Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 18

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Population of tigers in Polish zoos in 2000–2006

100%
Obecnie w środowisku naturalnym tygrysy zamieszkują tereny od wschodniej Turcji, przez południową Azję, do południowo-wschodniej Syberii, Półwyspu Malajskiego oraz Sumatrę, Jawę i Balię. Generalnie obszar występowania tych drapieżników kurczy się coraz bardziej, a niektóre podgatunki bezpowrotnie wyginęły, np. tygrys jawajski, tygrys balijski, tygrys kaspijski. Ogrody zoologiczne pozostają więc miejscami, gdzie można zobaczyć na żywo te wielkie koty. Utrzymywane są również w polskich zoo, gdzie coraz częściej prowadzi się tam programy hodowli i reprodukcji tego zagrożonego wymarciem gatunku. Celem niniejszej pracy była analiza pogłowia tygrysów i wybranych wskaźników reprodukcyjnych oraz śmiertelności w polskich ogrodach zoologicznych w latach 2000–2006. Na podstawie danych liczbowych z Informatora Ogrodów Zoologicznych oraz kart zwierząt dokonano analizy pogłowia tygrysów: amurskiego, bengalskiego, białego i syberyjskiego w Polsce w latach 2000–2006, uwzględniając wybrane wskaźniki reprodukcji. Populacja tygrysów w badanych latach zmniejszyła się o około 45%. Spadek ten dotyczył w większym stopniu samic. Liczba padłych zwierząt nie była rekompensowana liczbą urodzonego i odchowanego potomstwa. Utrzymanie stanu liczebności tygrysów w polskich ogrodach zoologicznych wymaga podjęcia intensywnych działań zmierzających do zwiększenia reprodukcji tego gatunku oraz zakupu lub „wypożyczenia” samic o sprawdzonej zdolności reprodukcyjnej.
Neurodegenerative lesions in cholinergic encephalopathies include an excessive activation of microglia, which may aggravate this process. Infl amatory cytokines were reported to affect viability of cultured cholinergic cells, through the infl uence on their acetyl-CoA metabolism. The aim of this work was to investigate whether phenotypic modifi cations of N9 microglia by common neuron-differentiating stimuli can alter its energy metabolism, viability and biological activity in neurodegenerative conditions. In basal conditions lipopolysaccharide (LPS) slightly decreased PDH activity and acetyl-CoA content and activated NO synthesis (600%). The cyclic AMP alone (0.25 mM), caused 15% increase of nonviable cells at 300% rise in NO synthesis and 50 and 30% decreases in acetyl-CoA and ATP contents, respectively. In such conditions LPS resulted in further increase of NO accumulation and aggravated loss of cell viability and their acetyl-CoA content. In basic conditions retinoic acid (RA) alone did not alter viability and NO synthesizing capacity but increased acetyl-CoA and blunted cytotoxic potencies of cAMP and LPS to N9. RA-evoked restoration of N9 cell viability was accompanied by the increase in their acetyl-CoA content. These data indicate that activation of microglia depletes their acetyl-CoA, making them more vulnerable to cytotoxic insults. On the contrary, rescue of microglia by RA-signaling pathways is connected with restoration their acetylCoA pool. Supported by MNiSW projects P05A 11030 and NN401 2333 33 and AMG fund St-57.
BACKGROUND AND AIMS: Excess of zinc ions and intermittent hypoxia both cause neurodegeneration by disruption in energy metabolism and oxidative stress, resulting in diminished pyruvate dehydrogenase complex (PDHC) and aconitase activity and consequent shortages in acetyl-CoA. This deficiency may be particularly dangerous for cholinergic neurons as they consume acetyl-CoA in additional pathway of acetylcholine synthesis apart from energy production. Aim of our study was to investigate effect of hypoxia on acetylCoA metabolism in neuronal cells under cytotoxic conditions. METHODS: The SH-SY5Y neuroblastoma cells were recognized as an in vitro model of brain cholinergic neurons after differentiating with all-trans-retinoic acid and cAMP. Hypoxic conditions were induced by 24 h (chronic) exposition of SH-SY5Y cells to cobalt ions (Co). Zinc (Zn) ions were used to evoke cytotoxicity. RESULTS: Chronic exposition of SH-SY5Y NC to 0.2 mM and 0.5 mM Co decreased cells number by 22% and 53%, respectively. The activities of PDHC and aconitase were reduced by 70% (0.2 mM Co) and over 75% (0.5 mM Co). IDH activity, in both concentrations, was decreased by 18%. The level of acetyl-CoA in SH-SY5Y NC was 28.4 pmol/mg of protein and chronic exposition of SH-SY5Y to 0.5 mM Co decreased acetyl-CoA level by about 60%. Chronic exposure of SH-SY5Y DC to 0.2 mM and 0.5 mM Co decreased number of cells by 28 and 60%, respectively, reduced activities of PDHC by 52% (0.2 mM) and 31% (0.5 mM Co). Aconitase activity was decreased by 77 and 90%, respectively. Activity of NADP-IDH and level of acetyl-CoA were also diminished regardless of the cobalt concentration by approximately 28% and 30%, respectively. In both groups addition of 0.1 mM Zn-aggravated cells mortality. CONCLUSION: Presented data indicate that hypoxia enhance cytotoxic effects of Zn in highly differentiated cholinergic cells. Supported by Ministry of Research and Higher Education projects: MN 01-0058/08 and ST-57, IP 2011046071.
Microglial cells, through the proinflammatory mediators play an important role in host defense and tissue repair in CNS. They contribute to pathomechanisms of Alzheimer’s and other neurodegenerative diseases. The aim of this work was to investigate modifying effects of non-activated migroglia on cholinergic neuronal SN56 cells subjected to common neuroprotective and/or neurotoxic signals. Chronic exposure to Zn or SNP caused loss of viability (30%), inhibition of pyruvate dehydrogenase (PDH) (40%), isocitrate dehydrogenase (60 and 50%) and aconitase activities as well as decrease of acetyl-CoA levels. These alterations in enzyme activities displayed strong direct correlation with depletion of acetylCoA (r=0.86, P<0.0001) and inverse correlation with cell viability (r=0.87, P<0.0001). Resveratrol, free radical scavenger, increased viability of Zn/SNP treated cholinergic cells but did not overcome suppresive effects of SNP and Zn on enzymes activities. Under same neurotoxic conditions, N9 microglial cells cultured on isoporated inserts and added to neuronal culture dishes, also overcame neurotoxic effect Zn and SNP maintaining control levels of acetyl-CoA, enzymes activites and high cell viability. These data sugest that in some specific, pathologic conditions, non-activated microglia may protect neuronal cholinergic neurons against neurotoxic insults by paracrine-like mechanism by protecting their energy metabolism. On the other hand resveratrol neuroprotection may depend on entirely different yet undefined mechanism. Supported by GUMed MN-15, MNiSW NN401029937, IP2010035370, GUMed ST-57 projects.
Cholinergic neurons of brain septum were found to be highly susceptible to neurodegenerative conditions. The sources of this particular sensitivity remain unclear. There is suggestion that their low resistance to cytotoxic conditions might be due to comprehensive consumption of acetyl-CoA. In cholinergic neurons the acetyl-CoA, except of intramitochondrial utilization for energy and NAA synthesis, serves as a precursor of acetycholine in their cytoplasmic compartment. The later pathway, present only in cholinergic neuronal cells, can cause temporary shortages of acetyl-CoA under cytotoxic conditions. The aim of our study was to investigate how these conditions affect N-acetylaspartate (NAA) synthesis as another acetylCoA consuming pathway in cholinergic SN56 neuroblastoma cells. These cells are recognized in vitro model of brain cholinergic neurons. Neurodegenerative conditions were induced by chronic exposition SN56 cells to zinc, a known excitotoxic agent. NAA in cholinergic neuroblastoma cells was assayed by HPLC preceded by one-dimension solid phase/ion exchange extraction. Levels of NAA in nondifferentiated (NC) and differentiated (DC) cells were equal to 70 and 56 nmol/mg protein, whereas rates of its release were 21.6 and 20.5 nmol/h/mg protein. Levels of acetyl-CoA and activities of choline acetyltransferase in NC and DC were equal to 29.5 and 23.8 pmol/mg of protein and to 0.106 and 0.232 nmol/min/ mg of protein, respectively. It indicates that 20% decrease of acetylCoA level in DC was caused by its increased utilization for acetylcholine synthesis. Zinc inhibited TCA cycle enzymes and pyruvate dehydrogenase activities at [IC50] values well below 0.10 mmol/L. Despite of that zinc concentrations up to 125 µM increased levels of acetyl-CoA and NAA both in DC and NC by 94 and 57% and by 27% and 22%, respectively. However, 0.175 mmol/L Zn resulted in impairment of 27 and 36% of NC and DC, as measured by lactate dehydrogenase release, respectively. In these conditions levels of acetyl-CoA in NC and DC were decreased by 68% and 45%, respectively. NAA levels were also suppressed by 63% and 51%, respectively. These data indicate the existence of significant, although differential interrelationships between rates of acetyl-CoA synthesis in mitochondria of cholinergic neurons and its utilization for NAA and acetylcholine synthesis. Increased acetylcholine synthesis may contribute to greater susceptibility of cholinergic neurons to cytotoxic conditions. On the other hand, NAA synthesis may not be a factor decreasing availability of acetyl-CoA in neurons with high expression of cholinergic phenotype. Its alterations seem to be secondary to respective shifts in acetyl-CoA levels. Supported by project IP2010035370 Ministry of Science and Higher Education.
Excessive activation of glutamatergic neurons in course of different encephalopathies is accompanied by marked increase of zinc concentration in the synaptic cleft. This cation is co-released with glutamate and subsequently taken up by cholinergic and other postsynaptic elements through ZIP transporters, NMDA and other voltage dependent Ca-channels. On the other hand, Zn distribution and clearance from cellular compartments is executed by multiple Zn-transporters (ZnT). The aim of this work was to investigate how variable levels of Zn in extracellular space affect its accumulation in cholinergic cells and their functions. Acute, 30 min exposure of differentiated and nondifferentiated SN56 cells to increasing concentrations of Zn yielded concave up, non saturable, super imposable accumulation plots. At 0.15 mM extracellular concentration, intracellular accumulation of Zn was about 60 nmol/mg protein. On the other hand, after 24 h cell culture with same Zn concentration its intracellular level was found to be equal to 6 nmol/mg protein, only. Atypical shape of concentration-dependent plots of Zn accumulation might be explained by the coexistence in cholinergic cell plasma membranes low density, high-affi nity and high density low affi nity Zn-transporting sites. On the other hand, time-dependent decrease of Zn accumulation might result from an adaptative increase of density of one of ZnT proteins, presumably ZnT4, thereby protecting cells against Zn overload. Supported by MNiSW grants NN401 2333 33 and P05A 110 30
Zinc is a trace element essential for living organisms. However, its excess in the aging human brain is claimed to contribute to patomechanisms Alzheimerís disease. The aim of this work was to fi nd out whether acute effects of Zn on neurons may be caused by alterations in their acetyl-CoA metabolism. Zn quickly accumulated in cholinergic SN56 cells in concentration-dependent fashion. In cell homogenates Zn caused, inhibition of pyruvate dehydrogenase (PDH), aconitase, isocitrate dehydrogenase and ketoglutarate dehydrogenase (KDH) activities, with Ki values equal to 0.058, 0.010, 0.005 and 0.0015 mM, respectively. For choline acetyltransferase [IC 0.5] for Zn was above 0.3 mM. No inhibition of succinate dehydrogenase activity was found. It also decreased cytoplasmic acetyl-CoA and ACh levels ([IC 0.5] 0.15 mM), and inhibited ACh release ([IC 0.5] 0.10 mM). Lipoamide (LA) or EDTA, added before or simultaneously with Zn prevented these inhibitions. When LA or EDTA were added 10 min after Zn, they did not reverse aconitase inhibition, partially restored KDH activity and totally reversed inhibition of PDH. Activities of PDH and KDH but not aconitase suppressed by 24 hour cell culture with Zn, were also restored by post culture additions of LA and EDTA to harvested cell homogenates. It indicates that, Zn could exert its acute effects on cholinergic cells through inhibitory-binding to crucial enzymes of energy metabolism, yielding acute depletion of cytoplasmic acetyl-CoA and suppression of cholinergic transmitter functions. Supported by MNiSW grants NN401 2333 33 and P05A 110 30
Preferential loss of septal cholinergic neurons is a main cause of cognitive deficits in various encephalopathies. Zinc excess is one of multiple pathologic signals contributing to mechanisms of Alzheimer’s and other neurodegenerative diseases. We suggest that zinc may be involved in early excitotoxic phase of neuronal injury. In homogenates of SN56 cholinergic neuroblastoma cells, Zn caused instant inhibition of pyruvate dehydrogenase (PDH), aconitase, isocitrate dehydrogenase (IDH) and ketoglutarate dehydrogenase (KDH) activities with Ki values equal to 0.08, 0.008, 0.005 and 0.005 mM, respectively. Short term, 30 minute exposition to Zn caused a concentration dependent increase in mortality of cAMP/retinoic acid differentiated SN56 cholinergic cells (DC) that was two times higher than that of differentiated ones (NC). Zn also decreased cytoplasmic acetyl-CoA as well as ACh content and inhibited its release. Exposition of DC and NC to increasing concentrations of Zn yielded concave up non saturable accumulation plots that reached level of 60 nmol/mg protein at 0,15 mM extracellular concentration of a cation. In these conditions no change in whole cell Ca level was observed. However the level of intramitochondrial Ca was decreased by 30%, at 100 % increase of cytoplasmic Ca. Significant, direct correlation between Zn accumulation and cytoplasmic Ca concentration (r=0.97, p=0.028) and the inverse one with mitochondrial Ca (r=- 0.96, p=0.028) were found, respectively. On the other hand, 24 h cell exposition to 0,15 mM Zn increased its intracellular content from 1.4 to about 6 nmol/mg protein at simultaneous 40% decrease of whole cell Ca level. Zn caused no significant changes in the density of ZnT1 and ZnT4 transporter proteins in the cells. Presented data indicate the coexistence in SN56 cell plasma membranes low density - high-affinity and high density - low affinity Zn-transporting sites. Inhibition of mitochondrial Na-Ca exchanger by accumulated Zn might cause depletion of Ca in mitochondria. In addition chronic exposition to Zn apparently induced adaptative mechanisms eliminating excess of the metal from the cells. These changes may directly inhibit intramitochondrial acetyl-CoA synthesis and its transport to cytoplasmic compartment, yielding impairment of cell viability and suppression their transmitter functions. Supported by MWiSW NN401 0299 37, St57 and W-109 MUG projects.
Zinc excess in the synaptic cleft may be one of pathologic signals triggering chronic neurodegenerative events. The aim of this work was to find relationships between Zn accumulation and integrity of cholinergic and astroglial cells. Exposition of cAMP/RA-differentiated (DC) and nondifferentiated cells (NC) cholinergic SN56 neuroblastoma and astroglial C6 cells to Zn yielded its concentration dependent accumulation. It caused inhibition of pyruvate dehydrogenase, aconitase and ketoglutarate dehydrogenase activities. Zn accumulation caused concentration-dependent death of both neuronal and astroglial cells. After 24 h exposition of SN56 cells to 0.15 mM Zn their death rates were equal to 35 and 50% for NC and DC at cation levels equal to 4.0 and 5.5 nmol/mg protein, respectively. In the same conditions, the death rates of astroglial NC and DC were close to 1–2% only, at intracellular Zn levels of 1.6 and 2.1 nmol/ mg protein, respectively. Higher about 0.25 mM Zn levels were required to evoke death rates of astroglial cells, similar to those seen in neuronal cells. In such conditions Zn levels in astroglia were about 6.4 and 27.0 nmol/mg protein, respectively. Such differential sensitivity of astroglial and neuronal cholinergic NC and DC to Zn may be due to respective differences in densities of ZnT1 transporters in their plasma membranes. Supported by M.S&H.E. project IP2010035370 and GUMed fund ST57.
BACKGROUND AND AIMS: Inhibition of brain energy metabolism, accompanied by inflammatory activation of microglial cells is a characteristic feature of several neurodegenerative brain diseases, including Alzheimer’s, aluminum or vascular encephalopathies. Microglial inflammatory response to neurotoxic signals may contribute to neuronal degeneration through excessive production of nitric oxide (NO) and a vast range of pro-inflammatory cytokines. The aim of this work was to investigate whether and how lipopolysaccharide (LPS), and its key mediator NO, may differentially affect energy and acetyl-CoA metabolism of microglial N9 and cholinergic SN56 neuroblastoma cells. METHODS: In experimential model cell cultures were used: N9 murine microglial cells and SN56.B5.G4 cholinergic murine neuroblastoma cells. RESULTS: Exposition of murine microglial N9 cells to LPS caused concentration-dependent several-fold increases of nitrogen oxide synthesis, accompanied by inhibition of pyruvate dehydrogenase complex (PDHC), aconitase and α-ketoglutarate dehydrogenase complex (KDHC) activities, and by depletion of acetyl-CoA, but by small losses in ATP content and cell viability. On the other hands, SN56 cells were insensitivity to LPS, which was probably caused by lower than in N9, expression of TLR4. However, exogenous NO caused inhibition of PDHC and aconitase activities, depletion of acetyl-CoA and loss of SN56 cells viability. Microglial cells appeared to be more resistant than neuronal cells to acetyl-CoA and ATP depletion evoked by these neurodegenerative condition. CONCLUSIONS: These data indicate that preferential susceptibility of cholinergic neurons to neurodegenerative insults may results from competition for acetyl-CoA between mitochondrial energyproducing and cytoplasmic acetylocholine synthesizing pathways. One of the reasons for greater resistance of microglial cells to cytotoxic inputs could be their lower energy demand. Supported by MNSW project MN 01-0067/08 and GUMed fund ST-57.
BACKGROUND AND AIMS: The aim of this work was to find relationships between Zn accumulation and integrity of cholinergic and astroglial cells. METHODS: Exposition of cAMP/RA-differentiated (DC) and nondifferentiated (NC) cells cholinergic SN56 neuroblastoma and astroglial C6 cells to Zn yielded its concentration dependent accumulation. The level of Zn was measured by fluorimetric method with TSQ. RESULTS: After 24 h exposition of SN56 cells to 0.15 mM Zn their death rates were equal to 35 and 50% for NC and DC at cation levels equal to 4.0 and 5.5 nmol/mg protein, respectively. In the same conditions, the death rates of astroglial cells were close to 1–2% only, at intracellular Zn levels of 1.6 and 2.1 nmol/mg protein, respectively. Higher, about 0.25 mM Zn levels were required to evoke death rates of astroglial cells, similar to those seen in neuronal cells. In such conditions Zn levels in astroglia were about 6.4 and 27.0 nmol/mg protein, respectively. In thisstudy we examined the effects of accumulation of Zn in cholinergic neurons and adjacent astrocytes on activity of enzymes involved in energy metabolism. It caused inhibition of PDHC, aconitase and IDH activities. The high susceptibility of cholinergic neurons and a relative high resistance of astrocytes induced by cytotoxic concentration of zinc. Higher levels of Zn may cause deeper inhibition of acetyl-CoAsynthesis and the flow rate of the TCAcycle, which leads to a decrease in ATP synthesis and cell damage. CONCLUSIONS: Chronic exposition to Zn apparently induced adaptative mechanisms eliminating excess of the metal from the cells. These changes may directly inhibit intramitochondrial acetyl-CoA synthesis and its transport to cytoplasmic compartment, yielding impairment of cell viability and suppression their transmitter functions. Chronic neurons are more susceptible to increase extracellular concentrations of zinc than astrocytes. Supported by MNiSW projects MN 01-0108/08/248 and MUG fund ST-57.
Inhibition of brain energy metabolism in demented subjects correlates with impairment their cognitive functions and loss of cholinergic neuron markers found in post mortem studies. However, mechanisms of preferential loss of brain cholinergic neurons in Alzheimer’s disease and other encephalopathies, remain unknown. We demonstrate that neuronal acetyl-CoA metabolism may be a primary target for neurodegenerative insults. Several putative encephalopathy-inducing pathogens, such as aluminum, amyloid-beta, zinc, NO excess, interleukin 1b, hypoglycemia and thiamine deficit were found to decrease viability and transmitter functions of cholinergic neuronal cells in cultures as well as in whole brain models of neurodegeneration. They caused inhibition of pyruvate dehydrogenase activity that correlated directly with respective alterations of acetyl-CoA level in neuronal mitochondria and inversely with rate of cell death. Moreover, these pathogens caused greater suppression mitochondrial acetyl-CoA and viability of differentiated than nondifferentiated cholinergic neuronal cells. Decreased availability of intramitochondrial acetyl-CoA apparently suppressed its transport to cytoplasm. In consequence, these neurotoxins decreased acetyl-CoA level in the cytoplasmic compartment. It resulted in a prominent decrease in ACh content and its quantal release in differentiated cells. In nondifferentiated cells neurotoxic effects were much smaller or negligible. Significant direct correlations were found between cytoplasmic acetyl-CoA levels and different parameters of cholinergic metabolism. Neurotoxic signals were less harmful for resting microglial and astroglial than for neuronal cells. Several compounds, known to improve pyruvate and acetyl-CoA metabolism, such as lipoamide, acetyl-L-carnitine, flavonoids, prevented neurotoxic activities through the maintenance proper level of acetyl-CoA in the mitochondrial compartment. They also, stabilized transmitter functions, when added simultaneously with neurotoxic compounds. However, delay in neuroprotectant application, abolished its beneficial effects on cell survival. It might be due to irreversible inhibition of aconitase and isocitrate dehydrogenase by some neurotoxins. Presented data indicate that in encephalopathic brains, cholinergic neurons viability and their transmitter functions are affected by alterations of two functionally independent pools of intramitochondrial and cytoplasmic acetyl-CoA, respectively. Supported by MNiSW projects NN401233333, 401029937 and GUMed fund St-57.
Preferential loss of brain cholinergic neurons in course of Alzheimerís disease (AD) and other encephalopathies might result from the fact that they utilize acetyl-CoA, not only for energy and N-acetylaspartate production but also for acetylcholine (ACh) synthesis. Therefore, acetyl-CoA metabolism might be a likely target for both cytotoxic signals and therapeutic procedures. The shortage of acetyl-CoA in cholinergic cell mitochondria caused their high susceptibility to amyloid-beta, NO, Al and Zn. They caused dose-dependent increase of nonviable cell fraction and cytoplasmic cytochrome c levels, decreases in mitochondrial enzyme and ChAT activities, intramitochondrial and cytoplasmic acetyl-CoA and ACh levels, with loss of morphologic differentiation. The expression of cholinergic phenotype positively correlated with compound-evoked alterations in cytoplasmic acetylCoA levels (r=0.90, P=0.002). On the other hand, cytoprotective properties correlated with their ability to maintain high level of acetyl-CoA in mitochondria. Accordingly nonviable cell fraction inversely correlated with pyruvate dehydrogenase activity (r=−0.79, P=0.002) and content of mitochondrial acetyl-CoA (r=−0.92, P=0.0002). These data indicate the existence in cholinergic neurons two independent pools of cytoplasmic and mitochondrial acetyl-CoA, that under pathologic conditions affect expression of cholinergic phenotype and their viability, respectively. Supported by MNiSW project 2P05A 110 30
Cognitive defi cits in Alzheimer’s disease (AD) are caused by preferential loss of septal cholinergic neurons. We postulate that utilization of acetyl-CoA for ACh synthesis creates its defi cit for energy production in cholinergic neurons. Therefore, we investigated whether higher expression of the cholinergic phenotype could make these neurons more susceptible to putative AD pathogens. Chronic exposure of nondifferentiated (NC) and differentiated (DC) cholinergic septal neuroblastoma SN56 cells to amyloid-β, NO excess and Al inhibited pyruvate dehydrogenase (PDH) and other oxidative enzymes activities in, with similar potencies. However, they caused much greater decrease of acetyl-CoA content, cholinergic functions and viability in DC than in NC, respectively. On the other hand, both in NC and DC, Zn caused acute inhibition of PDH, aconitase and NADP isocitrate dehydrogenase, with similar Ki values of about 0.058, 0.010 and 0.005 mM, respectively. Unexpectedly, Zn-Ki for ketoglutarate dehydrogenase (KDH) in DC was 0.0005 mM, whereas in NC 0.0040 mM, respectively. Signifi - cant correlations were found between acetyl-CoA in mitochondria and mortality as well as between cytoplasmic acetyl-CoA and expression of the cholinergic phenotype in SN56 cells. We postulate that these two partially independent pools of acetyl-CoA affect survival and transmitter functions of cholinergic neurons, respectively. Supported by MNiSW grants 2P05A 11030, NN401139933 and AMG project St-57.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.