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Results for “Lithium Chloride”

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At least 19 recordsLinked to original sources
PubMed1985

Thermodynamic characterization of the partially denatured states of ribonuclease A in calcium chloride and lithium chloride.

The denaturations of ribonuclease A by calcium chloride and lithium chloride were studied by circular dichroism measurements in the far-ultraviolet region. The temperature dependence of the equilibrium constant for the unfolding of the protein by calcium chloride and lithium chloride gave values of 46 and 52 kcal mol-1 (1 cal = 4.1868 J) for the enthalpy of denaturation at 25 degrees C and pH 7.0, respectively. Thermodynamic parameters for the denaturation by calcium chloride and lithium chloride are compared with those for the heat and guanidine hydrochloride denaturation. It has been observed that the thermodynamic quantity, be it free energy, entropy, or enthalpy, cannot be related quantitatively to the extent of unfolding measured by various conformational properties of the protein.

Animals↗
PubMed1986

Conditioned slowing of stomach emptying produced by Pavlovian pairings of a drug CS or a place with lithium chloride.

Lithium chloride, in common with other drugs with emetic effects, prolongs stomach emptying. In different experiments, a drug state induced by a low dose of pentobarbital in Experiment 1 and morphine in Experiment 2 or a distinctive place (Experiments 3, 4) was the conditioned stimulus paired with lithium chloride as the unconditioned stimulus. In each case, Pavlovian conditioning occurred and the conditioned response mimicked lithium's unconditioned effect on stomach emptying.

Animals↗
PubMed1978

Inhibition of fighting in isolated mice following repeated administration of lithium chloride.

Lithium was found to be a selective (i.e., it antagonized aggression at doses that did not produce concurrent neuromuscular impairment) antagonist of isolation-induced aggressive behavior in mice following repeated (subacute) administration for five days. Acute (single dose) administration of lithium failed to inhibit aggression. At atiaggressive doses, lithium did not produce ataxia as measured by the inclined-screen or rotarod procedures. The mechanism of this action is discussed in terms of a possible influence on serotonergic mechanisms.

Aggression↗
PubMed1989

A flavor paired with lithium chloride blocks the formation of a pentobarbital-lithium chloride association.

Thirsty rats were used in order to determine whether a vinegar solution, which had been paired with an injection of lithium chloride, could block the formation of an association between a pentobarbital- and a lithium chloride-induced state. During phase 1 the rats in the blocking group had a 2.0% vinegar solution paired with an injection of 240 mg/kg of lithium chloride, during phase 2 these rats were reexposed to the vinegar prior to each injection of 20 mg/kg of pentobarbital and 240 mg/kg of lithium chloride, and during phase 3 these rats were given access to a novel 0.75% saccharin solution and were injected with pentobarbital after saccharin removal. Animals with this history did not form an association between the pentobarbital- and lithium chloride-induced states during phase 2 as evidenced by their refusal to consume the saccharin solution over repeated pairings of saccharin with pentobarbital during phase 3. Control groups that received forward pairings of pentobarbital and lithium chloride, in the absence of a previously conditioned vinegar solution during phase 2, formed an association between pentobarbital and lithium chloride. These findings indicate that drug states and flavors can interfere with each others' capacity to predict the occurrence of lithium chloride.

Acetates↗
PubMed1993

Induction of the differentiation of HL-60 and WEHI-3B D+ leukemia cells by lithium chloride.

The use of lithium chloride in manic-depressive patients and in patients receiving myelo-suppressive cancer chemotherapeutic agents is accompanied by a sustained leukocytosis due to an increase in granulocyte production. This property suggests that lithium chloride may have effects on hematopoietic differentiation. Treatment of cultured WEHI-3B D+ murine myelomonocytic and HL-60 human promyelocytic leukemia cells with millimolar concentrations of lithium chloride resulted in concentration-dependent increases in the number of differentiated myeloid cells, as determined by the ability of the cells to reduce nitroblue tetrazolium and by the binding of myeloid specific antibodies, and was associated with an inhibition of cellular proliferation. The effects of lithium chloride on growth and differentiation were antagonized by KCl, whereas NaCl had little effect. The induction of leukemic cell maturation by lithium chloride was markedly enhanced by the addition of low levels of retinoic acid. In contrast, other differentiation inducing agents (i.e. dimethyl sulfoxide and selenazofurin) had no effect on the degree of maturation induced by lithium. These findings suggest that the combination of lithium chloride and retinoic acid may have clinical utility in the treatment of leukemia through the induction of terminal differentiation.

Animals↗
PubMed1982

Comparison of colony stimulating activities secreted into mouse lung conditioned medium in the presence and absence of lithium chloride.

Inclusion of lithium chloride during the process of secretion of granulocyte-macrophage colony stimulating activity (CSA) into mouse lung conditioned medium resulted in an increased production of CSA. CSA produced in the presence of lithium chloride was compared to the CSA produced in its absence by means of ammonium sulfate precipitation, Sephadex G-1CO (S) chromatography, concanavalin A-Sepharose chromatography and polyacrylamide gel electrophoresis. It was found that the two activities behaved identically, indicating that lithium-induced increase in CSA does not involve a qualitative change in the molecule of the colony stimulating factor, but reflects an increased production (or release) of a CSF molecule that is similar to the one produced in its absence.

Animals↗
PubMed2001

Dynamics of c-fos and ICER mRNA expression in rat forebrain following lithium chloride injection.

Lithium is commonly used as a treatment for affective disorders in humans and as a toxin to produce conditioned taste aversions in rats. LiCl administration in rats has been correlated with activation of c-fos and cAMP-mediated gene transcription in many brain regions; however, little is known about the timing or duration of gene activation. We hypothesized that c-fos gene transcription is rapidly stimulated by LiCl, followed later by the expression of the inducible cAMP early repressor (ICER) transcription factor, a negative modulator of cAMP-mediated gene transcription. By in situ hybridization, we analyzed the timecourse of c-fos and ICER mRNA expression in the central nucleus of the amygdala (CeA), the paraventricular nucleus of the hypothalamus (PVN) and the supraoptic nucleus (SON) at seven time points (0, 0.3, 1, 3, 6, 9 and 12 h) after intraperitoneal LiCl injection (0.15 M, 12 ml/kg, 76 mg/kg). Expression of c-fos mRNA peaked between 20 min and 1 h and returned to baseline by 3 h in the CeA, PVN and SON. ICER mRNA was detected in these regions at 20 min, peaked at 1-3 h and returned to nearly baseline 9 h following LiCl injection. The time lag between c-fos mRNA expression and ICER mRNA expression within the same regions is consistent with ICER terminating c-fos gene transcription. However, no refractory period was detected for restimulation of c-fos transcription by a second injection of LiCl during the period of peak ICER mRNA expression, suggesting the involvement of other transcriptional modulators.

Amygdala↗
PubMed1984

Lithium chloride: protective and antisecretory properties in rats.

Lithium chloride was evaluated as a potential protective agent against ethanol-induced hemorrhagic gastritis in rats. Rats received lithium chloride intragastrically (30, 60, or 90 mg/kg i.g.) or subcutaneously (3, 5, 10, 15, 20, 30, 60, or 90 mg/kg s.c.), or a placebo (H2O i.g. or 0.9% NaCl s.c.). Ninety minutes later 1 cm3 of 95% ethanol was administered intragastrically. After 30 min, the rats were killed and their stomachs were removed and visually scored for gross hemorrhagic gastritis. Lithium chloride at all doses less than 3 mg/kg significantly improved hemorrhagic gastritis when compared with the placebo. Moreover, rats treated with lithium chloride intragastrically had significantly less hemorrhagic gastritis than those treated subcutaneously even though serum lithium levels were similar. To determine if lithium's protective properties related to acid inhibition, pylorus-ligated and gastric fistula rats were studied. The median effective dose for lithium chloride was 20-30 mg/kg and the nonantisecretory dose was 3 mg/kg. No difference in hemorrhagic gastritis was noted between controls and animals receiving the nonantisecretory dose. However, at higher doses (LiCl 30, 60, and 90 mg/kg), lithium's protective properties persisted in spite of adding 150 mM HCl to the intragastrically administered ethanol (p less than 0.001). To determine further if lithium chloride stimulated endogenous prostaglandins, indomethacin, a prostaglandin inhibitor, was administered. Indomethacin did not alter lithium chloride's protective properties. In fact, when compared with exogenously administered 16,16-dimethyl prostaglandin E2 (5 and 500 micrograms/kg), high-dose LiCl (30, 60, or 90 mg/kg) resulted in significantly more protection against ethanol-induced injury (p less than 0.001). In contrast, when both nonantisecretory doses were compared, 16,16-dimethyl prostaglandin E2 (5 micrograms/kg) gave significantly better protection than LiCl (3 mg/kg). These data indicate that LiCl is a potent gastric antisecretory and protective agent. The protective properties of LiCl appear to be related to acid inhibition and be independent of endogenous prostaglandins, although other protective mechanisms may be present at higher LiCl doses. Additionally, this study indicates that LiCl may have clinical application in protecting the gastric mucosa against hemorrhagic gastritis.

Animals↗
PubMed1981

[Morphofunctional changes in the thyroid glands of rats following lithium chloride administration].

The effect of lithium chloride on the morphological characteristics and function of the thyroid gland of male white rats was studied by histological, histochemical, radioimmunological and radiometric methods. Significant changes in the thyroid parenchyma proper and in the population of parafollicular or C cells were recorded in response to the increased dosage of the substance injected. The lowering of J-accumulative and hormone-binding functions indicates the inhibitory action of lithium chloride both on the phase of hormonogenesis in thyrocytes and on the phase of secretion of thyroid hormones into the blood. Reduction of TTH level in the animals blood plasma suggests that lithium chloride produces the adenohypophysis-mediated action on the thyroid gland.

Animals↗
PubMed1984

Free energy changes in denaturation of ribonuclease A by mixed denaturants. Effects of combinations of guanidine hydrochloride and one of the denaturants lithium bromide, lithium chloride, and sodium bromide.

The denaturation of ribonuclease A by guanidine hydrochloride, lithium bromide, and lithium chloride and by mixed denaturants consisting of guanidine hydrochloride and one of the denaturants lithium chloride, lithium bromide, and sodium bromide was followed by difference spectral measurements at pH 4.8 and 25 degrees C. Both components of mixed denaturant systems enhance each other's effect in unfolding the protein. The effect of lithium bromide on the midpoint of guanidine hydrochloride denaturation transition is approximately the sum of the effects of the constituent ions. For all the mixed denaturants tested, the dependence of the free energy change on denaturation is linear. The conformational free energy associated with the guanidine hydrochloride denaturation transition in water is 7.5 +/- 0.1 kcal mol-1, and it is unchanged in the presence of low concentrations of lithium bromide, lithium chloride, and sodium bromide which by themselves are not concentrated enough to unfold the protein. The conformational free energy associated with the lithium bromide denaturation transition in water is 11.7 +/- 0.3 kcal mol-1, and it is not affected by the presence of low concentrations of guanidine hydrochloride which by themselves do not disrupt the structure of native ribonuclease A.

Animals↗
PubMed2005

Early gene response in lithium chloride induced apoptosis.

Depending on the cellular context, lithium chloride can lead to enhanced proliferation, cell cycle arrest or apoptosis in mammalian cells. Although substantial work has been made to elucidate the downstream events in the case of lithium chloride-induced cellular proliferation, the molecular response to lithium chloride treatment in the apoptotic scenario is largely undefined. We have used quadruplicate human cDNA arrays with 8000 targets to analyze the early gene response in cultures of human T/C28a cells that undergo apoptosis in response to 20 mM lithium chloride treatment. Incubation of cell cultures with 20 mM lithium chloride for five hours caused alterations in the steady-state mRNA levels of a large number of genes. RT-PCR and real-time RT-PCR confirmed the array results for ten of eleven selected targets. In addition to one protein primarily associated with apoptosis, genes identified as differentially expressed based on microarray data mainly encode proteins involved in basic cellular functions such as signaling, cell cycle control and growth, cell-cell interaction, solute transport and transcription control. We present a list of 50 genes that were differentially expressed in response to lithium chloride treatment and which may represent a reference for further studies to define the pathways governing the apoptotic response to lithium chloride.

Apoptosis↗
PubMed2000

The myoneural effects of lithium chloride on the nerve-muscle preparations of rats. Role of adenosine triphosphate-sensitive potassium channels.

The potential effects of lithium chloride on the neuromuscular transmission and muscular contraction were studied using in vitro and in vivo nerve-muscle preparations of rats. Addition of lithium chloride to the fluid bathing the isolated rat diaphragm produced a concentration-dependent inhibition of diaphragmatic contractions elicited by either indirect or direct electrical stimulation. The threshold concentrations were 1 mmol l(-1)and 3 mmol l(-1), respectively. Similarly, the intravenous administration of lithium chloride as bolus injections, produced a dose-dependent progressive inhibition of the indirectly- and directly-induced gastrocnemius muscle contractions during the 2-h period of investigation. The indirectly-induced contractions were much more sensitive to the inhibitory effect of lithium chloride than directly-induced contractions. Also, lithium chloride was found to be capable of enhancing the paralysis of the indirectly stimulated rat diaphragm in vitro and gastrocnemius muscle in vivo induced by either pipecuronium or succinylcholine. The combination of lithium chloride and pipecuronium led to a synergistic inhibition of the neuromuscular transmission, while the combination of lithium chloride and succinylcholine led to additive inhibition. Pretreatment with lithium chloride at the threshold concentrations enhanced the inhibitory effects of verapamil on diaphragmatic contractions elicited either indirectly or directly. The inhibitory effects of verapamil on the indirectly- and directly-induced rat gastrocnemius muscle contractions were potentiated by lithium chloride administration to rats. Glibenclamide was found to be capable of inhibiting the relaxant effects of lithium chloride on the indirectly- and directly-elicited contractions of rat diaphragm in vitro and rat gastrocnemius muscle in vivo, in a concentration- and dose-dependent manner, respectively. Doubling the concentration of magnesium in the bathing fluid potentiated the inhibitory effects of the threshold concentrations of lithium chloride on the diaphragmatic contractions induced either indirectly or directly. Pretreatment with 4-aminopyridine or barium chloride inhibited the relaxant effects of lithium chloride on the indirectly- and directly-elicited diaphragmatic contractions. The inhibitory effects of diazoxide on the indirectly-evoked contractions of rat diaphragm in vitro and rat gastrocnemius muscle in vivo were potentiated by lithium chloride. Pretreatment with glibenclamide inhibited markedly the combined effects of lithium chloride and diazoxide on the contractions of the diaphragm and gastrocnemius muscles induced indirectly. Additionally, the intravenous administration of lithium chloride into rats as bolus injections produced a dose-dependent progressive increase in plasma potassium level and a dose-dependent progressive decrease in the intracellular levels of adenosine triphosphate in the sciatic nerve and gastrocnemius muscle. It is concluded that lithium chloride, via activation of adenosine triphosphate- sensitive potassium channels, acts presynaptically to inhibit the neuromuscular transmission and acts at the muscle membrane to inhibit the muscular contraction.

ATP-Binding Cassette Transporters↗
PubMedDate not supplied

Effects of lithium chloride on muricidal behavior in rats.

Lithium chloride at two different doses (1 mEq/kg and 2 mEq/kg) IP BID for 10 days failed to inhibit muricidal behavior in rats. Lithium chloride at the higher dose caused neurotoxicity in 6 of 11 rats as measured by the rotorod. These dosages generated serum levels of 0.70 and 1.00 mEq/L respectively. The same behavior was blocked by imipramine HC1 at an ED50 of 8.5 mg/kg 45 min following a single IP injection without evidence of neurotoxicity by the rotorod method. These results indicate that lithium chloride is unlike the tricyclic agents in the muricide test. Therefore, if its clinical antidepressant activity is substantial, it may be most effective in a neurochemically different class of depressives than the tricyclics.

Aggression↗