Rubidium (Rb)

Rb – Rubidium is found in igneous rocks at 90 ppm; shale at 140 ppm; sandstone at 60 ppm; limestone at 3 ppm; freshwater at 0.00 15 ppm; sea water at 0. 12 ppm; soil at 100 ppm (fixed by clay soils); marine plants at 7.4 ppm; land plants at 20 ppm; marine animals at 20 ppm; land animals at 17 ppm (highest levels in liver and muscle – lowest levels in bone).

Rubidium can replace the electrolyte function of potassium in many species including bacteria, algae, fungi and certain invertebrates (echinoderms -starfish).

As another element in the potassium family group, rubidium, also shows some properties of essentiality. Rubidium is widely distributed both in seawater (120 ppb) and in the earth’s crust (100 ppm). Normal human adults contain about 300 mg in all tissues, more than most of the other ultratrace elements. The metabolism of rubidium and cesium are closely related to that of potassium, and they show interchangeability with potassium in a variety of biological systems with little evidence for any toxicity. In a recent paper, Lombeck, et al. (1980) reported a homeostatic control of rubidium levels in the blood of children (12 ñ 3 ppm), which they interpreted as suggestive of an essential role for rubidium. Rubidium is a good example of an element that cannot be excluded.

Biological interest in rubidium and cesium has been stimulated by their close physicochemical relationship to potassium and their presence in living tissues in higher concentrations, relative to those of potassium, than in the terrestrial environment. Over a century ago Ringer observed that rubidium was similar to potassium in its effect on the contractions of isolated frog heart. Relationships between potassium and rubidium, and between cesium and potassium, have been found in a variety of physiological processes. These relationships exist in such diverse actions as their ability to neutralize the toxic action of lithium on fish larvae, or to affect the motility of spermatozoa, the fermentative capacity of yeast, and the utilization of Krebs cycle intermediates by isolated mitochondria. Their extracellular ionic concentrations also influence the resting potential in nerve and muscle preparations and the configuration of electrocardiograms.

The described metabolic interchangeability suggests that rubidium or cesium might have the ability to act as a nutritional substitute for potassium. Rubidium, and to a lesser extent cesium, can replace potassium as a nutrient for the growth of yeast and of sea urchin eggs. This nutritional replaceability can be extended to bacteria, but higher animals are more discriminating. Additions of rubidium or cesium to potassium-deficient diets prevent the occurrence of characteristic lesions in the kidneys and muscles in rats and, for a short period, permit almost normal growth until death inevitably supervenes.

Glendening et al. obtained no evidence that rubidium is an essential element for rats fed purified diets with variable supplements of rubidium, sodium, and potassium. However, there were indications that rubidium partially substituted for potassium and was more toxic in low-than in high-potassium diets. Purified diets containing up to 200 mcg/g rubidium were nontoxic, but levels of 1000 mcg/g or more depressed growth, reproductive performance, and survival time in rats.

In addition to its possible interchangeability role with potassium, there is some evidence suggesting that rubidium has a role involving some neurophysiological mechanism. In heart, rubidium was found to be lower in conductive tissue than in adjacent muscle tissue. The rubidium content of brain differs significantly between defined functional regions and also decreases with age. Rubidium apparently can enhance the turnover of brain norepinephrine. Vis et al suggested that because rubidium causes electroencephalogram activation in monkeys and rats, perhaps the depletion of rubidium prevents the normalization of low-wave power values in dialysis patients. They found that rubidium rapidly diffused through the membranes of the artificial kidney. However, electroencephalogram activation by rubidium has not been demonstrated in humans.

Rubidium is rapidly and highly absorbed and excreted by the digestive tracts of mammals. Rubidium resembles potassium in its pattern of absorption, distribution, and excretion in animals. On the basis of studies with brush border membrane vesicles isolated from rabbit jejunum, potassium and rubidium apparently share a transport system. All plant and animal cells are apparently permeable to rubidium and cesium ions at rates comparable with those of potassium. All soft tissues of the body have rubidium concentrations that are high compared with many trace elements, with a total-body content of approximately 360 mg in the adult man. Rubidium does not accumulate in any particular organ or tissue and is normally relatively low in bones.

Varo and co-workers included rubidium in their mineral analyses of Finnish foods. Their results indicated that most foods contained 0.5-5 mcg/g rubidium and that the daily intake of rubidium was 4.2 mg. This compares well with the reported rubidium intakes of 4.35 +or-1.54 mg/day with English total diets, 1.28-4.98 mg/day with U.S. diets and 2.5 mg/day with Italian diets. Diets with the highest rubidium levels were probably rich in meats and dairy products. Brazil nuts are very rich in rubidium. Becker et al. found that the rubidium content for swine feeds, piglet starter rations, and various mixed feeds ranged from 2.6 to 26.1 mcg/g dry weight. Based on the analyses by Varo and associates. many animal feeds probably contain rubidium at these levels.
Biol Trace Elem Res 1996 Feb;51(2):199-208

Effect of low dietary rubidium on plasma biochemical parameters and mineral levels in rats.
Yokoi K, Kimura M, Itokawa Y

Department of Social Medicine, Graduate School of Medicine, Kyoto University, Konoe-cho Yoshida, Sakyo-ku, Japan.

The effects of low dietary rubidium on plasma biochemical parameters and mineral levels in tissues in rats were studied. Eighteen male Wistar rats, weighing about 40 g, were divided into two groups and fed the diets with or without supplemental rubidium (0.54 vs 8.12 mg/kg diet) for 11 wk. Compared to the rats fed the diet with supplemental rubidium, the animals fed the diet without rubidium supplementation had higher urea nitrogen in plasma; lower rubidium concentration in tissues; lower sodium in muscle; higher potassium in plasma, kidney and tibia, and lower potassium in testis; lower phosphorus in heart and spleen; lower calcium in spleen; higher magnesium in muscle and tibia; higher iron in muscle; lower zinc in plasma and testis; and lower copper in heart, liver, and spleen, and higher copper in kidney. These results suggest that rubidium concentration in tissues reflects rubidium intake, and that rubidium depletion affects mineral (sodium, potassium, phosphorus, calcium, magnesium, iron, zinc, and copper) status.

Cytobios 1979; 24(94): 99-101

The effects of rubidium on mammary tumor growth in C57 blk/6J mice.
Brewer AK, Clarke BJ, Greenberg M, Rothkopf N

A high pH therapy for cancer arrived at theoretically was tested in mice by feeding them rubidium carbonate. Tumors were transplanted in the abdomen of mice and allowed to grow for 8 days. The mice were then divided into two groups. The control group was continued on conventional mouse chow. The test group, in addition to the mouse chow, was force-fed 1.11 mg of rubidium carbonate dissolved in distilled water. At the end of 13 more days the tumors in the controls had grown to a large size so all the mice were sacrificed. The tumors were then removed and weighed. The tumors in the test animals weighed essentially one eleventh of those in the controls. In addition the test animals were showing no adverse effects from the cancers. The probability that this marked difference in tumor size could have come about by chance is exceedingly small.