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PubMed2005

Lithium-mediated downregulation of PKB/Akt and cyclin E with growth inhibition in hepatocellular carcinoma cells.

We studied in vitro effects of glycogen synthase kinase 3beta (GSK3beta)-inhibitor lithium on the growth of hepatocellular carcinoma (HCC) cells. Lithium induced strong growth inhibition (> 70%) in 75% (n = 9 of 12) of cell lines, apparently independent from the status of major genes that are mutated in HCC including p53, p16(INK4a), beta-catenin and Axin1. Comparative studies with a growth-sensitive Huh7 and growth-resistant Hep40 cell lines showed that lithium induces growth arrest in Huh7 cells but not in Hep40 cells. Lithium induced the accumulation of N-terminally phosphorylated inactive form of GSK3beta with concomitant increase in beta-catenin and beta-catenin/TCF transcriptional activity in both cell lines. This suggests that lithium-mediated HCC growth inhibition is independent of its well-known stimulatory effect on Wnt-beta-catenin signaling. The main differences between Huh7 and Hep40 responses to lithium treatment were observed at the levels PKB/Akt and cyclin E proteins. Lithium induced depletion of both proteins in growth-sensitive Huh7, but not in growth-resistant Hep40 cells. PKB/Akt and Cyclin E are 2 major proteins that are known to be constitutively active in HCC. The targeting of both proteins with lithium may be the main reason why most HCC cells are responsive to lithium-mediated growth inhibition, independent of their p53, retinoblastoma and Wnt-beta-catenin pathways. The exploration of molecular mechanisms involved in lithium-mediated growth inhibition in relation with PKB/Akt and cyclin E downregulation may provide new insights for therapy of liver tumors.

Carcinoma, Hepatocellular↗
PubMed1999

Lithium chloride-induced cardiovascular changes in rabbits are mediated by adenosine triphosphate-sensitive potassium channels.

The effect of lithium chloride on the mean arterial blood pressure, heart rate and heart contractility was evaluated in rabbits. The intravenous administration of 50 mg kg-1 lithium chloride as a bolus injection into rabbits produced a progressive decrease in the mean arterial blood pressure, heart rate and heart contractility during the 2-h period of investigation. Pretreatment of animals with 5 mg kg-1 glibenclamide, a potent inhibitor of adenosine triphosphate-sensitive potassium channels, markedly inhibited the cardiovascular changes induced by lithium chloride. Doubling the dose of glibenclamide nearly abolished these effects of lithium chloride. Similarly, lithium chloride produced a concentration- dependent relaxation of noradrenaline-induced contractions in isolated aortic strips of rabbits. This relaxant effect of lithium chloride was inhibited by pretreatment of the aortic strips with glibenclamide. Doubling the concentration of glibenclamide in the bathing fluid nearly abolished the effect of lithium. Diazoxide and verapamil potentiated the relaxant effect of lithium chloride on the isolated noradrenaline-contracted aortic strips. Pretreatment with glibenclamide markedly reversed the effect of diazoxide but not that of verapamil. The intravenous administration of lithium was also found to be capable of increasing the plasma potassium level and of decreasing the intracellular levels of adenosine triphosphate in cardiac and vascular tissues in a time-dependent manner. The plasma sodium and calcium levels were not changed. These results provide evidence that the hypotensive and cardiac depressant effects of lithium chloride are mediated by activation of adenosine triphosphate-sensitive potassium channels.

Adenosine Triphosphate↗
PubMed1980

Transmembrane distribution of lithium and sodium in erythrocytes of depressed patients.

In this investigation the intracellular: extracellular distribution of lithium across the erythrocyte membrane (RBC lithium distribution) was studied in vitro and in vivo. The in vitro studies were conducted by incubating cells from drug-free subjects in lithium-containing physiologic media. The in vivo studies consisted of measurements of plasma and erythrocyte (RBC) lithium and sodium concentrations during lithium carbonate treatment. Previous observations of a correlation between in vitro and in vivo RBC lithium distribution values were verified, and it was found that addition of 0.1 mM ouabain to the in vitro incubation media abolished this correlation. To examine the relationship between RBC lithium distribution and specific clinical features of depression, in vitro studies were conducted with RBCs from 20 depressed patients and 14 nondepressed control subjects. The patients were categorized as having bipolar (manic-depressive), unipolar, or secondary depressive disorders. After in vitro incubation with lithium for 48 h, the RBCs from bipolar patients had lithium distribution values that were similar to those observed in ouabain-treated cells. It appears that the lithium transport characteristics of RBCs of bipolar patients may differ from those of other depressed patients or nondepressed subjects.

Depression↗
PubMed1995

Myo-inositol attenuates the enhancement of the serotonin syndrome by lithium.

Lithium elicits opposite effects on two behavioural syndromes in rats: enhancement of the 5-HT1A-linked serotonin syndrome and attenuation of the 5-HT2-linked wet dog shakes. The ability of intracerebroventricular (ICV) myo-inositol or forskolin to reverse the enhancement of the serotonin syndrome by lithium was tested in rats that were fed chronic dietary lithium or control diet and injected with the serotonin agonist 5-MeODMT (5-methoxy-N, N-dimethyltryptamine). Lithium enhanced the total serotonin syndrome score and particularly flat posture and tremor. Inositol, but not forskolin, mitigated the effects of lithium. Inositol was also injected in the lateral ventricle of rats pretreated with chronic dietary lithium or regular rat chow for 3 weeks and injected with carbidopa and L-5-hydroxytryptophan (5-HTP). Lithium attenuated wet dog shakes, but inositol had no significant effect on lithium-treated or control rats. These findings suggest that the enhancement of the serotonin syndrome by lithium may be related to lithium-induced inositol depletion.

5-Hydroxytryptophan↗
PubMedDate not supplied

An attempt to predict daily erythrocyte lithium fluctuations.

Erythrocyte lithium concentration, which is a better predictor of brain lithium levels than plasma lithium concentrations, possesses the disadvantage of precise hourly determination following the last intake. The variability in RBC lithium accumulation increases as the extracellular lithium concentration increases. This increase is also time dependent and it would be very useful if the pharmacokinetic rate constant were known. Unfortunately, low lithium levels do not allow measurements within confidence intervals. In this work, we tried to determine, in vitro, the kinetic rate constants in erythrocytes of healthy volunteers. Different high lithium loaded plasma-like media were used for an extrapolation procedure of constants allowing the determination of an erythrocyte load constant namely K0 = 0.0161 +/- 0.0005 h-1 at corresponding plasma lithium concentrations. The abnormalities of lithium transport determined by in vitro procedures would be very useful in understanding the etiology of affective illness. Lithium flux pre-controls corrected with this rate constant would be very helpful in enlarging laboratory time management.

Antimanic Agents↗
PubMed2003

Lithium in the long-term treatment of bipolar disorders.

Usefulness of lithium in the prophylaxis of bipolar disorders has been challenged for five major reasons. The authors review the empirical basis of these criticisms and come to the following conclusions. 1. Lithium efficacy is high and beyond reasonable doubt in classic manic-depressive illness. Bipolar patients presenting atypical features show a much poorer response rate to lithium. 2. There is no empirical evidence for a loss of lithium efficacy over time. 3. There is little evidence for discontinuation-induced refractoriness to lithium. 4. Lithium withdrawal phenomena are well established but seem to be rather specific to certain subgroups. Withdrawal phenomena seem to be common in atypical bipolar disorder but rare in fully stabilized classic manic-depressive illness. 5. Other factors limiting lithium efficacy in clinical practice (e. g., non-compliance) are not specific to lithium. In conclusion, prophylactic lithium does have major drawbacks and there is a clear need for more efficacious alternatives in non-classic bipolars. Compared to existing alternatives, lithium currently is to be considered the golden standard. This status might, however, be challenged by major alternative mood-stabilizers that are presently under clinical investigation.

Antimanic Agents↗
PubMed1981

Lithium carbonate in patients with small cell lung cancer receiving combination chemotherapy.

Lithium administration has been shown to attenuate the leukopenia associated with systemic chemotherapy. The results of a randomized trial of lithium in 45 patients with small cell lung cancer who received combination chemotherapy and radiation therapy are reported. Patients randomized to receive lithium were started on 300 mg three times daily for 18 days of every 21 day chemotherapy cycle. Patients who received lithium experienced significantly less mid-cycle leukocyte and neutrophil count depression and spent fewer days with leukopenia and neutropenia than control patients regardless of age or extent of disease. Patients who received lithium spent fewer days hospitalized and fewer days with fever in the presence of severe neutropenia than control patients. The cumulative risk of fever with signs of infection was greater in control patients regardless of age, disease extent or the presence of marrow involvement. Patients who were given lithium received significantly more chemotherapy than control patients. Patient survival was greatest in those with limited disease, in complete responders and in those who received more than 75 percent of their induction chemotherapy although it did not differ between the two study groups. The majority of patients required either reduction or discontinuation of lithium. Those who received lithium continuously demonstrated a higher objective response rate and longer survival than either patients in whom the lithium had to be discontinued or those randomized to the control group. Infection was an important cause of death in the control group and cardiovascular event occurred frequently in the lithium group, but the major cause of death in this patient population remains progressive malignant disease.

Carcinoma, Small Cell↗
PubMed1987

Mechanism of action of lithium on acetylcholine receptor metabolism in skeletal muscle.

Changes in the levels of cations within skeletal muscle are thought to mediate the neural regulation of turnover of extrajunctional acetylcholine receptors (AChRs). We have used lithium as a probe of these cation influences because of its resemblance to calcium and other ions. In the present experiments we studied the mechanism of action of lithium on AChR metabolism in cultured mammalian skeletal muscle. We measured the effects of lithium on AChR turnover (using [125I]alpha-bungarotoxin binding), and evaluated the resemblance of lithium and calcium in producing their effects on AChR metabolism. Our results provide insight into the mechanisms of action of lithium and the cellular processes controlling AChR metabolism in muscle. Lithium reduces the number of AChRs in skeletal muscle in vitro to a degree similar to that which we previously reported in vivo. Lithium appears to enter cells via both sodium and calcium channels. It then produces its effect on levels of AChRs primarily by selectively reducing AChR synthesis and insertion into the surface membrane. Lithium induces this change in AChR metabolism in a manner resembling neural and calcium-mediated effects on AChRs. Phosphoinositide pathways may be involved in the lithium-induced effects. Further analysis of the effects of lithium on AChR turnover should provide new information about the mechanisms underlying the cellular control of receptor metabolism.

Animals↗
PubMed1992

Lithium mimics dexamethasone in stimulating DNA synthesis by WI-38 cells.

Lithium interferes with the responses of neural and secretory cells to calcium-mobilizing agonists by blocking the generation of phospholipase C-dependent second messengers. However, the mechanism by which lithium stimulates the proliferation of other cells in response to agonists that do not activate phospholipase C remains obscure. We investigated the pathways that mediate the mitogenic action of lithium on WI-38 cells in a defined, serum-free medium. Lithium, like dexamethasone (Dex), potentiated DNA synthesis in response to the combination of insulin+epidermal growth factor (EGF) (+50%), but not in response to either growth factor alone or with Dex. As in the case of Dex, lithium could be added as late as 8 h following stimulation of quiescent cells by insulin+EGF without loss of potentiating activity. While DNA synthesis in control cultures was essentially complete by 24 h, lithium and Dex stimulated "late" DNA synthesis (24-30 h) 10-fold and 5-fold, respectively. The potentiating activity of Dex, but not that of lithium, was blocked by the specific glucocorticoid receptor antagonist, RU486. Both lithium and Dex stimulated log-phase growth, but only Dex increased saturation density. These data indicate that both lithium and Dex recruit into the cell cycle a subpopulation of cells with a longer mean prereplicative phase (G1). The effect of lithium on DNA synthesis in WI-38 cells may be mediated by the glucocorticoid response pathway at some point distal to activation of the glucocorticoid receptor, or by an independent mechanism that can be switched on late in G1.

Cell Line↗
PubMed1984

Plasma and erythrocyte choline concentrations in rats following chronic treatment with lithium or choline.

Rats were given daily injections of choline, lithium or lithium plus choline for either 11 or 18 days and red cell choline, glycine and glutathione levels were measured using proton nuclear magnetic resonance spectroscopy. In addition, plasma choline, plasma lithium and red cell lithium levels were measured 4 hr after the last dosage. Choline (1 mmol/kg) alone increased plasma but not red cell choline concentrations. Lithium (0.94 mmol/kg) elevated red cell choline levels but did not affect plasma choline concentrations. In contrast, red cell choline levels were not elevated in rats treated with a higher dose of lithium (1.88 mmol/kg). When choline was given in addition to the lower dose of lithium, a similar accumulation of red cell choline was observed suggesting that the lithium-induced choline accumulation was not enhanced by a greater availability of free choline. No differences were detected in red cell glycine or glutathione levels between any of the treatment groups. Therefore, lithium produced a specific (dose-dependent) accumulation of choline in rat erythrocytes. However, the 100% increase observed in rats was not as marked as the increased red cell choline levels reported in patients maintained on lithium (8 to 10-fold). This discrepancy supports the concept that species differences exist in red cell choline transport or metabolism.

Animals↗
PubMed1987

Effects of lithium on the pituitary-gonadal axis in the rat: evidence for dose-dependent changes in plasma gonadotropin and testosterone levels.

The purpose of the present study was to examine the effects of lithium, a drug which is now used rather widely in the treatment of acute mania and the prophylaxis of manic-depressive bipolar disorders, on the pituitary-gonadal function in the laboratory rat. Sexually adult male rats, maintained under standardized laboratory conditions (LD 14: 10; lights on at 06:00 h, CST), were injected (ip) with lithium chloride both acutely for 1 day and chronically for 5 days, and by utilizing a low and high dose. For the low dose, lithium was injected twice daily (at 10:00 and 15:00 h) at 2.5 meg/Kg for 1 and 5 days, whereas in the high dose groups, also receiving lithium twice daily and at the same hours, the dosages were 5 meq/Kg for 1 day and 3.5 meq/Kg for 5 days. Animals were sacrificed 4 hours after the last lithium (or saline) injections. Plasma and pituitary levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH), and plasma levels of testosterone (T) were measured by radioimmunoassay (RIA). The administration of the low dose led to a significantly higher (P less than 0.001) plasma FSH, but unaltered plasma LH, levels after 5 days. In contrast, the high dose lithium led to significant suppressions of plasma LH (P less than 0.02; on day 5) and FSH (P less than 0.001; on both day 1 and 5) levels. The levels of plasma T also showed a significant reduction following the low dose (P less than 0.02; on day 5), as well as the high dose lithium treatment, as evident after both 1 (P less than 0.02) and 5 (P less than 0.02) days. Regardless of the dosage, or the duration of treatment, pituitary gonadotropin levels remained unaltered following lithium. The results of our present experiments suggest that lithium administration, either acutely or on a chronic basis, might be associated with significant adverse effects on the pituitary-testicular axis. Furthermore, since some of the hormonal changes were evident when plasma lithium concentration was within the therapeutic range, our data may have potential clinical implications.

Aggression↗
PubMed1982

In vitro and in vivo inhibition by lithium of enkephalin binding to opiate receptors in rat brain.

The in vitro and in vivo effects of lithium ions on opiate receptor binding were studied in the cerebral cortex, the hippocampus and the basal ganglia of the rat. In vitro, lithium ions inhibited enkephalin binding to opiate receptors through a reduction in the number of binding sites, whereas the affinity was unchanged or only slightly decreased. In vivo, long term ingestion of lithium (3 weeks), during which the rats were maintained at a serum lithium level of approximately 1 mM, also inhibited enkephalin binding to rat neuronal membranes (P2-fractions) through a reduction of the number of opiate receptor binding sites, whereas the affinity was unchanged. No lithium could be detected in the suspension of neuronal membranes from the lithium-treated rats, and no difference in the concentration of endogenous opioid peptides was found between control rats and lithium-treated rats. The opiate receptors from control rats and lithium-treated rats did no display any difference in lithium sensitivity. This data suggest that administration of lithium to rats in small doses reduces opiate receptor binding of enkephalin.

Animals↗
PubMed1990

Effects of treatment with a lithium-imipramine combination on components of adenylate cyclase in the cerebral cortex of the rat.

This study was aimed at investigating the effects of treatment with a lithium-imipramine combination on the activity of adenylate cyclase in membranes from the cerebral cortex of the rat. Treatment with (1) lithium for 2 weeks, yielding a level of lithium in serum of 0.54 +/- 0.12 mmol/l, (2) imipramine for 4 weeks (10 mg/kg i.p. twice per day) and (3) a combination of the two drugs reduced isoprenaline-induced stimulation of adenylate cyclase by GTP, with a greater decrement with the combined treatment. None of the treatments exerted any effect on the activity of the enzyme stimulated by GTP alone. Lithium ex vivo inhibited the calcium (Ca2+)- and Gpp(NH)p-stimulated activity of adenylate cyclase, but imipramine ex vivo did not affect the activity of adenylate cyclase, stimulated by these activators. The lithium-imipramine treatment reduced Ca2(+)- and Gpp(NH)p-stimulated activity of adenylate cyclase, but this was not different from that observed in the lithium-treated group. In conclusion, the beta-adrenoceptor-stimulated adenylate cyclase was affected markedly by administration of lithium and imipramine together. In contrast to lithium ex vivo, imipramine ex vivo did not impair the activity of either the guanine nucleotide regulatory protein or the catalytic subunit, since no change in activity was observed in the presence of beta,gamma-imidoguanosine-5' triphosphate (Gpp(NH)p) or Ca2+. Furthermore, lithium ex vivo exerted its post-receptor effects on the adenylate cyclase, independent of imipramine. The decrement in activity of beta-adrenergic adenylate cyclase, induced by administration of the two drugs together may partly be involved in the therapeutic action of the augmentation of antidepressants by lithium in refractory depression.

Adenylyl Cyclases↗
PubMed1992

Prospective multicentre study of pregnancy outcome after lithium exposure during first trimester.

Lithium carbonate is an effective drug for prophylaxis and treatment of major affective disorders. In-utero exposure to lithium during the first trimester of pregnancy might be associated with an increased risk of cardiac malformations, especially the rare Ebstein's anomaly. We prospectively recruited and followed 148 women (mean age 30 years, SD 5 range 15-40) using lithium during the first trimester of pregnancy, who consulted four teratogen information centres in the USA and Canada. Pregnancy outcome was compared with that of controls matched for maternal age. We had complete follow-up of pregnancy outcome in 138 of 148 patients recruited. In the other 10, fetal echocardiograms were available but postnatal follow-up was not done. Mean daily dose of lithium was 927 mg (SD 340). Rates of major congenital malformations did not differ between the lithium (2.8%) and control (2.4%) groups. 1 patient in the lithium group chose to terminate pregnancy after Ebstein's anomaly was detected by a prenatal echocardiogram. There was 1 ventricular septal defect in the controls. Birthweight was significantly higher in the lithium-exposed infants than in the controls despite identical gestational ages (3475 [660] g vs 3383 [566] g, p = 0.02). The true difference in birthweight might have been even larger, since significantly more women using lithium than controls were cigarette smokers (31.8% vs 15.5%, p = 0.002). These results indicate that lithium is not an important human teratogen. Women with major affective disorders who wish to have children may continue lithium therapy, provided that adequate screening tests, including level II ultrasound and fetal echocardiography, are done.

Abnormalities, Drug-Induced↗
PubMed1985

Lithium and twenty-four hour rhythms of serum corticosterone, prolactin and growth hormone in pigmented eye rats.

Lithium, a widely used substance for the treatment of manic-depressive illness, has been reported to alter the phase relationships of a variety of biological rhythms. We have previously found that lithium affects serum melatonin differently in albino compared to pigmented eye rats. The present study was undertaken to investigate the effect of lithium on pituitary rhythms in pigmented eye rats. Six point 24 hour maps were generated throughout a 12 hour light/12 hour dark lighting regime on separate groups of individually housed adult male Long Evans rats (with pigmented eyes), maintained for six weeks on ad lib water and either normal lab chow or lab chow supplemented with 50 mM/Kg of lithium chloride. Animals were sacrificed by rapid decapitation with care to ensure that blood samples were obtained from subjects in the resting, undisturbed state. Plasma lithium levels were 0.57 +/- 0.02 mEq/1. In comparison to normal controls, lithium treatment suppressed body weight by 19%, and increased water intake by 100%. Absolute corticosterone levels were not altered by lithium, but the 24-hour pattern was significantly changed. Growth hormone levels were significantly reduced by lithium treatment without alteration of the 24-hour pattern. Prolactin levels were significantly reduced by lithium and the normal 24-hour variation was attenuated. Comparison of these effects of lithium in pigmented eye rats with similar data from albino rats suggests that the effects on growth hormone, body weight and water intake were similar; however, the effects on prolactin and corticosterone differed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Conditions that lithium inhibits or potentiates vasopressin V1-receptor-mediated platelet aggregation and [Ca++]i mobilization.

1. Besides clinical use, there are many explanations for the mechanism of action of lithium. Although it is shown that lithium may reduce the supply of inositol that is required to sustain phosphoinositide synthesis, evidence exists concerning the potentiating effect of lithium on this pathway. We therefore decided to evaluate conditions in which lithium inhibits or potentiates platelet aggregation and calcium response induced by vasopressin. 2. Platelet aggregation was measured by the photometric method, and changes in intracellular free calcium were measured using fura-2/AM. 3. We show an inhibitory action of neomycin on vasopressin-induced platelet aggregation. Lithium, according to the preincubation time, could both potentiate or inhibit platelet aggregation and calcium responses induced by vasopressin. The inhibitory effect of lithium on platelet aggregation is dependent on concentrations of both lithium and vasopressin and also the presence of indomethacin, for example, in the absence of indomethacin there was no clear inhibitory action of lithium on vasopressin-induced platelet aggregation. 4. These results show the importance of arachidonate metabolites concerning lithium effects on platelet V1-receptor signaling. In conclusion, because the arachidonate metabolites are responsible for the release of other active substances from platelets' granules, the aggregatory responses in the absence of indomethacin may be amplified, and this subsequently may change the net inhibitory action of lithium.

Arachidonic Acid↗
PubMed1990

Lithium enhances neuronal muscarinic excitation by presynaptic facilitation.

The mechanisms underlying the psychotropic actions of lithium are not established, but modulation of endogenous brain neurotransmitter systems is likely to be important. Several interactions of lithium with muscarinic responses have been reported, including a marked potentiation of seizures produced by muscarinic agonists. Because the mechanism by which lithium augments muscarinic seizures may be related to the mechanism by which it produces its psychotropic effects, we have studied the interaction of lithium and muscarinic agonists in vitro. Using rat hippocampal slices, we found that a muscarinic agonist, pilocarpine, increased postsynaptic neuronal excitability, but simultaneously decreased synaptic transmission because of presynaptic inhibition. Lithium did not alter pilocarpine's postsynaptic excitatory actions, but reversed its presynaptic inhibitory action, leading to markedly increased action potential firing. These presynaptic effects are not caused by alterations in presynaptic action potential shape or reliability of conduction, and do not involve pertussis toxin-sensitive G proteins. Activation of protein kinase C with phorbol-12,13-dibutyrate, or inhibition with H-7 and sphingosine, did not affect muscarinic presynaptic inhibition, but abolished lithium's ability to enhance synaptic transmission, suggesting that this effect of lithium involves protein kinase C. We propose that presynaptic facilitation accounts for lithium's potentiation of muscarinic seizures. Since these effects occur with concentrations of lithium used clinically, similar presynaptic effects in endogenous brain neurotransmitter systems may be important for lithium's psychotropic actions.

Animals↗
PubMed1995

In vitro binding of lithium using the cation exchange resin sodium polystyrene sulfonate.

Sodium polystyrene sulfonate, a cation exchange resin, should be useful in the treatment of lithium overdosage. This in vitro study was conducted to assess the ability of sodium polystyrene sulfonate to bind lithium, effects of pH on binding, binding efficacy in comparison to charcoal, and affinity for lithium versus potassium. Stock solutions of lithium were added to fixed amounts of sodium polystyrene sulfonate and charcoal. Lithium and potassium concentrations in supernatant were measured by flame photometry. Increasing concentrations of sodium polystyrene sulfonate bound more lithium. Changes in pH had little effect on lithium binding. Lithium is bound to sodium polystyrene sulfonate more readily than to charcoal. Potassium is preferentially bound to sodium polystyrene sulfonate over lithium. Sodium polystyrene sulfonate may provide a useful therapeutic modality in the treatment of lithium overdosage.

Binding Sites↗