Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D03575 (CoCl2)
 1,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Ion-sensitive glass micro-electrodes were used to measure the intracellular pH (pHi) and the intracellular sodium ion concentration, [Na+]i, in identified Helix aspersa neurones. 2. The injection of small volumes of 0-1 McaCl2, which increased the membrane potential by 10-15 mV for 1-2 min, had little or no effect on [Na+]i. Increases of up to 1 mM in [Na+]i could be reversibly induced by larger injections. 3. Calcium injection caused an immediate decrease in pHi, which appeared to be directly proportional to the amount of calcium injected. Injections causing hyperpolarizations of 10-20 mV which recovered in 2-5 min caused pHi decreases of 0-04-0-15 units. After each of these injections both pHi and the membrane potential recovered exponentially but with different time constants. 4. The injection of calcium at a low rate could decrease pHi without affecting the membrane potential. 5. Neither membrane potential nor pHi were affected by the injection of small volumes of 0-1 M-MgCl2, Injection of CoCl2 produced a large transient decrease in pHi but no significant change in membrane potential. 6. Exposure of the cell to saline equilibrated with 2-5% CO2 greatly reduced the pHi decrease caused by calcium injection but had only small effects on the membrane potential response. 7. It is concluded that most of the injected calcium is exchanged for protons inside the cell.
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PMID:The effect of calcium injection on the intracellular sodium and pH of snail neurones. 1 26

Growth of Methanobacterium thermoautotrophicum on H2 and CO2 as sole energy and carbon sources was found to be dependent on Ni, Co, and Mo. At low concentrations of Ni (less than 100 nM), Co (less than 10 nM) and Mo (less than 10 nM) the amount of cells formed was roughly proportional to the amount of transition metal added to the medium; for the formation of 1 g cells (dry weight) approximately 150 nmol NiCl2, 20 nmol CoCl2 and 20 nmol Na2MoO4 were required. A dependence of growth on Cu, Mn, Zn, Ca, Al, and B could not be demonstrated. Conditions are described under which the bacterium grew exponentially with a doubling time of 1.8 h up to a cell density of 2 g cells (dry weight)/l.
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PMID:Nickel, cobalt, and molybdenum requirement for growth of Methanobacterium thermoautotrophicum. 12 Jul 28

Similarities in properties of ribulose diphosphate carboxylase and oxygenase activities further substantiate the hypothesis that the same protein catalyzes both reactions. The Km (ribulose diphosphate) is 0.33 mM for the ribulose diphosphate oxygenase, when assayed in air with an oxygen electrode. Maximum activity is obtained with 10 to 35 mM MgCl2. Higher MgCl2 concentrations are inhibitory, but they shift the pH optimum from 9.3 or 9.4 to 8.7 or 9.0. MnCl2 is an effective cofactor of the oxygenase and some activity is obtained with CoCl2. Both the ribulose diphosphate carboxylase and oxygenase activity of the purified protein from spinach leaves are slowly inactivated by storage at 0 degrees and reactivated in 10 min at 50 degrees, provided both 25 mM MgCl2 and 1 mM dithiothreitol are present. The sulfhydryl groups of the enzyme which react rapidly with 5,5'-dithiobis(2-nitrobenzoic acid) are approximately 4 at pH 7.8 and 11 at pH 9.4. At both pH values ribulose diphosphate prevents two of these sulfhydryl groups from reacting with this reagent. About 50% inhibition of the oxygenase activity at pH 9.0 occurs with 50 mM bicarbonate in the presence of 3 mM ribulose diphosphate, and from variations in these parameters the inhibition is attributed to the CO2 species. The purified enzyme of acrylamide gels prevented the reduction of nitroblue tetrazolium in the presence of the superoxide radical, but the enzyme in solution did not react as a superoxide dismutase.
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PMID:Ribulose diphosphate carboxylase/oxygenase. III. Isolation and properties. 23 14

The hypothesis that sympathoexcitatory neurones within the rostroventrolateral medulla (RVLM) may be chemosensitive was tested in chloralose-anaesthetized cats by artificial perfusion of the RVLM via the left vertebral artery. The baroreceptors and peripheral chemoreceptors were denervated by bilaterally dissecting the carotid sinus and vagus nerves. Either white ramus T3 (WR-T3) or the renal nerve was recorded to monitor sympathetic activity. Perfusion with saline or Ringer solution bubbled with CO2 (10%-100%) produced a rapid and pronounced increase in sympathetic activity and blood pressure. Solutions adjusted to the same pH (pH 5.2 for 100% CO2) with HCl resulted in a much weaker excitation. A linear relationship between PCO2 and sympathetic activity was demonstrated. During prolonged perfusion (90 s) sympathetic activity returned to the control level after initial excitation and fell below control levels when perfusion ceased. The sympathetic activity response to CO2-bubbled solutions was unaffected by blockade of synaptic input by microinjection of CoCl2 into the RVLM, whereas spontaneous sympathetic activity and the supraspinal somato-sympathetic reflex from intercostal nerve T4 to WR-T3 were markedly reduced. It is therefore concluded that sympathoexcitatory bulbospinal neurones in the RVLM are directly chemosensitive to changes in arterial PCO2 and pH.
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PMID:Chemosensitivity of sympathoexcitatory neurones in the rostroventrolateral medulla of the cat. 212 39

The phenacetin breath test (PBT) has been proposed as an alternative to the aminopyrine breath test (ABT) for the assessment of hepatic function. To investigate the clinical utility of the PBT, we compared the PBT with the ABT in 9 healthy subjects and 18 patients with biopsy-proven liver disease. We also investigated the effects of cytochrome P-450 inducers in humans and rats, and the effect of cobaltous chloride (CoCl2) in rats on the PBT to elucidate the relationship between the rate of phenacetin deethylation and exhaled labeled CO2 derived from phenacetin. In humans with abnormal ABTs, the PBT correlated with the ABT (r = 0.77), but in healthy humans there was no correlation between the two breath tests. Rifampin pretreatment in healthy humans induced the ABT by 27%, but did not induce the PBT. In rats the PBT was not induced by 3-methylcholanthrene pretreatment at phenacetin doses of 1 mg per kg, but was induced by both 3-methylcholanthrene (178%) and phenobarbital (142%) at 10 mg per kg phenacetin. Pretreatment of rats with CoCl2, which reduces cytochrome P-450 content, decreased the PBT by 40% and the ABT by 84%. The insensitivity of the PBT to induction except at high doses of phenacetin suggests that phenacetin deethylation is not the rate-limiting process modulating exhaled labeled CO2 in healthy subjects, and that the PBT does not generally reflect normal or induced phenacetin dealkylation rates. The PBT, however, did reflect hepatic damage and may even be better than the ABT for grading the severity of hepatic damage.
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PMID:Comparison of the phenacetin and aminopyrine breath tests: effect of liver disease, inducers and cobaltous chloride. 392 Jan 35

We describe a K+ transport system in Methanospirillum hungatei cells depleted of cytoplasmic K+ via an ammonia/K+ exchange reaction (Sprott, G. D., Shaw, K. M., and Jarrell, K. F. (1984) J. Biol. Chem. 259, 12602-12608). Ammonia-treated cells contained low concentrations of ATP and were unable to make CH4 or to transport 86Rb+. All of these properties were restored by CaCl2, MgCl2, or MnCl2, and not by CoCl2 or NiCl2. The Rb+ transport system had a Km of 0.42 and Vmax of 29 nmol/min X mg; K+ inhibited competitively. Both H2 and CO2 were required for appreciable transport, whereas air, valinomycin, or nigericin were potent inhibitors. The influx of Rb+ was electrogenic and associated with proton efflux, producing a delta pH (alkaline inside) in acidic media. In the absence of K+ (or Rb+), the activation of CH4 synthesis by Mg2+ produced little change in the cytoplasmic pH, showing that methanogenesis did not elicit a net efflux of protons. The pH optimum for transport was in the range 6.0-7.3 where the transmembrane pH gradient would contribute minimally to the proton motive force. Protonophores at pH 6.3 caused a partial decline in CH4 synthesis and the ATP content and dramatically collapsed Rb+ transport. These and other inhibitor experiments, coupled with the fact that the Rb+ gradient was too large to be in equilibrium with the proton motive force alone, suggest a role for both ATP and the proton motive force in Rb+ transport. Also, a role for K+ in osmoregulation is indicated.
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PMID:Methanogenesis and the K+ transport system are activated by divalent cations in ammonia-treated cells of Methanospirillum hungatei. 401 70

Prior results from this laboratory have demonstrated that the respiratory response to hypercapnia is enhanced by microinjection of GABA antagonists or GABA synthesis inhibitors into the caudal hypothalamus of both cats and rats. However, no evidence was found for modulation of the respiratory response to hypoxia by a hypothalamic GABAergic mechanism. The purpose of the present study was to determine if synaptic input other than GABAergic onto caudal hypothalamic neurons affects the respiratory responses to hypoxia. The respiratory (diaphragmatic EMG) responses to hypoxia (10% O2) and hypercapnia (5% CO2) were recorded in anesthetized rats before and after bilateral microinjection of a blocker of synaptic transmission (CoCl2, 100 mM) or an excitatory amino acid receptor antagonist (kynurenic acid, 50 mM) into the caudal hypothalamus. Both hypoxia and hypercapnia elicited increases in tidal diaphragmatic activity and respiratory frequency prior to the microinjections. The respiratory response to hypercapnia was increased (+10.5%) after CoCl2 microinjections, which is consistent with prior results obtained with blockade of GABAergic input. Kynurenic acid did not alter the respiratory response to hypercapnia. A new finding was that the respiratory response to hypoxia was diminished after both CoCl2 (-13.0%) and kynurenic acid (-25.0%) microinjections. The results of this study support our prior findings that neurons in the caudal hypothalamus modulate the respiratory response to hypercapnia. In addition, our findings suggest that an excitatory input acting through excitatory amino acid receptors in the caudal hypothalamus modulates the respiratory responses to hypoxia.
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PMID:Modulation of the respiratory responses to hypoxia and hypercapnia by synaptic input onto caudal hypothalamic neurons. 789 38

Hypoxia is an important regulator of hypoxia inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) expression. Using Dunning rat prostate tumour cells (MatLyLu) we examined the induction of HIF-1alpha and VEGF by hypoxia and if the induction of these proteins would lead to angiogenesis in the chick chorioallantoic membrane (CAM). MatLyLu cells were exposed to 1% O2, in 5.25% CO2 and 94.75% N2, or treated with 100 mM CoCl2 to simulate hypoxia. Conditioned medium was analyzed using Western blots for HIF-1alpha or VEGF. VEGF levels were quantified using ELISA. Hypoxia significantly increased both HIF-1alpha and VEGF protein production. MatLyLu cells (1x10(6) viable cells in 50 microl of medium) grown under normoxic conditions induced in angiogenesis in the CAM, evaluated by the formation of a spoke wheel, and in cross sections by the number of blood vessels, following 5-day culture. This response was significantly increased using CoCl2-treated cells. Culture medium alone with or without CoCl2 was not angiogenic. These results provide direct evidence for the role of hypoxia in the induction of HIF-1alpha and VEGF which act as key angiogenic signals.
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PMID:A hypoxic response induced in MatLyLu cells by cobalt chloride results in an enhanced angiogenic response by the chick chorioallantoic membrane. 1288 12

Corneal nociceptors terminate at the trigeminal subnucleus interpolaris/caudalis (Vi/Vc) transition and subnucleus caudalis/upper cervical spinal cord (Vc/C1) junction regions of the lower brain stem. The aims of this study were to determine if local GABAA receptor activation modifies corneal input to second-order neurons at these regions and if GABAA receptor activation in one region affects corneal input to the other region. In barbiturate-anesthetized male rats, corneal nociceptors were excited by pulses of CO2 gas, and GABAA receptors were activated by microinjections of the selective agonist muscimol. Local muscimol injection at the site of recording inhibited all Vi/Vc and Vc/C1 units tested and was reversed partially by bicuculline. To test for ascending intersubnuclear communication, muscimol injection into the caudal Vc/C1 junction, remote from the recording site at the Vi/Vc transition, inhibited the evoked response of most corneal units, although some neurons were enhanced. Injection of the nonselective synaptic blocking agent, CoCl2, remotely into the Vc/C1 region inhibited the evoked response of all Vi/Vc units tested. To test for descending intersubnuclear communication, muscimol was injected remotely into the rostral Vi/Vc transition and enhanced the evoked activity of all corneal units tested at the caudal Vc/C1 junction. These results suggest that GABAA receptor mechanisms play a significant role in corneal nociceptive processing by second-order trigeminal brain stem neurons. GABAA receptor mechanisms act locally at both the Vi/Vc transition and Vc/C1 junction regions to inhibit corneal input and act through polysynaptic pathways to modify corneal input at multiple levels of the trigeminal brain stem complex.
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PMID:GABA(A) receptor activation modulates corneal unit activity in rostral and caudal portions of trigeminal subnucleus caudalis. 1289 Jul 97

Hydrothermal reaction of CoCl2 with the potassium salt of pyridine-2,3-dicarboxylic acid and excess base yields [Co3(NC5H3(CO2)2-2,5)2(mu3-OH)2(OH2)2], which has a three-dimensional structure based on hydroxide-bridged triangular chains. The magnetic behavior of this compound shows the presence of three distinct regions of magnetic bistability.
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PMID:Multiple areas of magnetic bistability in the topological ferrimagnet [Co3(NC5H3(CO2)2-2,5)2(mu3-OH)2(OH2)2]. 1547 73


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