged periods of low temperature, often accompanied by low levels of dissolved oxygen. They must do so with the energy stores acquired prior to the onset of winter. Overwintering mortality is a significant factor in their life history, occasionally reaching 100% due to freezing and/or anoxia. Many species of northern ranid frogs overwinter in the tadpole stage, which increases survival during hypoxic episodes relative to adults, as well as allowing for larger sizes at metamorphosis. At temperatures below 5 °C, submerged ranid frogs are capable of acquiring adequate oxygen via cutaneous gas exchange over a wide range of ambient oxygen partial pressures (PO2), and possess numerous physiological and behavioural mechanisms that allow them to maintain normal rates of oxygen uptake across the skin at a relatively low PO2. At levels of oxygen near and below the critical PO2 that allows for aerobic metabolism, frogs must adopt biochemical mechanisms that act to minimise oxygen utilisation and assist in maintaining an aerobic state to survive overwintering. These mechanisms include alterations in mitochondrial metabolism and affinity, changes in membrane permeability, alterations in water balance, and reduction in cellular electrochemical gradients, all of which lead to an overall reduction in whole-animal metabolism. Winter energetic requirements are fueled by the energy stores in liver, muscle, and fat depots, which are likely to be sufficient when the water is cold and well oxygenated. However, under hypoxic conditions fat stores cannot be utilised efficiently and glycogen stores are used up rapidly due to recruitment of anaerobiosis. Since ranid frogs have minimal tolerance to anoxia, it is untenable to suggest that they spend a significant portion of the winter buried in anoxic mud, but instead utilise a suite of behavioural and physiological mechanisms geared to optimal survival in cold, hypoxic conditions. [source] Mitochondrial metabolism in the rat during bladder regeneration induced by small intestinal submucosaBJU INTERNATIONAL, Issue 3 2004Rozbeh Faramarzi-Roques OBJECTIVE To assess mitochondrial metabolism of bladder tissue induced by small-intestinal submucosa (SIS), by comparing the mitochondrial enzyme metabolism in this tissue with that in normal bladder tissue and thus evaluate intracellular normality. MATERIAL AND METHODS In all, 70 rats were grouped into healthy controls (10), surgical controls with a simple bladder incision (15) and rats treated by partial cystectomy with replacement by the SIS graft (45). At 1, 3 and 6 months the rats were killed, the enzymes of mitochondrial respiratory chain complexes assayed, and the respiration of permeabilized bladder fibres assessed using polarographic analysis. RESULTS The enzyme activities of control and treated rats at 3 months were identical. The results from the polarographic analysis of respiration were also similar to that in normal tissue apart from a decrease in the number of mitochondria. Histologically, there was complete regeneration at 6 months. CONCLUSION After a phase of inflammation the bladder regenerates after a patch is placed. The new tissue has the same enzymatic and histological features as normal bladder tissue. [source] The Role of Mitochondria in the Pathogenesis of Neurodegenerative DiseasesBRAIN PATHOLOGY, Issue 3 2000Giovanni Manfredim MD A growing body of evidence indicates that mitochondrial dysfunction may play an important role in the pathogenesis of many neurodegenerative disorders. Because mitochondrial metabolism is not only the principal source of high energy intermediates, but also of free radicals, it has been suggested that inherited or acquired mitochondrial defects could be the cause of neuronal degeneration as a consequence of energy defects and oxidative damage. Mitochondrial respiratory chain dysfunction has been reported in association with primary mitochondrial DNA abnormalities, and also as a consequence of mutations in nuclear genes directly involved in mitochondrial functions, such as SURF1, frataxin, and paraplegin. Defects of oxidative phosphorylation and increased free radical production have also been observed in diseases that are not due to primary mitochondrial abnormalities. In these cases, the mitochondrial dysfunction is likely to be an epiphenomenon, which, nevertheless, could be of importance in precipitating a cascade of events leading to cell death. In either case, understanding the role of mitochondria in the pathogenesis of neurodegenerative diseases could be important for the development of therapeutic strategies in these disorders. [source] Eicosapentaenoic acid and docosahexaenoic acid effects on tumour mitochondrial metabolism, acyl CoA metabolism and cell proliferationCELL BIOCHEMISTRY AND FUNCTION, Issue 2 2001Alison Colquhoun Abstract In order to investigate the effects of high-fat diets rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), Wistar rats bearing subcutaneous implants of the Walker 256 tumour were fed pelleted chow containing low DHA/EPA or high DHA/EPA. The presence of n -3 polyunsaturated fatty acids (PUFAs) led to a marked suppression (35,46%) of tumour growth over a 12 day period. Both the whole tumour homogenate and the Percoll-purified mitochondrial fraction presented significant changes in fatty acid composition. The levels of EPA increased in both n -3 dietary groups while the levels of DHA increased only in the high DHA/EPA group, in comparison with the control chow-fed group. The presence of n -3 PUFAs led to an increase in mitochondrial acyl CoA synthetase activity, but neither the cytoplasmic acyl CoA content nor the n -3 fatty acid composition of the cytoplasmic acyl CoAs was altered by the diet. The content of thiobarbituric acid-reactive substances (TBARS) was increased in the low DHA/EPA group but was unchanged in the high DHA/EPA group. In vitro studies with the Walker 256 cell line showed a 46% decrease in cell growth in the presence of either EPA or DHA which was accompanied by a large decrease in the measured mitochondrial membrane potential. The TBARS content was increased only in the EPA-exposed cells. Cell cycle analysis identified a decrease in G0,G1 phase cells and an increase in G2,M phase cells and apoptotic cells, for both EPA and DHA-exposed cells. The data show that the presence of n -3 PUFAs in the diet is able to significantly after the growth rate of the Walker 256 tumour. The involvement of changes in mitochondrial membrane composition and membrane potential have been indicated for both EPA and DHA, while changes in lipid peroxidation have been identified in the presence of EPA but not of DHA. Copyright © 2001 John Wiley & Sons, Ltd. [source] Novel intramolecular coordination chemistry of some new metallocene complexesCHINESE JOURNAL OF CHEMISTRY, Issue 11 2001Yan-Long Qian Abstract The metabolic thermogenic curves of liver mitochondria isolated from the livers of Cyprinus Carpio vol and its parents were determined at 28°C by using an LKB-2277 Bioactivity Monitor. The results indicated that their thermogenic curves are different The total heat output and total time of the metabolism of the liver mitochondria of the hybrid F1 (Cyprinus Carpio val) are more than those of its parents, and its maximum heat power is between that of the female parent and male parent. The relationship between their metabolic thermogenic curves and character of mitochondrial metabolism, and thermokinetics and the heterosis were analyzed and discussed. The character of the mitochondrial thermogenic curves reflected the physiologic character of heterosis. The microcalorimetric method proved to be a probable and sensitive tool for the assessment of heterosis. [source] Microcalorimetric studies on the mitochondria metabolism of Cyprinus Carpio val and its parentsCHINESE JOURNAL OF CHEMISTRY, Issue 11 2001Feng-Jiao Deng Abstract The metabolic thermogenic curves of liver mitochondria isolated from the livers of Cyprinus Carpio vol and its parents were determined at 28°C by using an LKB-2277 Bioactivity Monitor. The results indicated that their thermogenic curves are different The total heat output and total time of the metabolism of the liver mitochondria of the hybrid F1 (Cyprinus Carpio val) are more than those of its parents, and its maximum heat power is between that of the female parent and male parent. The relationship between their metabolic thermogenic curves and character of mitochondrial metabolism, and thermokinetics and the heterosis were analyzed and discussed. The character of the mitochondrial thermogenic curves reflected the physiologic character of heterosis. The microcalorimetric method proved to be a probable and sensitive tool for the assessment of heterosis. [source] | |||||||||||||