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PubMed2000

In vitro iontophoretic release of lithium chloride and lidocaine hydrochloride from polymer electrolytes.

Ionically conducting polymers, frequently known as polymer electrolytes, are potential candidates as hosts for drugs to be delivered iontophoretically. The iontophoretic delivery of lithium or lidocaine from polymer electrolyte films through a cellophane membrane was examined using different delivery current regimes. Thin, mechanically strong, polymer electrolyte films were fabricated from poly(ethylene oxide) (PEO) with lithium chloride or lidocaine hydrochloride. Experiments showed that iontophoretic transport of both lithium chloride and lidocaine hydrochloride might be achieved from these PEO-based films. Cation transport number determinations give values for PEO-based films of about 0.4 for lithium chloride systems and 0.12 for lidocaine hydrochloride systems. The mechanism of transport from these PEO-based polymer electrolyte films allows the delivery of ionic salts such as lithium chloride and lidocaine hydrochloride to be controlled solely by current, thus providing a system that can deliver precise amounts of drug.

Anesthetics, Local↗
PubMed1992

Relationship between vomiting and taste aversion learning in the ferret: studies with ionizing radiation, lithium chloride, and amphetamine.

The relationship between emesis and taste aversion learning was studied in ferrets (Mustela putorius furo) following exposure to ionizing radiation (50-200 cGy) or injection of lithium chloride (1.5-3.0 mEq/kg, ip). When 10% sucrose or 0.1% saccharin was used as the conditioned stimulus, neither unconditioned stimulus produced a taste aversion, even when vomiting was produced by the stimulus (Experiments 1 and 2). When a canned cat food was used as the conditioned stimulus, lithium chloride, but not ionizing radiation, produced a taste aversion (Experiment 3). Lithium chloride was effective in producing a conditioned taste aversion when administration of the toxin was delayed by up to 90 min following the ingestion of the canned cat food, indicating that the ferrets are capable of showing long-delay learning (Experiment 4). Experiment 5 examined the capacity of amphetamine, which is a qualitatively different stimulus than lithium chloride or ionizing radiation, to produce taste aversion learning in rats and cats as well as in ferrets. Injection of amphetamine (3 mg/kg, ip) produced a taste aversion in rats and cats but not in ferrets which required a higher dose (> 5 mg/kg). The results of these experiments are interpreted as indicating that, at least for the ferret, there is no necessary relationship between toxin-induced illness and the acquisition of a CTA and that gastrointestinal distress is not a sufficient condition for CTA learning.

Amphetamine↗
PubMed2001

The effect of lithium chloride on the biooxidation of aqueous methanol/acetone mixtures.

Lithium chloride, more specifically the lithium cation, has been implicated in interference in biological systems. In the case of Escherichia coli, interference involves the Na+(Li+)/H+ antiporter transport system. The study reported here concerns the effects of LiCl on a mixed enrichment culture that is able to biodegrade both methanol and acetone under aerobic conditions. The results obtained using unsteady state continuous flow culture techniques demonstrate a significant disruptive effect of LiCl on culture performance. In addition, a reduction in the substrate-based biomass yield coefficient, which is a clear advantage as far as biotreatment process performance is concerned, also occurs. The ultimate fate of the LiCl was not determined.

Acetone↗
PubMed2002

Highly efficient separation of lithium chloride from seawater.

A complexing reagent composed of two bipyridine moieties enabled the efficient separation of lithium chloride through liquid membrane from seawater, in which 0.005% lithium chloride is contained (more than 99% metal chlorides are NaCl, KCl, MgCl2, and CaCl2). That is, two separations by our liquid membrane changed the molar ratio of LiCl from 0.005% to 80%. The striking characteristic of this compound is that the lithium ion is separated efficiently from alkali and alkaline earth metal ions without the lipophilic anion. Thus this new membrane system contructed by us offers a low-energy, low-cost, and environmentally friendly method to enable the routine use of lithium chloride separation from seawater.

Journal Article↗
PubMed1975

Effects of lithium chloride on parameters biosynthetic capacity for 5-hydroxytryptamin in rat brain.

Administration of lithium chloride to rats resulted in a biphasic, temporally related alteration in the brain's biosynthetic capacity for 5-hydroxytryptamine (5-HT). After 3 to 5 days of drug administration, the Vmax of the high affinity uptake of [14-C]tryptophan into striate nerve ending synaptosomes increased to 140% of control values. The stimulated uptake of radioactive precursor apparently resulted in an augmentation of tryptophan-to-5-HT conversion activity of the same magnitude in these synaptosomes. These events were succeeded by an apparently compensatory decrease in the Vmax of midbrain cell body and nerve-ending solubilized tryptophan-5-hydroxylase (EC 1.99.1.4). After 21 days of drug administration, [14-C]tryptophan uptake remained above control levels, but striate synaptosomal conversion activity had returned to control levels. In contrast, soluble midbrain and solubilized striate synaptosomal enzyme activity remained significantly below control values. In vitro lithium chloride at 10 or 53 mM had no effect on soluble tryptophan hydroxylase activity, but either concentration of lithium chloride significantly enhanced the uptake of [14-C]tryptophan into striate synaptosomes, and consequently also the synaptosomal conversion of tryptophan to 5-HT. Increasing tryptophan levels either by preincubation of synaptosomes with L-tryptophan or by administration of L-tryptophan loads (20-60 mg/kg) resulted in augmented [14-C]tryptophan uptake and conversion activity. The sequence of events that we observed after lithium treatment is consistent with receptor-mediated neuronal feedback regulation of tryptophan hydroxylase activity after stimulation of tryptophan uptake and conversion of 5-HT.

Animals↗
PubMed1985

The influence of lithium chloride on experimental autoimmune thyroid disease.

Lithium administration is known to be associated with the development of thyroid dysfunction; it also exerts an effect on the immune system. The effect of lithium on experimental autoimmune thyroid disease was studied in female August rats. Following immunization with rat thyroglobulin in Freund's complete adjuvant, lithium chloride was administered i.p. for 30 days to four groups at varying stages of the disease. Control animals received i.p. saline. Anti-thyroglobulin antibody levels (measured by ELISA) were significantly increased in rats given lithium immediately post-immunization (group B) compared to control animals (661 +/- 42 OD vs 448 +/- 68; mean +/- s.e., P less than 0.02). In contrast, animals which received lithium during the spontaneous resolution of the disease (group D) showed a significant fall in anti-TG antibody compared to controls (99 +/- 15 vs 27 +/- 15; P less than 0.001). Anti-TG antibody levels remained undetectable in animals which received lithium but were not immunized. The splenic T cell blastogenic response (as measured following phytohaemagglutinin stimulation) was significantly increased in rats receiving lithium prior to and during immunization (group A) (stimulation index 63.4 +/- 6.9 vs 10.2 +/- 2.4; P less than 0.001). Spontaneous cell proliferation of splenic lymphocytes was decreased in two lithium treated groups (group A P less than 0.005, group C P less than 0.05). There was no alteration in splenic weight or the degree of thyroid lymphocytic infiltration in any of the treated group. Lithium exerted both positive and negative influences on the immune system in rats immunized with thyroglobulin in adjuvant but did not induce autoantibody production in normal rats.

Animals↗
PubMed1984

Acute effects of lithium chloride on noradrenergic neurons from rat cerebral cortex.

Acute effects of lithium chloride upon the parameters of central noradrenergic function were assessed at either a therapeutic dose (2 m-equiv/kg) or a toxic one (10 m-equiv/kg) on rats. Lithium chloride lacked a direct effect on tyrosine hydroxylase (TH), monoamine oxidase (MAO), or catechol-O-methyltransferase (COMT) in concentrations up to 2 mM. A single i.p. injection of both studied doses inhibited MAO a hr later. Endogenous NA levels in frontal cerebral cortex were increased by a therapeutic dose and slightly increased by a toxic dose. Uptake of [3H]NA was increased in pretreated tissues at a therapeutic level but decreased by a toxic dose. The unmetabolized [3H]NA was always increased over controls.

Animals↗
PubMed1990

Plasma lithium as a marker of lithium chloride in wild Norway rats (R. norvegicus).

A parametric study was conducted to determine the efficacy of plasma lithium as a marker of lithium chloride ingestion and dose in conditioned taste aversion research with rats. Separate groups of male wild Norway rats were given 60, 120 and 240 mg/kg doses of a lithium chloride solution by gavage. At 0.5, 1, 2, 24, 48 and 72 hr after dosing, 2-3 cc samples of blood were taken from each rat: these were centrifuged and 0.5-1.0 cc specimens of plasma were frozen for later analysis. Flameless atomic absorption spectroscopy was then used to determine quantities (ppm) of lithium in these specimens. Analyses of the data revealed that plasma lithium was both dose and time dependent; however, uptake and elimination of the lithium was rapid (less than or equal to 48 hr for 60 and 120 mg/kg-dosed rats). Results showed that measurements of plasma lithium has some utility as a marker of lithium chloride ingestion in laboratory studies, but limited potential in field studies, of conditioned taste aversion with rats.

Animals↗
PubMed1999

Lithium chloride induces the expression of tyrosine hydroxylase in hNT neurons.

In the present study, several doses of lithium chloride were tested for their ability to induce the expression of tyrosine hydroxylase (TH) in neurons derived from a human teratocarcinoma cell line (hNT) after 5 and 10 days in vitro (DIV). Following immunocytochemical staining for tyrosine hydroxylase, the percentage of TH-positive neurons was determined and morphometric analysis, including mean soma profile area and neuritic length, was performed. hNT neurons responded to lithium treatment in a dose-dependent manner. In 5 DIV, the most effective dose of lithium chloride (1.0 mM) increased the number of TH-positive neurons approximately sixfold. In addition, both TH-positive hNT neuron mean soma profile area and neurite length were significantly larger than controls by 60 and 70%, respectively. Moreover, even after withdrawal of lithium chloride on day 5, the number of TH-positive neurons in 10 DIV cultures remained significantly increased. These data suggest that hNT cells are indeed responsive to lithium exposure and may serve as a continual source of TH-expressing neurons in new therapeutic approaches to degenerative brain disease.

Cell Differentiation↗
PubMed1986

Sex differences in gastric mucosal protection after 16, 16-dimethyl PGE2 and lithium chloride.

While the incidence of duodenal ulcer disease has been documented to be greater in men than in women, this observation has not been previously noted in animal studies of the upper gastrointestinal tract. In this study, we questioned whether the cytoprotective properties of 16, 16-dimethyl PGE2 were sex-related by comparing the degree of ethanol-induced hemorrhagic gastritis in male and female rats pretreated with 16,16-dimethyl PGE2 or lithium chloride. Animals receiving 16,16-dimethyl PGE2 or lithium chloride had significantly less ethanol-induced hemorrhagic gastritis (1.17 +/- 0.15 and 1.24 +/- 0.13, respectively, p less than 0.001) when compared with controls (2.69 +/- 0.10). Female rats treated with 16,16-dimethyl PGE2 had 59% less hemorrhagic gastritis than male rats treated similarly (0.76 +/- 0.14 vs 1.86 +/- 0.19 respectively, p less than 0.001). This sex-related difference in hemorrhagic gastritis was not noted in male and female rats receiving lithium chloride (1.24 +/- 0.15 vs 1.23 +/- 0.27, respectively). However, female rats treated with 16, 16-dimethyl PGE2 had significantly less hemorrhagic gastritis when compared with female rats receiving lithium chloride (0.76 +/- 0.14 vs 1.24 +/- 0.15 respectively, p less than 0.05).

16,16-Dimethylprostaglandin E2↗
PubMed1994

The effects of lithium chloride on the activity of the afferent nerve fibers from the abdominal visceral organs in the rat.

The effect of lithium chloride on the activity of the afferent nerve fibers from the abdominal organs was studied in anesthetized rats. The administration of the lithium chloride solution (0.15 M) over the mesentery increased afferent discharge rate of the splanchnic and vagal gastric nerve. Injection of the same solution into the portal vein caused an increase in afferent activity of the vagal hepatic nerve. Further, infusion of the same solution into the duodenum resulted in facilitation of the afferent activity of the splanchnic as well as vagal celiac nerves. The results may explain the mechanism played by lithium chloride as unconditioned stimulus in the conditioned taste aversion paradigm.

Abdomen↗
PubMed1980

The effect of lithium chloride on the replication of herpes simplex virus.

Lithium chloride inhibited the replication of type 1 and type 2 Herpes simplex virus at concentrations which permitted host cell replication. Virus polypeptide and antigen synthesis were unaffected while viral DNA synthesis was inhibited. The replication of two other DNA viruses, pseudorabies and vaccinia virus, was inhibited but there was no inhibition of two RNA viruses, namely, EMC and influenze virus.

Antigens, Viral↗
PubMed1992

Lithium chloride and immunomodulation in taste aversion conditioning.

Lithium chloride has been used in many studies of conditioning to induce taste aversion behaviour, and in some experiments investigating conditioning effects on immunity it has been used on the assumption that it is immunologically neutral. The studies reported here, however, indicate that LiCl is not immunologically neutral and when used to endow a UCS with noxious properties to enhance the behavioural response in taste aversion conditioned immunosuppression, it may antagonize the residual immunosuppression following initial UCS administration and also the conditioned immunosuppression occurring after CS reexposure. Therefore, conclusions drawn from studies of behaviourally conditioned immunomodulation where LiCl is used as part of either the CS or UCS may require reevaluation.

Animals↗
PubMed1980

Localization and quantitation of lithium in rat tissue following intraperitoneal injections of lithium chloride. II. Brain.

The distribution of lithium in the rat brain following chronic i.p. injections of lithium chloride has been determined by a radiographic dielectric track registration technique. The study indicated significant differences in lithium distribution in various areas of the brain. Consistently high levels were observed in the neocortex and putamen, and low concentrations in the cerebellum and white matter structures such as the corpus callosum and basis pedunculi. Intermediate levels were found in the thalamus, hypothalamus, septal nuclei, dentate gyrus, hippocampus and substantia grisea centralis.

Animals↗
PubMed1975

Changes in rat brain monoamine metabolism following the acute administration of lithium chloride in combination with antidepressant drugs.

The acute administration of lithium chloride resulted in a decrease in the concentration of serotonin, tyrosine, dopamine and noradrenaline in the rat brain. The antidepressant drugs imipramine, amitriptyline and Org GB94 did not reverse or potentiate the effect of lithium chloride on these monoamines or tyrosine. It is concluded that the ability of lithium salts to enhance the effect of antidepressant drugs in the treatment of endogenous depression cannot readily be explained by their synergistic action on brain monoamine metabolism.

Amitriptyline↗
PubMed2003

Effects of dextroamphetamine, lithium chloride, sodium valproate and carbamazepine on intraplatelet Ca2+ levels.

OBJECTIVE: To explore the possible involvement of second-messenger pathways in the pathophysiology of bipolar disorder and the mechanism of action of mood stabilizers, we investigated the effects of dextroamphetamine (a model for mania) and the most widely used mood stabilizers, lithium chloride, sodium valproate and carbamazepine, on intraplatelet levels of calcium ion ([Ca2+). DESIGN: In the first part of the study, dextroamphetamine was administered in vivo in a double-blind, placebo-controlled, crossover design. In the second part of the study, platelets from untreated subjects were incubated in vitro with dextroamphetamine, lithium chloride, sodium valproate or carbamazepine. PARTICIPANTS: Fifteen healthy men between 18 and 45 years of age. OUTCOME MEASURES: Basal, thrombin-induced and serotonin- (5-HT) induced intraplatelet [Ca2+] determined by means of fura-2 fluorescent intensity. RESULTS: In vivo administration of dextroamphetamine had no effect on basal or agonist-induced intraplatelet [Ca2+]. However, in vitro basal platelet [Ca2+] was significantly higher in samples incubated with dextroamphetamine (86.8 nmol/L [standard error of the mean, SEM, 3.9], p < 0.001), lithium chloride (76.4 nmol/L [SEM 3.1], p < 0.002), sodium valproate (82.7 nmol/L [SEM 3.7], p < 0.001) and carbamazepine (84.8 nmol/L [SEM 3.3], p < 0.001) than in the controls (58.2 nmol/L [SEM 2.3]). Thrombin-induced and 5-HT-induced peak cytosolic [Ca2+] were significantly greater than control levels in samples incubated with carbamazepine (277.1 nmol/L [SEM 19.9] v. 195.8 nmol/L [SEM 12.2], p < 0.002; and 153.0 nmol/L [SEM 8.2] v. 115.4 nmol/L [SEM 5.7], p < 0.003, respectively). CONCLUSIONS: This study does not support the involvement of intraplatelet [Ca2+] in the dextroamphetamine model of mania; however, the modulation of intraplatelet [Ca2+] by the mood stabilizers lithium chloride, sodium valproate and carbamazepine implicates intracellular [Ca2+] in the therapeutic mechanisms of these drugs and the pathophysiological basis of mania.

Adolescent↗