Disease relevance of lithium chloride

• METHODS: Pheochromocytoma PC-12 cells were treated with varying concentrations of LiCl (0 to 30 mM) [1].
• Finally, Trichodion, a potent nuclear factor-kappaB (NF-kappaB) inhibitor, could not affect LiCl-induced TRAIL sensitization, although GSK-3beta inhibitors significantly blocked TRAIL-reduced NF-kappaB activity in prostate cancer cells [2].

Psychiatry related information on lithium chloride

• Failure of CCK-8 to affect feeding behavior like LiCl is indirect evidence that the reduction of food intake by CCK-8 is not merely the result of aversiveness, but is an extremely potent and specific behavioral effect [3].
• Effects of CCK-8 and LiCl on food intake were then compared in the hour (hr) following 8 hr of food deprivation; rats were on this food deprivation schedule for a relatively long time (78 days) throughout testing [3].

High impact information on lithium chloride

• In this study we have established that exposure of murine Dexter cultures to LiCl (4 mEq/L) causes an increase of colony-forming cell megakaryocytes (CFU-meg) over 1 to 6 weeks of culture in both supernatant (188% to 611%) and stromal phases (123% to 246%) [4].
• To examine the effect of lithium (Li) on early megakaryocytopoiesis, murine marrow megakaryocytic (CFU-M) and granulocyte-macrophage (CFU-C) progenitors were assayed in vitro with and without addition of lithium chloride (LiCl) to culture [5].
• Here we show that the TNF-sensitizing effect of lithium chloride (LiCl) is independent of the type of cell death, either necrosis or apoptosis [6].
• TNF-induced activation of NF-kappa B-dependent gene expression is not modulated by LiCl treatment [6].
• LiCl also potentiates cell death induced by artificial oligomerization of a fusion protein between FKBP and the TNF receptor-associated death domain protein [6].

Biological context of lithium chloride

• Using concentrations of 1-30 mM LiCl we also showed that cell proliferation is inhibited in a dose-dependent manner [7].
• The increasing ratio of second field EPSP, which was examined by paired-pulse stimulation, was reduced about 10% by 5 mM LiCl [8].
• In Experiment I, three groups of female rats were water deprived and conditioned to avoid a 0.025 M Polycose, a 0.1 M sucrose, or a 0.1 M maltose solution by pairing solution consumption with a lithium chloride (LiCl) injection; in a control group water consumption was paired with the LiCl injection [9].
• Here we report that lithium chloride (LiCl) is a potent stabilizer of the lens epithelial phenotype [7].
• Although a very high dose of LiCl (120 mg/kg) decreased food intake markedly, the rats were obviously distressed, not satiated [3].

Anatomical context of lithium chloride

• Confocal microscopy and immunohistochemistry for ZO-1 and E-cadherin showed that LiCl treatment maintained tight junctions at the apical margins of cells [7].
• We now report the effect of various levels of LiCl on the high proliferative potential colony-forming cell (HPP-CFC) in Dexter culture and on the induction of growth factors from Dexter stromal cells [10].
• We have previously reported that the addition of lithium chloride (LiCl) to murine Dexter cultures results in increased numbers of progenitor and mature hematopoietic cells of the granulocyte, macrophage, and megakaryocyte lineages [10].
• Lithium (Li) concentrations have been estimated in several peripheral tissues (serum, heart, kidney, liver and skeletal muscle) and different brain areas (cortex, caudate nucleus, hypothalamus, diencephalon, midbrain, pons-medulla and cerebellum) at different intervals (0.5 to 48 h) after administrations of 3 mEq/kg of lithium chloride (LiCl) [11].
• Rats with lesions of the area postrema or with sham lesions were given pairings of a novel taste with either intraperitoneally or intragastrically administered lithium chloride (LiCl; 10 mg/kg of a 0.15 M solution of lithium chloride) or a similar concentration of NaCl (control groups) [12].

Associations of lithium chloride with other chemical compounds

• 2. In guinea-pig and rat cerebral cortex slices the accumulation of total [3H]-inositol phosphates due to the cholinoceptor agonist carbachol was inhibited by the excitatory amino acid L-glutamate, but only when LiCl was present [13].
• In the in vitro studies, no effects of LiCl on iodide uptake or efflux were observed [14].
• Our previous study demonstrated that 2 mEq/kg/day of lithium chloride (LiCl) is not a toxic dose; and therefore, this dose of LiCl in 1 ml vehicle (5% glucose solution) or 1 ml of vehicle alone was injected intraperitoneally for 7 days into Wistar rats [15].

Gene context of lithium chloride

• Using a gelshift assay, we found that LiCl significantly decreased activating protein 2 (AP-2)-binding activity, and protein levels of the AP-2 alpha and AP-2 beta but not of the AP-2 gamma subunits in the frontal cortex [16].
• Furthermore, LiCl treatment resulted in a slight, but non-significant increase of beta-catenin levels in ES cell-derived embryoid bodies [17].
• Additionally, LiCl increased PHA-induced IL-2 production in both normal subjects and ARC patients [18].
• The ability of antidepressant drugs, electroconvulsive treatment (ECT), or lithium chloride (LiCl), to modify prolactin secretion in the rat was studied [19].
• Similar effects were observed when LiCl was added to the MLR assays in both the normal and the ARC patient groups [18].

Analytical, diagnostic and therapeutic context of lithium chloride

• In both rat and human capsulorhexis explants, LiCl treatment effectively blocked the accumulation of alpha-SMA and maintained the cells in a polarized, adherent, cobblestone-packed monolayer [7].
• Perfusion of 2-10 mM lithium chloride (LiCl) produced a dose-dependent increase in the amplitude of field EPSPs, whereas change in the population spikes was variable [8].
• Additionally, LiCl-treated TT xenograft mice had a significant reduction in tumor volume compared with those treated with control [20].

References