[Harmful elements versus iron, zinc and copper: their interactions in animals and humans. I. Mercury, tin, nickel, selenium, fluorine and aluminum]. / Pier wiastki szkodliwe a zelazo, czynk i miedz: interakcje w organizmie zwierzat i ludzi. Cz. I. Rtec, cyna, nikiel, selen, fluor, glin.

A literature survey was made of the interactions--in the organism--between some food contaminating elements (mercury, tin, nickel, selenium, fluorine, aluminium) and iron, zinc and copper. The harmful elements may disturb the mineral metabolism already at the stage of intestinal absorption. Moreover, they bring about changes in microelement distribution in the tissues and cells. On account of their approximately similar chemical structure, they compete for the sites of binding to some proteins, including enzymic ones. In this respect a special role is played by ++metallothionein, a protein with the ability of regulating free metal contents in the tissues and thus possibly displaying some detoxifying properties. Many mechanisms and relationships determining the interactions between the surveyed food contaminants and iron, zinc and copper remain, however, not elucidated.

Modulation of fluoroaluminate-induced inositol phosphate formation by increases in tissue cyclic AMP content in bovine tracheal smooth muscle.

1. The effect of fluoroaluminate complexes (AlCl3 plus NaF) upon smooth muscle tone, [3H]-inositol phosphate accumulation and [3H]-cyclic AMP accumulation has been investigated in slices of bovine tracheal smooth muscle. 2. Fluoroaluminate (10 microM AlCl3 + various concentrations of NaF) elicited concentration-dependent contractions of bovine tracheal smooth muscle strips at concentrations of NaF in the range 1-10 mM. The resultant contractile response was reversed by isoprenaline (50 nM) and was preserved in calcium-free medium. 3. Fluoroaluminate stimulated [3H]-inositol phosphate formation at concentrations of NaF over 1 mM. The response to 20 mM NaF + 10 microM AlCl3 was 164 +/- 29% of the response to 1 mM histamine. Fluoroaluminate also increased the incorporation of [3H]-myo-inositol into membrane phospholipids. 4. Fluoroaluminate produced a small rise in [3H]-cyclic AMP levels (2.1 fold increase over basal with 20 mM NaF). The response to forskolin (1 microM, 8.6 fold over basal) was reduced by fluoroaluminate in a concentration-dependent manner, but still remained significantly (P less than 0.05) elevated over the response to fluoroaluminate alone. 5. The [3H]-inositol phosphate response to fluoroaluminate was inhibited by salbutamol (maximum inhibition 60%, IC50 = 0.08 microM), forskolin (1 microM, 46% inhibition) and isobutylmethylxanthine (1 mM, 73% inhibition). 6. These data suggest that inhibition of agonist-induced inositol phospholipid turnover by cyclic AMP in this tissue can occur at the post-receptor level.

[The role of Streptococcus mutans in human caries]. / Ruolo dello Streptococcus mutans nella carie umana.

Definite proof has been found that S. mutans, and probably S. sobrinus and lactobacilli, are responsible for caries in man. The aciduria of S. mutans encourages the selection inside the plaque and is directly responsible for its cariogenicity. Other aciduric species, as S. sobrinus, cause caries on the smooth surface of the tooth, where the principal causes of the rampant caries reside. If during the eruption of the tooth the fissures become colonized in depth by S. mutans, the development of caries becomes a highly probable event. Instead, if the colonization of the tooth by S. mutans takes place after the fissure depth have been occupied by other microbic species not cariogenic, it is probable that the caries will not manifest or will appear in a less severe form. In conclusion, the knowledge already acquired on the ecology of S. mutans and the mechanism of cariogenesis clearly indicate that all factors that interfere with the colonization of the tooth by S. mutans can greatly reduce the incidence of caries in man.