Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy per cent of the phospholipid in mitochondria from sweet potato roots was removed by aqueous acetone treatment. The amount of phospholipid that could be rebound to these lipid-depleted mitochondria roughly corresponded to the amount of phospholipid in untreated mitochondria. The activities of NADH-cytochrome c oxidoreductase, succinate-cytochrome c oxidoreductase, cytochrome oxidase, and succinoxidase in lipid-depleted mitochondria were restored by addition of mitochondrial phospholipid to about 60, 50, 15, and 35%, respectively, in comparison to untreated mitochondria. The capacity of lipid-depleted mitochondria from 14-day cold-stored tissue to bind mitochondrial phospholipid from healthy tissue was lower than that from healthy tissue. However, there was no large difference in activities of NADH-cytochrome c oxidoreductase and succinate-cytochrome c oxidoreductase between both phospholipid rebound lipid-depleted mitochondria from healthy and 14-day cold-stored tissues. On the other hand, activity of succinoxidase in phospholipid rebound lipid-depleted mitochondria from 14-day cold-stored tissue was decreased by about 50% of that from healthy tissue. Furthermore, the capacity of lipid-depleted mitochondria from 2-day cold-stored tissue to bind mitochondrial phospholipid from healthy tissue was higher than that from healthy tissue.
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PMID:Mechanism of Chilling Injury in Sweet Potato: X. Change in Lipid-Protein Interaction in Mitochondria from Cold-stored Tissue. 1665 33

We investigated whether low-pressure reperfusion may attenuate postischemic contractile dysfunction, limits necrosis and apoptosis after a prolonged hypothermic ischemia, and inhibits mitochondrial permeability transition-pore (MPTP) opening. Isolated rats hearts (n = 72) were exposed to 8 h of cold ischemia and assigned to the following groups: 1) reperfusion with low pressure (LP = 70 cmH(2)O) and 2) reperfusion with normal pressure (NP = 100 cmH(2)O). Cardiac function was assessed during reperfusion using the Langendorff model. Mitochondria were isolated, and the Ca(2+) resistance capacity (CRC) of the MPTP was determined. Malondialdehyde (MDA) production, caspase-3 activity, and cytochrome c were also assessed. We found that functional recovery was significantly improved in LP hearts with rate-pressure product averaging 30,380 +/- 1,757 vs. 18,000 +/- 1,599 mmHg/min in NP hearts (P < 0.01). Necrosis, measured by triphenyltetrazolium chloride staining and creatine kinase leakage, was significantly reduced in LP hearts (P < 0.01). The CRC was increased in LP heart mitochondria (P < 0.01). Caspase-3 activity, cytochrome c release, and MDA production were reduced in LP hearts (P < 0.001 and P < 0.01). This study demonstrated that low-pressure reperfusion after hypothermic heart ischemia improves postischemic contractile dysfunction and attenuates necrosis and apoptosis. This protection could be related to an inhibition of mitochondrial permeability transition.
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PMID:Controlled reperfusion after hypothermic heart preservation inhibits mitochondrial permeability transition-pore opening and enhances functional recovery. 1679 30

Protein molecules typically unfold (denature) when subjected to extremes of heat, cold, pH, solvent composition, or mechanical stress. One might expect that shearing forces induced by a nonuniform fluid flow would also destabilize proteins, as when a protein solution flows rapidly through a narrow channel. However, although the protein literature contains many references to shear denaturation, we find little quantitative evidence for the phenomenon. We have investigated whether a high shear can destabilize a small globular protein to any measurable extent. We study a protein (horse cytochrome c, 104 amino acids) whose fluorescence increases sharply upon unfolding. By forcing the sample through a silica capillary (inner diameter 150-180 microm) at speeds approaching 10 m/s, we subject the protein to shear rates dv(z)/dr as large as approximately 2 x 10(5) s(-1) while illuminating it with an ultraviolet laser. We can readily detect fluorescence changes of <1%, corresponding to shifts of < approximately 0.01 kJ/mol in the stability of the folded state. We find no evidence that even our highest shear rates significantly destabilize the folded protein. A simple model suggests that extraordinary shear rates, approximately 10(7) s(-1), would be required to denature typical small, globular proteins in water.
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PMID:Do protein molecules unfold in a simple shear flow? 1689 74

Cold ischemia--warm reperfusion (CI/WR) injury of liver transplantation involves hepatocyte cell death, the nature and underlying mechanisms of which remain unclear. Isolated hepatocytes and isolated perfused livers were used to determine the prevalence of necrosis and apoptosis as well as mitochondrial dysfunction. In isolated cells, propidium iodide and Hoechst 33342 staining showed a cold-storage, time-dependent increase in necrosis, whereas apoptosis was minimal even after 48 h of hypothermia. Nonetheless, a progressive loss of mitochondrial membrane potential was observed. Translocation of mitochondrial cytochrome c toward microsomes occurred within 24 h of CI/WR, with cytochrome c reaching the cytosol later. Mitochondria isolated from whole livers subjected to CI/WR also display reduced metabolic parameters and increased susceptibility to swelling. These events are associated with increased activity of major initiator (caspase 9) and effector (caspase 3) caspases. The results demonstrate that CI/WR induces mitochondrial dysfunction in isolated cells and in the whole organ; only in the latter is that sufficient to trigger the classical mitochondrial pathway of apoptosis. Our study also provides evidence for the involvement of endoplasmic reticulum stress in CI/WR hepatocyte injury. Combined protection of mitochondria and endoplasmic reticulum may thus represent an innovative therapeutic avenue to enhance liver graft viability and functional integrity.
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PMID:Implication of mitochondrial dysfunction and cell death in cold preservation--warm reperfusion-induced hepatocyte injury. 1690

In this study, experiments were designed to determine if peroxisome proliferator-activated receptor (PPAR) alpha agonists could decrease myocardial ischemia/reperfusion injury after cardioplegia-induced cardiac arrest under cardiopulmonary bypass, attenuate the appearance of cardiomyocytic apoptosis, and decrease the damage of reactive oxygen species. Cardiomyocytic apoptosis occurs after cardiopulmonary bypass surgery. Reactive oxygen species and peroxynitrite generated during ischemia/reperfusion initiate the formation of single-strand DNA breaks. Peroxisome proliferator-activated receptors (PPARs) activators had an important role in alleviating myocardial apoptosis. Four groups of New Zealand white rabbits (10 in each group, each 2.5-3.5 kg) underwent cardiopulmonary bypass. Thirty minutes before surgery, one group received WY14643 (a PPAR-alpha agonist, 1 mg kg(-1)) and another received 15D-PGJ2 (a PPAR-gamma agonist; 0.3 mg kg(-1)). The ascending aorta was cross-clamped for 60 min, whereas intermittent cold crystalloid cardioplegic solution was infused into the aortic root every 20 min. The myocardium of the reperfused hearts and control hearts were harvested and studied in vitro for evidence of apoptosis using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling method and Western blot analyses of cytochrome c and apoptosis-inducing factor. The reactive oxidative insults were checked using enzyme-linked immunosorbent assay to detect plasma cytokine levels. The occurrence of cardiomyocytic apoptosis and elevation of plasma cytokines were significantly lower in the group receiving PPAR-alpha agonists than in the other groups. Western blot analysis of apoptosis-inducing factor and cytochrome c revealed similar patterns. PPAR-alpha activation could diminish postischemic cardiomyocytic apoptosis and reactive oxygen species injuries after global cardiac arrest under cardiopulmonary bypass, possibly via prevention of both caspase-dependent and caspase-independent apoptotic pathways.
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PMID:Cardiomyocytic apoptosis following global cardiac ischemia and reperfusion can be attenuated by peroxisome proliferator-activated receptor alpha but not gamma activators. 1691 51

Within cetartiodactyl species, both New and Old World camelids are uniquely adapted to the extremely hot and dry climates of African-Asian territories and to the high altitude cold and hypoxic environment of the whole Andean area. In order to investigate the potential association between these particular adaptations and mitochondrial aerobic energy production, we examined the camelid genes of cytochrome c oxidase subunits I, II, and III and the replacement of amino acids inferred. We found that all subunits had undergone a number of replacements in sites otherwise conserved in other cetartiodactyls. Changes of COXI and COXIII were mainly located in the transmembrane helices of proteins. For COXII, although most of the changes did not occur in sites directly involved in electron transfer, a shift of D by T at 115 position of Old World camelid might modify electrostatic interactions with cytochrome c. COXII also showed an increased relative evolutionary rate respect to other cetartiodactyls compared.
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PMID:Rapid evolution of cytochrome c oxidase subunit II in camelids (Tylopoda, Camelidae). 1715 35

Nitric oxide (NO) prevents the myocardial apoptosis and dysfunction resulting from cardioplegia-induced cardiac arrest (CCA) under cardiopulmonary bypass (CPB). Inasmuch as CCA-induced myocardial dysfunction is associated with acute ischemia/reperfusion (I/R) and inflammatory response, which activates nuclear factor kappaB (NF-kappaB) translocation, we assessed the hypothesis that the detrimental effects of CCA under CPB result from NO imbalance inducing NF-kappaB activation. New Zealand white rabbits (10 in each group, each 2.5-3.5 kg) received total CPB. Rabbits were weaned from CPB and reperfused for 4 h before the hearts were harvested. Blood was sampled at various time points. Nitric oxide donor or NO synthase inhibitor was added into the cardioplegic solution. The ascending aorta was cross-clamped for 60 min, whereas cold crystalloid cardioplegic solution was intermittently infused into the aortic root every 20 min. The myocardia of the reperfused hearts and control hearts were harvested and studied for evidence of apoptosis, I/R-induced proinflammatory gene expression, and inflammatory cytokine production by cardiomyocytes. Pretreatment of the cardiomyocytes with exogenous NO prevented the I/R-induced proinflammatory effects. The inflammatory and apoptotic responses of cardiomyocytes could be lessened by restoring NO concentration via modulation of the (1) nuclear translocation of NF-kappaB, (2) inducible NO synthase mRNA expression, (3) cytochrome c production, and (4) occurrence of apoptosis. Cardioplegia-induced cardiac arrest under CPB can decrease endogenous NO production, which can be restored with exogenous NO supplementation. Exogenous NO can ameliorate the myocardial inflammatory response by inhibition of NF-kappaB translocation, inflammatory gene expression, inducible NO synthase expression, and cytochrome c production.
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PMID:Cardioplegia-induced cardiac arrest under cardiopulmonary bypass decreased nitric oxide production which induced cardiomyocytic apoptosis via nuclear factor kappa B activation. 1741 26

Adaptation to the extrauterine environment at birth relies upon the onset of postnatal function and increased metabolism in the lungs, liver and kidney, mediated partly by activation of mitochondrial proteins such as the voltage-dependent anion channel (VDAC), cytochrome c and, in the lung only, uncoupling protein (UCP)2. The magnitude of adaptation is dependent on the maternal metabolic and endocrine environment. We, therefore, examined the influence of maternal cold exposure (MCE) induced by winter shearing of pregnant sheep in conjunction with nutrient restriction (NR; 50% reduction in maternal food intake from 110 days gestation up to term). The effect of parity was also examined, as the offspring of nulliparous mothers are growth restricted compared with multiparous offspring. All sheep were twin bearing. One twin was sampled after birth and its sibling at 30 days. In the lung, both MCE and maternal nulliparity enhanced UCP2 abundance. However, whilst VDAC abundance was decreased in both the offspring of nulliparous mothers and by NR, it was transiently raised by MCE. Kidney VDAC abundance was reduced by MCE and nulliparity, adaptations only influenced by NR in multiparous mothers. Cytochrome c abundance was raised by MCE and by NR in multiparous controls and raised in offspring of nulliparous mothers. Liver VDAC and cytochrome c abundance were transiently reduced by MCE and persistently lower in offspring of nulliparous mothers. In conclusion, changes in the maternal metabolic environment have marked tissue-specific effects on mitochondrial protein abundance in the lungs, liver and kidney that may be important in enabling the newborn to effectively adapt to the extrauterine environment.
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PMID:Different effects of maternal parity, cold exposure and nutrient restriction in late pregnancy on the abundance of mitochondrial proteins in the kidney, liver and lung of postnatal sheep. 1763 78

Photoreduction of cytochrome c (Cyt c) has been reinvestigated using femtosecond-to-nanosecond transient absorption and stationary spectroscopy. Femtosecond spectra of oxidized Cyt c, recorded in the probe range 270-1000 nm, demonstrate similar evolution upon 266 or 403 nm excitation: an ultrafast 0.3 ps internal conversion followed by a 4 ps vibrational cooling. Late transient spectra after 20 ps, from the cold ground-state chromophore, reveal a small but measurable signal from reduced Cyt c. The yield phi for Fe3+-->Fe2+ photoreduction is measured to be phi(403) = 0.016 and phi(266) = 0.08 for 403 and 266 nm excitation. These yields lead to a guess of the barrier E(f)(A) = 55 kJ mol(-1) for thermal ground-state electron transfer (ET). Nanosecond spectra initially show the typical absorption from reduced Cyt c and then exhibit temperature-dependent sub-microsecond decays (0.5 micros at 297 K), corresponding to a barrier E(A)(b) = 33 kJ mol(-1) for the back ET reaction and a reaction energy DeltaE = 22 kJ mol(-1). The nanosecond transients do not decay to zero on a second time scale, demonstrating the stability of some of the reduced Cyt c. The yields calculated from this stable reduced form agree with quasistationary reduction yields. Modest heating of Cyt c leads to its efficient thermal reduction as demonstrated by differential stationary absorption spectroscopy. In summary, our results point to ultrafast internal conversion of oxidized Cyt c upon UV or visible excitation, followed by Fe-porphyrin reduction due to thermal ground-state ET as the prevailing mechanism.
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PMID:Transient and stationary spectroscopy of cytochrome c: ultrafast internal conversion controls photoreduction. 1817 20

The essential oil of Tanacetum gracile (Accession no. AT-01 termed AT-01 in the manuscript), a cold desert alpine highly aromatic herb, has 40 constituents including lavendulol (21.5 %), lavendulol acetate (1.7 %), alpha-pinene (11.2 %), 1,8-cineole (15.2 %), CIS-beta-ocimene (6.9 %), borneol (6.1 %), limonene (5.1 %) and chamazulene (3.7 %). AT-01 was evaluated for its anticancer activity. It inhibited HL-60 cell proliferation with an IC (50) of 27 microg/mL. Furthermore, AT-01 induced apoptosis in human leukemia HL-60 cells as measured by several biological end points. AT-01 induced apoptotic body formation, enhanced annexinV-FITC binding of the cells, increased sub-G (0) DNA fraction, loss of mitochondrial membrane potential (Deltapsi (mt)) and release of cytochrome c from mitochondria, activated caspase-9 as well as caspase-3, and increased cleavage of PARP in HL-60 cells. Thus, AT-01 induced apoptosis through the mitochondrial dependent pathway in HL-60 cells.
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PMID:Induction of mitochondrial-dependent apoptosis by an essential oil from Tanacetum gracile. 1840 43


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