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The presented review summarizes literature data on pathways of the inorganic fluoride intake into the plant, animal, and human organisms, on its metabolism, distribution, and accumulation in the organism, forms of fluoride in biological tissues, toxic effects of fluoride on physiological and reproductive functions of living organisms of various phylogenetic groups, as well as clinical symptoms of deficient and excessive fluoride intake into the human organism.

The K+ transport in isolated erythrocytes from the frog Rana ridibunda has been studied using 86Rb as a tracer at the temperature of 18-20 degrees C. At physiological K+ concentration (3 mM) in C1- medium ouabain and furosemide inhibited K+ influx by approximately 42 and 47%, respectively. Furosemide had no effect on the Na+ (22Na) transport under the same conditions. The replacement of C1- by NO-3 in medium resulted in significant decrease of total K+ influx, which was not inhibited by furosemide. The ouabain- and furosemide-sensitive components of K+ influx hyperbolically increased as a function of external K+e concentration (1-90 mM) in C1- medium and calculated values of Vmax were 2.2 +/- 0.14 and 5.8 +/- 1.2 mmol/1 cells/h, respectively. K+ influx into frog erythrocytes in the presence of both ouabain and furosemide in NO-3 medium was significantly lower compared with C1- medium. C1--dependent, furosemide-insensitive component of K+ influx increased in a saturable fashion in the range of K+e concentration from 1 to 90 mM. Residual component of K+ transport in NO3 medium in the presence of the blockers was a linear function of K+e concentration and is characterized by the constant of K+ influx rate equal to 0.028 +/- 0.002 h-1. The data obtained indicate that in parallel with the Na, K-pump specific K, C1-transporter participates in K+-transport in the frog erythrocyte membrane. The latter mechanism was only partially blocked by 1 mM furosemide.