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PubMed1997

[Effects of lithium chloride and harringtonine on the differentiation, proliferation and c-myc proto-oncogene expression of HL-60 cells].

This research was to observe the effects of lithium chloride (LiCl) and Harringtonine (HT) on the proliferation and differentiation of HL-60 leukemia cells. The results obtained by liquid suspension culture, semi-solid colony culture and 3H-TdR incorporation into HL-60 cells indicated that different concentrations of LiCl (5-20 mmol/L) and HT (10(-8)-10(-5)mol/L) exerted the inhibitory effects in a dose-dependent manner on HL-60 cell proliferation respectively. When LiCl (10 mmol/L) and HT (10(-7) mol/L) were added together in the liquid culture or semi-solid culture of HL-60 cells, they showed much greater inhibitory effect than that by each agent separately. It was discovered that there was induction of the differentiation of HL-60 cells by lithium and HT and the induction of HL-60 cells differentiation by HT was markedly enhanced by the addition of low concentration of lithium. This work also showed that by treating HL-60 cells with lithium and HT, the expression of the c-myc proto-oncogene was markedly decreased as measured by RT/PCR-mRNA (P < 0.01). These findings provide some evidence of the mechanismcausing leukemic change and of the potential use of lithium and HT in the treatment of leukemia and in vitro purging of leukemic cells for autologous bone marrow transplantation.

Antineoplastic Agents↗
PubMed1988

Effects of lithium chloride and ethacrynic acid on experimental polycystic kidney disease.

Hydrocortisone acetate is known to produce polycystic kidney disease when administered to susceptible animals in the perinatal period. To assess whether sodium and water transport mechanisms are involved in cyst pathogenesis, we administered lithium, an inhibitor of such transport in the distal nephron, and ethacrynic acid, an inhibitor of sodium transport in the Loop of Henle, to hydrocortisone acetate treated newborn rats. Hydrocortisone acetate alone resulted in significant polycystic kidney disease with the development of uremia, hypokalemia, and shortened life span. Co-administration of lithium and hydrocortisone acetate increased the severity of cystic tubular change and further compromised renal function. Ethacrynic acid reduced the degree of cyst formation induced by the combination of lithium chloride and hydrocortisone acetate but otherwise had no effect. We conclude that fluid and electrolyte disturbance plays a significant role in cyst formation, but we are unable to ascribe that effect to a single ion. We also conclude that the antinatriuretic effect of glucocorticoids is not the principal factor in glucocorticoid induced polycystic kidney disease.

Animals↗
PubMedDate not supplied

Effect of lithium chloride on spermatogenesis, testicular delta 5- 3 beta- and 17 beta-hydroxysteroid dehydrogenase activities in toad (Bufo melanostictus).

The purpose of the present study was to show the effects of lithium on testicular activities in the toad. Adult male toads were injected with lithium chloride (200 micrograms/toad) of alternate days for 21 days. At the moment of sacrifice on 22nd day, lithium treated animal showed decreases in testicular weight and Leydig cell nuclear area along with inhibition of spermatogenesis and testicular delta 5-3 beta as well as 17 beta-hydroxysteroid dehydrogenase activities. The results of our present experiment suggest that lithium administration might be associated with significant adverse effects on testicular activity in toad.

17-Hydroxysteroid Dehydrogenases↗
PubMed1998

Separate populations of neurons within the paraventricular hypothalamic nucleus of the rat project to vagal and thoracic autonomic preganglionic levels and express c-Fos protein induced by lithium chloride.

The role of different hypothalamic nuclei, particularly the paraventricular nucleus (PVN), in the control of food intake and feeding behaviour is well known. It is also well established that lithium chloride (LiCl) causes various disorders in feeding behaviour. In this study, we analyzed the precise distribution of hypothalamic neurons activated by i.p. LiCl administration (LCA neurons) and compared it to that of hypothalamic neurons which project to autonomic preganglionic levels (HAP neurons). We also analysed the possibility that some neurons belong to both populations of nerve cells. To this end, a multiple-labelling technique, using two retrograde fluorescent tracers together with c-Fos-like immunohistochemistry, was performed. Fast Blue was injected in the dorsal motor nucleus of the vagus and Fluorogold (FG) in the thoracic intermedial-lateral cell column, to trace parasympathetic and sympathetic pathways, respectively. LiCl was used as stimulus for c-Fos-like immunohistochemistry. HAP neurons were located mainly in the dorsal, ventral and lateral regions of the parvocellular PVN, while LCA neurons were observed predominantly in the magnocellular region of the PVN rostrally to HAP neurons. A significant number of FG/Fos double-labelled neurons were located in the dorsal parvocellular subnucleus of the PVN (dp) in the LiCl-stimulated rats. We concluded that there is a clear segregation of LCA neurons from HAP neurons within the PVN. The presence of FG/Fos double-labelled neurons in the dp suggests that this nucleus could mediate a sympathetic response after LiCl administration.

Animals↗
PubMed2002

Chronic lithium chloride administration to rats decreases brain protein level of epsilon (epsilon) subunit of eukaryotic initiation factor-2B.

The eukaryotic initiation factor-2B (eIF-2B) can regulate translation and protein synthesis. We used Western blot analysis to quantify the protein level of the catalytic epsilon (epsilon) subunit of eIF-2B in brains of rats fed lithium chloride (LiCl) for 6 weeks so as to produce a brain lithium concentration that is therapeutically effective in bipolar disorder. The ratio of eIF-2B (epsilon) to actin protein was significantly reduced (P<0.01) in LiCl-fed rats, 0.86+/-0.06 (SE) compared to 1.2+/-0.07 in control rats. These results suggest that a therapeutic level of lithium may downregulate the synthesis of proteins whose translation depends on eIF-2B.

Animals↗
PubMed1988

Naloxone potentiation of effects of cholecystokinin and lithium chloride on oxytocin secretion, gastric motility and feeding.

Neurohypophyseal secretion of oxytocin (OT) in response to dehydration, hypovolemia, restraint, and parturition in rats is known to be potentiated by the opioid antagonist naloxone. The present studies demonstrated that stimulation of OT secretion by systemic injections of cholecystokinin (CCK) and lithium chloride (LiCl) likewise are potentiated by naloxone pretreatment. Moreover, the inhibitory effects of CCK and LiCl on gastric motility and feeding similarly were enhanced by naloxone. Because neurohypophyseal hormone secretion and inhibition of gastric motility are known to be mediated by oxytocinergic neurons projecting from the paraventricular nucleus of the hypothalamus, this parallel potentiation by naloxone of CCK- and LiCl-induced effects on OT secretion, gastric motility, and food intake suggests that one of the pathways involved in the central control of feeding behavior also may be oxytocinergic. These findings therefore provide evidence in support of an important role of endogenous opioid peptides in regulating OT secretion in a diffuse neuronal system that mediates an integrated neuroendocrine, autonomic, and behavioral response to CCK, LiCl, and perhaps other treatments that similarly affect ingestive behavior in rats.

Animals↗
PubMed1987

Preexposure and extinction effects of lithium chloride induced taste-potentiated aversions for spatially contiguous auditory food cues in rats.

Taste potentiated illness-induced aversions for noisy food were studied in Sprague-Dawley rats. The rats ate from receptacles containing salty food and a contiguous tone produced by speakers under the food followed by lithium chloride injections. In preference tests, the rats then avoided noisy food in favor of quiet food followed by extinction and spontaneous recovery of the auditory aversion over repeated nonreinforced trials. Other rats were given either 4 or 10 days of exposure to the noisy food prior to taste-toxicosis treatment. None of these rats subsequently avoided noisy food. The importance of spatial contiguity and methodological variation in associating nongustatory food cues with illness is discussed.

Animals↗
PubMed1991

Effect of lithium chloride on testicular steroidogenesis and gametogenesis in immature male rats.

The present study was performed on immature male rats aged 35 days. Subcutaneous injections of lithium chloride at a daily dose of 2.0 mg/kg for 15 days resulted in significant inhibition of spermatogenesis at stage VII of the seminiferous epithelial cycle. Spermatogonia A, preleptotene spermatocytes and step 7 spermatids were decreased in number in comparison to controls. Serum levels of FSH, LH, PRL, and testosterone were decreased. Activities of testicular delta 5-3 beta-hydroxysteroid dehydrogenase and 17 beta-hydroxysteroid dehydrogenase were suppressed along with a low caudal epididymal sperm count in comparison with controls. When the treatment was prolonged for 20 and 25 days, it showed an additional significant diminution in accessory sex organ weights and number of midpachytene spermatocytes at stage VII in comparison to control animals of corresponding age. It is concluded that lithium has an adverse effect on testicular function in immature rats by reducing serum levels of FSH, LH, PRL, and testosterone. Furthermore, since hormonal changes and altered spermatogenic activities were evident when the serum concentration of lithium was within the therapeutic range, our data may have some potential clinical implications.

17-Hydroxysteroid Dehydrogenases↗
PubMed1976

Influence of lithium chloride on rabbit's EEG and behavior.

The effects of intravenous or intrahippocampal injections of lithium chloride dissolved in bidistilled water were investigated on rabbits with chronically implanted canniulas and electrodes. Bioelectric activity of the limbic structures and behavior were analyzed. Electrical activity was recorded by means of bipolar electrodes implanted chronically in the dorsal hippocampus, the gyrus cinguli, the amygdaloid complex and the medial hypothalamus, LiCl inhibited electric activity of the limbic structures and caused a reduction of spontaneous motor and exploratory activity of rabbits.

Animals↗
PubMed2005

Lithium chloride increases the production of amyloid-beta peptide independently from its inhibition of glycogen synthase kinase 3.

Glycogen synthase kinase 3 (GSK3) is able to phosphorylate tau at many sites that are found to be phosphorylated in paired helical filaments in Alzheimer disease. Lithium chloride (LiCl) efficiently inhibits GSK3 and was recently reported to also decrease the production of amyloid-beta peptide (Abeta) from its precursor, the amyloid precursor protein. Therefore, lithium has been proposed as a combined therapeutic agent, inhibiting both the hyperphosphorylation of tau and the production of Abeta. Here, we demonstrate that the inhibition of GSK3 by LiCl induced the nuclear translocation of beta-catenin in Chinese hamster ovary cells and rat cultured neurons, in which a decrease in tau phosphorylation was observed. In both cellular models, a nontoxic concentration of LiCl increased the production of Abeta by increasing the beta-cleavage of amyloid precursor protein, generating more substrate for an unmodified gamma-secretase activity. SB415286, another GSK3 inhibitor, induced the nuclear translocation of beta-catenin and slightly decreased Abeta production. It is concluded that the LiCl-mediated increase in Abeta production is not related to GSK3 inhibition.

Amyloid beta-Peptides↗
PubMed2003

Chronic lithium chloride treatment has variable effects on motor behaviour and survival of mice transgenic for the Huntington's disease mutation.

Expression of the Huntington's disease (HD) mutation in mice (R6/2 line) causes a progressive neurological phenotype that includes deterioration of motor function resembling that seen in HD. The current study sought to determine whether or not chronic treatment of R6/2 mice with lithium chloride would have an effect on the progression of the phenotype, in light of lithium's reported neuroprotective and anti-depressive properties. Treatment began either before or after the onset of symptoms. Chronic treatment with lithium caused a significant improvement in rotarod performance when treatment was started post- but not pre-symptomatically. There was no overall effect on survival in either group, but further analysis revealed that in the post-symptomatic group, mice could be assigned to one of two distinct groups, depending on the effects of lithium. One subgroup of mice lost weight faster, died earlier and showed rotarod performance similar to the vehicle-treated controls. The other subgroup lost weight at a normal rate, died at a similar age, but showed greatly improved motor performance compared to controls. The improvement in rotarod performance suggests that lithium may improve motor symptoms as well as depression in some HD patients.

Aging↗
PubMed1994

The lymphoblast beta-adrenergic receptor in bipolar depressed patients: effect of chronic incubation with lithium chloride.

We have recently reported a study of beta-adrenergic receptor binding characteristics in lymphoblast cell lines derived from patients with bipolar disorder (BD) and healthy, matched control subjects. In the present study we have investigated the effects of incubating cells from the same subjects with lithium chloride (1 mM) for 7 days prior to assay. There was no difference in beta-adrenergic receptor number between control and BD cell lines and incubation with lithium had no effect on receptor number in either group. Exposure of the cells to isoprenaline (1 nM) for 24 h immediately prior to assay caused significantly less down-regulation in BD cells (15 +/- 5%) than control cells (39 +/- 4%), as described previously. Incubation with lithium significantly increased the down-regulation response to isoprenaline in BD cells (39 +/- 6%) but not in control cells (30 +/- 7%). After lithium, the agonist-induced decrease in beta-AR number in BD cells was no longer significantly different from that in control cells. We conclude that lithium selectively enhanced the agonist down-regulation of beta-adrenergic receptors in cells derived from patients with bipolar disorder. The functional significance of this result and the potential biochemical mechanisms responsible for this effect are discussed.

Adult↗
PubMed1981

[Effect of chronic administration of lithium chloride on the development of dopamine receptor sensitivity during morphine withdrawal in rats].

The morphine withdrawal syndrome was studied in male Wistar rats. Spontaneous aggressiveness, enhanced apomorphine aggressiveness, lowered pain threshold and decreased dopamine turnover were observed after withdrawal of 10-day treatment with the increasing doses of morphine (30-300 mg/kg). These changes attested to the increased sensitivity of dopamine receptors. Administration of morphine in conjunction with lithium chloride in a dose of 2 mekv/kg prevented the development of dopamine receptor hypersensitivity. Also, this method did not produce the increased spontaneous and apomorphine aggressiveness or the decreased dopamine turnover. Meanwhile the pain threshold remained lowered.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Lithium chloride induces partial responsiveness to LPS in nonresponder B cells.

The lipopolysaccharide (LPS)-nonresponder mouse strains C3H/HeJ, C57BL/10ScCR and C57BL/10ScN do not respond to LPS acting as a polyclonal B-cell activator, a mitogen, or an adjuvant. The genetic basis for the defective LPS response has been extensive studied in C3H/HeJ and C57BL/10ScCR mice, in which it was demonstrated that a single gene locus on chromosome 4 was responsible for LPS unresponsiveness. Lithium chloride, a potent inhibitor of adenylate cyclase, not only improved lymphocyte activity in a patient with adenosine deaminase deficiency but also enhanced the phytohaemagglutinin (PHA)-induced responses of normal human lymphocytes. Therefore, we investigated whether LiCl could restore LPS responsiveness in spleen cells of C3H/HeJ mice. We show here that LPS, in the presence of LiCl, induced polyclonal IgM and IgG antibody formation and DNA synthesis in C3H/HeJ mouse spleen cells in vitro. Moreover, LiCl (10 mM), which by itself is non-mitogenic, increased RNA synthesis in spleen cells from both LPS-nonresponder and high responders strains; in contrast, LPS failed to increase RNA synthesis in cells from such LPS-nonresponder strains as C3H/HeJ and B10ScCr mice.

Animals↗
PubMed1982

[Fatal granulocyte function defect in a male infant. Results of in vitro and in vivo stimulation with ascorbic acid as well as in vitro stimulation with levamisol and lithium chloride].

We report about a boy who suffered from repeated bacterial infections starting at the age of 4 weeks. A severe defect of chemotactic activity of the neutrophils, and an additional deficient phagocytosis were discovered. The child died at the age of 3 months from septicemia. Chemotactic activity could be stimulated in vitro by ascorbic acid and levamisole but not by lithium chloride. In vivo, however, the effect of ascorbic acid was minimal and treatment with this vitamin could not prevent the lethal end.

Ascorbic Acid↗
PubMed1992

Effects of lithium chloride and retinoic acid on the expression of genes from the Xenopus laevis Hox 2 complex.

We show that Xenopus laevis has a Hox 2 complex, and that this complex is strongly conserved with the mammalian one, both in structure and in the rules of spatial and temporal sequential expression of its genes during the early stages of development. Lithium chloride and retinoic acid, two reagents known to alter axial patterning of the body when applied to Xenopus embryos, produce, respectively, embryos with reduced posterior but exaggerated anterior structures and embryos with truncation of anterior structures. We report here on the effect of these reagents on the expression of Hox 2 genes in the Xenopus embryos. LiCl has a dramatic effect on Hox genes, suppressing the expression of these genes during gastrulation and early neurulation. However, later on expression of these genes reaches significant levels, suggesting the existence of two phases in the control of Hox gene expression. Retinoic acid increases the steady state level of transcripts from Hox genes with the greatest effect on Hox 2.7, the most anterior of the genes studied. This suggests that the results obtained in EC cells (Simeone et al., 1990, 1991) reflect what occurs in vivo. Neither LiCl nor RA change the sequential order of the onset of expression of the genes, showing that these reagents do not perturb the molecular mechanisms used to establish the sequential activation of the genes of the Hox complexes.

Amino Acid Sequence↗