ABSTRACT
Cesium is an alkali group element, the most basic and electropositive metal known, and it reacts explosively in contact with oxygen or water. In mammals, cesium is a biologically important trace element due to its similarity and relationship with potassium in a number of biochemical and physiological processes. The amount detected in serum and packed blood cells was about 0.74 and 4.82 µg/kg net weight, respectively (1). Cesium also closely approximates the other biologically active alkali metals, e.g., Li, Na, and Rb, in function and toxicity, and its salts exhibit no acute or chronic effects that significantly depart from similar compounds derived from the other group IA elements. A number of the more common salts of cesium were screened for acute toxicity in standard animal tests (skin/eye irritation, cutaneous sensitization, oral LD50) and were found to be of low toxicity, with the exception of the hydroxide, which was irritating to abraded skin (2). In animals, also in common with other alkali metals, Cs was shown to affect various CNS functions, mainly involving K transfer, with which it competes for transport across cell membranes. 133Cs nuclear magnetic resonance (NMR) studies carried out on suspended human erythrocytes showed that Cs is taken up at approximately one-third the rate of K (3). It is due to such metabolic similarities with potassium that cesium can be potentially harmful in mammals. Elevated cesium levels were observed in brain tissue of schizophrenic patients and depleted in those with Alzheimer’s disease (AD) (4). Seen in conjunction with the persistent imbalances observed for Na, K, and Rb in various brain tissues of AD patients, this supports the argument of membrane abnormality associated with AD (5). In that study it was also noted that sodium, with its relatively small ionic radius, showed elevated values in AD patients, whereas the other alkali metals studied, with larger ionic radii, are generally depleted in brain tissue.
