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PubMed1993

Interleukin-1 mediates the behavioral hyperalgesia produced by lithium chloride and endotoxin.

The sickness-inducing agents lithium chloride (LiCl) and lipopolysaccharide (LPS) produce a long-lasting facilitation of the nociceptive tailflick reflex. Many of the behavioral and physiological changes produced by illness are mediated by interleukin-1 (IL-1) released from monocytes stimulated by the pathogenic substance. Monocytes also produce an IL-1 receptor antagonist (IL-1ra) which has been sequenced and cloned. The present experiments report that IL-1 can itself produce hyperalgesia as assessed by tailflick to radiant heat, and that recombinant IL-1ra blocks the hyperalgesia produced by LiCl and LPS.

Animals↗
PubMed1985

[Effect of lithium chloride on thyroid structural elements in the rat and on the balance of calcitropic hormones].

Chronic experiments were performed to study the effect of lithium chloride on morphological and functional characteristics of rat thyroid and on the endocrine regulation of calcium metabolism. As a result of a prolonged exposure to low doses of lithium the thyroid manifests the signs of activation of tissue structures. As the lithium dose is raised, the thyrostatic effect of lithium occurs according to the mechanism similar to the Wolff-Chaikoff effect (colloid accumulation by follicles and suppression of hormones secretion into blood). Lithium chloride stimulates calcitonin production by C cells of the thyroid. However, the increase of the basal level of calcitonin has no substantial effect on calcium metabolism in the animals, since such an increase is accompanied by increment of the production of the physiological antagonist parathyroid hormone by the secretory cells of the parathyroid glands.

Animals↗
PubMedDate not supplied

[The effect of lithium chloride on the desynchronization of "reserpine-induced depression"].

Lithium chloride (5 mg/kg i.m. for 10 days in the morning but not in the evening) prevented effectively desynchronization of "reserpine depression" in mice and rats: the spectra and structure of the rhythms of behavioral parameters (open field), body temperature, content of serotonin and its metabolites in the brain and that of glucocorticoids in blood plasma were almost the same as those in intact animals; the circadian harmony of all parameters were correlated in the best manner and their mean circadian values were restored.

Adrenergic Uptake Inhibitors↗
PubMed1994

Effect of lithium chloride on testicular delta 5-3 beta, 17 beta-hydroxy steroid dehydrogenase, acid phosphatase and gametogenesis in Bufo melanostictus.

Injection of lithium chloride at the dose of 200 micrograms/toad/alternate day for 7, 14 and 21 days caused a significant reduction in the activities of testicular delta 5-3 beta, 17 beta-hydroxysteroid dehydrogenase and acid phosphatase enzymes. There was a marked inhibition in spermatogenesis in lithium chloride treated toad for 14 and 21 days of treatment, but 7 days of treatment has no effect.

17-Hydroxysteroid Dehydrogenases↗
PubMed1999

Altered intracellular calcium level in association with neuronal death induced by lithium chloride.

In this study, we examined the effects of lithium chloride (LiCl) on the intracellular calcium levels ([Ca2+]i), and the survival of immature and mature cultured cerebellar granule neurons (CGNs) grown in medium containing high (25 mmol/L) or normal (5 mmol/L) potassium (K+) levels. LiCl dramatically reduced [Ca2+]i in immature CGNs maintained in high K+ (HK) medium and in those switched to serum containing normal K+ (NK) medium for 1 to 2 days. This reduction in [Ca2+]i led to massive neuronal death of immature neurons developed in both HK and NK medium. In mature (cultured 5-8 days in vitro) CGNs, LiCl exhibited potent toxicity when cells were grown in HK medium, and led to increased [Ca2+]i. Exposing mature CGNs to serum deprivation and normal extracellular K+ concentrations decreased [Ca2+]i and induced cell death, while the addition of LiCl in these conditions further decreased [Ca2+]i but prevented cell death. The morphologic features revealed by Nomarski optics further confirmed these effects of LiCl on neuronal survival. Together, these findings indicate that the effects of LiCl on [Ca2+]i and neuronal death, and the association between [Ca2+]i and cell death, depend on the developmental stage of CGNs and the growth conditions to which they are subjected. These findings may help in understanding the mechanism of neurotoxicity of LiCl during therapy.

Animals↗
PubMed1983

Acquisition of lithium chloride- and radiation-induced taste aversions in hypophysectomized rats.

The effects of hypophysectomy on the acquisition of conditioned taste aversions following injection of lithium chloride and following exposure to ionizing radiation were studied using a two-bottle preference test. Hypophysectomy did not disrupt the acquisition of a taste aversion following either treatment. The results are interpreted as: (a) suggesting that pituitary/adrenal hormones do not mediate the acquisition of a conditioned taste aversion following injections of lithium chloride or following exposure to ionizing radiation in a two-bottle preference test, and (b) consistent with other research suggesting that the involvement of pituitary/adrenal hormones in taste aversion learning may be related to the conflict induced by using a one-bottle test and not to the learning itself.

Animals↗
PubMed1988

Haloperidol, chlorpromazine and lithium chloride antagonize the excitatory action of forskolin and of some gut peptides on guinea-pig myenteric neurones.

The effects of haloperidol, chlorpromazine and lithium chloride on electrical behaviour of AH/type 2 myenteric neurones from guinea-pig ileum as well as on the excitatory action of forskolin and of some gut peptides were studied. Haloperidol and chlorpromazine decreased the excitability of AH/type 2 myenteric neurones which was evidenced from the inhibition of spontaneous and electrically-evoked action potentials recorded intracellularly from neurones. Forskolin caused excitation in AH/type 2 neurones which mimicked the changes in neuronal behaviour that occur during the slow synaptic excitatory potentials (EPSP) in the same type of neurones: membrane depolarization, augmented excitability and increased input membrane resistance. Haloperidol, chlorpromazine and lithium chloride blocked the excitatory action of forskolin. Vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK) and bombesin excited the AH/type 2 myenteric neurones in a manner similar to that of forskolin. Haloperidol and chlorpromazine antagonized the excitatory actions of VIP, CCK, and bombesin. The results indicated that the antipsychotic drugs tested decrease the excitability of the AH/type 2 myenteric neurones and this could partly account for their side effects observed in clinical practice. The present data provided supporting evidence for the role of cyclic adenosine-3', 5'-monophosphate (cyclic AMP) in the regulation of excitability of AH/type 2 myenteric neurones and for the function of cyclic AMP as a second messenger in the action of some gut peptides.

Action Potentials↗
PubMedDate not supplied

Inhibition of experimental allergic encephalomyelitis by lithium chloride: specific effect or nonspecific stress?

Intraperitoneal injections of lithium chloride inhibited development of experimental allergic encephalomyelitis (EAE) in rats. The degree of inhibition was inversely related to the intensity of the immunologic stimulation, which depended on the choice of adjuvant. High dosage of lithium, the intraperitoneal route, and an intermittent schedule of administration were required to achieve suppression of EAE. This suggested that the immunosuppression was a toxic effect, mediated, at least in part, through the hypothalamic-pituitary-adrenal cortex axis. This hypothesis was supported by evidence that the lithium treatment schedule, especially the intermittent schedule, had caused adrenal cortical activation with thymolysis in intact rats and that it was lethal to adrenalectomized rats. Lithium also inhibited EAE produced by adoptive immunization, thus implicating the efferent arm of the immune response. A single dose of lithium was effective in this form of EAE, even in adrenalectomized rats. Therefore lithium affects EAE by both specific immunosuppressive and nonspecific adrenocortical-dependent mechanisms.

Adrenal Glands↗
PubMed1990

Effects of lithium chloride on testicular steroidogenic and gametogenic functions in mature male albino rats.

The present study was undertaken to evaluate the effects of lithium, an antimanic drug, on steroidogenic and gametogenic functions of testis in the laboratory rat. Adult male rats of Wistar strain maintained under standard laboratory conditions (L:D, 14h:10h), were injected (S.C) with lithium chloride at the dose of 0.1 mg, 0.2 mg and 0.4 mg/100 g body weight/day for 21 days. All the treated animals along with the vehicle treated controls were sacrificed 24 hours after the last injections. Testicular steroidogenic activity was evaluated by measuring the activities of two steroidogenic key enzymes, delta 5-3 beta hydroxysteroid dehydrogenase (delta 5-3 beta-HSD) and 17 beta hydroxysteroid dehydrogenase (17 beta-HSD). Gametogenic capacity was determined by counting the number of germ cells at stage VII of seminiferous cycle. Plasma levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL) and testosterone (T) were measured by radioimmunoassay (RIA). Administration of lithium chloride at a dose of 0.1 mg/100 g body wt. for 21 days led to insignificant changes of plasma FSH, LH, PRL and T along with unaltered activities of testicular delta 5-3 beta-HSD, 17 beta-HSD activities and gametogenesis. In contrast, 0.2 mg of lithium treatment for 21 days causes a significant reduction of plasma FSH (P less than 0.01), LH (P less than 0.001), PRL (P less than 0.001) and T (P less than 0.001) along with inhibition of testicular delta 5-3 beta-HSD activity (P less than 0.01) and 17 beta-HSD activity (P less than 0.001). Gametogenic activity does not exhibits any significant reduction in the number of preleptotene spermatocytes (PLSc) and midpachytene spermatocytes (mPSC) while significant reduction in the number of spermatogonia A (Asg) (P less than 0.01) and Step 7 spermatids (7Sd) (P less than 0.001) were observed at stage VII of seminiferous cycle when compared to control. The degree of detrimental effects of lithium on testicular activity became more prominent at the dose of 0.4 mg/100 g body wt. The results of our experiments suggest that lithium administration might be associated with significant adverse effects on testicular activities. Furthermore, since hormonal changes and altered gametogenic activities were evident when plasma lithium concentration was below or within the therapeutic range, our data may have some potential clinical implications.

Animals↗
PubMed1988

Rabbit lung after inhalation of lithium chloride.

Rabbits were exposed to aerosols of lithium chloride in metal concentrations of 0.6 and 1.9 mg/m3 (mass median aerodynamic diameter of 1 micron) for 4-8 weeks, 5 days/week, 6 h/day. The lungs were studied by light and electron microscopy, with particular reference to inflammatory changes, structure of alveolar macrophages and alveolar epithelial cells. Macrophages recovered by lung lavage were studied by light and electron microscopy and their oxidative metabolic activity was measured. The content of phospholipids was analysed in lung tissue. Exposure to lithium produced no significant effects. It thus seems that Li+ is less toxic to the lung than the other metals investigated with the same test system, e.g. Ni2+, Cd2+, Co2+, Cr3+ and Cr6+.

Administration, Inhalation↗
PubMed1998

Lithium chloride does not inhibit the proliferation of L6 myoblasts by decreasing intracellular free inositol.

We conducted a series of experiments to determine whether lithium chloride (LiCl) inhibited the proliferation of L6 myoblasts by reducing the availability of intracellular free inositol. After the myoblasts were plated in DMEM + 10% fetal bovine serum (FBS) for 24 h, medium was replaced with DMEM + 10% FBS containing 0 (control), 5, 10, or 20 mM LiCl. Cell number, protein content, and [3H]thymidine incorporation into DNA were determined at 24-h intervals. Control cells exhibited a 3.8-fold increase in cell number by 96 h in culture. Although 5 mM LiCl did not affect the rate or extent of proliferation, 10 and 20 mM LiCl caused 36 and 86% decreases, respectively (P < .05), in cell number by 96 h in culture. The effects of LiCl could not be overcome by the addition of free inositol (up to 20 mM) to the medium. Lithium chloride caused 4.6- and 7.3-fold increases (P < .05) in lactate dehydrogenase activity in culture media after 96 h of exposure to 10 and 20 mM LiCl, respectively, indicating loss of viability after chronic treatment. However, the acute effects of LiCl after 24 h of treatment were reversible, as indicated by a rapid resumption of proliferation following removal of LiCl. Concentrations of 5, 10, and 20 mM LiCl caused 4.7-, 8.2-, and 9.1-fold increases (P < .05), respectively, in the accumulation of [3H]inositol within the inositol monophosphate pool. Treatment of cells with 10 and 20 mM LiCl also increased (P < .05) label recovered as inositol bisphosphate. Rather than depress phosphoinositide synthesis, the addition of 10 and 20 mM LiCl dose-dependently increased (P < . 05) the incorporation of [3H]inositol into phosphatidylinositol and phosphatidylinositol-4-phosphate. These results indicate that LiCl does not decrease proliferation of L6 myoblasts via a depletion in the intracellular free inositol pool. Instead, LiCl may block the hydrolysis of phosphatidyl inositides.

Animals↗
PubMed1985

Inhibition of dimethyl sulfoxide-induced Friend erythroleukemia cell differentiation in vitro by lithium chloride.

This report describes the ability of ultra-pure lithium chloride (LiCl) to influence the growth kinetics and differentiation of Friend erythroleukemia cells in vitro. LiCl (0.2-50 mEq/l) was effective in reducing the ability of Friend cells to grow in liquid suspension culture (p less than or equal to 0.001). In addition, the capacity of these erythroleukemic cells to respond to the inducing agent dimethyl sulfoxide (DMSO) was also significantly reduced (p less than or equal to 0.001). These results demonstrate that LiCl can influence not only the proliferation of erythroleukemia cells but also their subsequent differentiation after exposure to such chemical inducers.

Animals↗
PubMed1976

The effect of lithium chloride on morphine- and pyrogen-induced hyperthermia in rats.

In rats, doses of morphine between 2.5 and 20 mg/kg produced hyperthermia, 50-400 mg/kg lithium chloride induced dose-dependent hypothermia. These doses of lithium chloride inhibited morphine- and pyrogen-induced hyperthermia. The hypothermic effect of lithium may be due to the replacement of sodium ions by lithium ions in the hypothalamus. The antagonism between morphine and lithium is nonspecific.

Animals↗
PubMed1982

The influence of age and sex on weight variation in rats treated chronically with lithium chloride.

Weight increase is a common side-effect after chronic lithium salt treatment in man. This effect has not always been found in animal models using the rat. The possibility that the age and sex of animals might interfere with the results was studied, using groups of male and female rats, 2, 5, and 12 months old, injected intraperitoneally twice daily for 28 days with a solution of lithium chloride, or sodium chloride as control. The dose used was 1.5 meq./kg body weight (total daily dose of 3.0 meq./kg). In 2 month old animals, lithium induced an increase in weight significantly greater than that of the controls in the female group, while the weight of the male rats in this age group remained indistinguishable from the control rats. The 5 and 12 month old lithium treated female rats showed no differentiation in weight. Lithium treatment of the males in these two age groups caused a large number of deaths and, considering only those animals which survived, average weights were significantly less than those of control in the 5 month olds rats, and equal to control in the 12 month olds. It is concluded that age and sex have to be taken into consideration when studying the effects of chronic lithium treatment on the weight of rats.

Age Factors↗
PubMed1991

The effect of lithium chloride on granulocyte-macrophage progenitor cells (CFU-GM) and clonogenic leukaemic blasts (CFU-L) in the cultures in vitro.

The influence of lithium chloride on the proliferation of normal granulocyte-macrophage progenitor cells (CFU-GM) and clonogenic blasts (CFU-L) from patients with acute myeloid leukaemia in the semisolid cultures in vitro was investigated. It was observed that while lithium chloride with the concentration of 2 mmol/l increases the number of CFU-GM colonies, it does not increase the number of CFU-L colonies and clusters. Our studies indicate that lithium salts can be used for the treatment of patients with acute myeloid leukaemia after intensive chemotherapy.

Cell Division↗
PubMedDate not supplied

Effects of histamine and H1 and H2-receptor antagonists on the wet-dog-shaking episodes in rats induced with lithium chloride.

In the experiments carried out on Wistar rats it was demonstrated that histamine administered intraventricularly had no effect on the number of wet-dog-shaking episodes induced with lithium chloride. Thenalidine and antazoline, antagonists of the H1 receptor, and cimetidine and ranitidine, antagonists of the H2 receptor reduced the number of shaking episodes proportionally to the dose. These results may suggest that the reduction of the number of shaking episodes induced with lithium chloride was connected with blockade of histamine receptors, although an indirect effect of H1 and H2-receptor antagonists on the serotoninergic and cholinergic systems cannot be ruled out.

Animals↗
PubMed1978

Acute and chronic effects of lithium chloride on physiological and psychological measures in normals.

In the acute experiment six healthy volunteers were given orally two doses of lithium chloride, 16 and 32 mmol, and placebo sodium chloride 32 mmol in a double-blind standardized procedure, with a 1-week interval between treatments. Compared to sodium, lithium produced a decrease in subjective well-being, decrease of skin conductance fluctuations, and increase in plasma calcium concentrations. Dose-related effects were maximal at the first hour after ingestion, decreasing or disappearing at 3--5 h. Most effects did not correlate with plasma or erythrocyte lithium concentrations, but drug effects and feelings of nausea were highly correlated. Accordingly, most acute effects seemed due to peripheral drug effects. In the chronic experiment six healthy volunteers were given orally 16 mmol of lithium chloride or sodium chloride (placebo) twice a day for 1 week in a double-blind standardized procedure with a 2-week interval between treatment weeks. Compared to placebo, lithium produced feelings of subjective impairment, an increase in EEG slow waves and of auditory evoked response variability, a deficit in long-term memory, and an increase in plasma magnesium concentrations. Most lithium effects did not correlate with plasma or erythrocyte lithium concentrations.

Adult↗