Lithium cellular distribution

Figure 2. Effects of lithium on the cellular distribution ofAQPl in mpkCCD cells. ConfluentmpkCCD monolayers were left untreated (a), treated with 1 nM dDAVP for 96 h (b), or treated with both dDAVP for 96 h and either I mM lithium for24h (c) or48h (d) or 10 mM lithium for24h(e) or48h (f). (Reproduced with permission from Yeudan etal [138]).

Newer uses have appeared in the treatment of viral diseases including AIDS, alteration of the immune response, and cancer. The lithium salt of 7-linolenic acid (LiGLA) has a significant anticancer effect against certain cancers. The neurochemical basis for lithium action is difficult to define. Lithium carbonate induces a wide range of intra- and extracellular changes—most emphasis has been naturally on the similarities with Na/K/Ca/Mg ions. Lithium selectively interferes with the inositol lipid cycle, representing a unified hypothesis of action. The biochemistry, distribution, and cellular localization of lithium has been extensively documented. 

Lithium disrupts almost every measurable cellular activity pertaining to nerve transmission as well as many other vital functions. In addition, its distribution is fairly uniform throughout the central nervous system, with no known areas of specific concentration. It produces what Wilson et al. (1975) called a nonselective diminution in neuronal activity. The neurophysiology of lithium, even without supporting clinical data, renders absurd the notion of a specific biochemical treatment for a specific disease and confirms the brain-disabling effect. 

Lithium is readily absorbed when administered orally and is widely distributed in the body, mainly intra-cellularly. It is carried into the red blood cells by the sodium transport carrier and enters the central nervous system. Lithium can penetrate the placental barrier. It is excreted in the urine - excretion depends on sodium and water balance and the glomerular filtration rate. 

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