L-carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) act as natural antioxidants with hydroxyl-radical-scavenging and lipid-peroxidase activities.

Carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) are natural imidazole-containing compounds found in the non-protein fraction of mammalian tissues. Carcinine was synthesized by an original procedure and characterized. Both carnosine and carcinine (10-25 mM) are capable of inhibiting the catalysis of linoleic acid and phosphatidylcholine liposomal peroxidation (LPO) by the O2(-.)-dependent iron-ascorbate and lipid-peroxyl-radical-generating linoleic acid 13-monohydroperoxide (LOOH)-activated haemoglobin systems, as measured by thiobarbituric-acid-reactive substance. Carcinine and carnosine are good scavengers of OH. radicals, as detected by iron-dependent radical damage to the sugar deoxyribose. This suggests that carnosine and carcinine are able to scavenge free radicals or donate hydrogen ions. The iodometric, conjugated diene and t.l.c. assessments of lipid hydroperoxides (13-monohydroperoxide linoleic acid and phosphatidylcholine hydroperoxide) showed their efficient reduction and deactivation by carnosine and carcinine (10-25 mM) in the liberated and bound-to-artificial-bilayer states. This suggests that the peroxidase activity exceeded that susceptible to direct reduction with glutathione peroxidase. Imidazole, solutions of beta-alanine, or their mixtures with peptide moieties did not show antioxidant potential. Free L-histidine and especially histamine stimulated iron (II) salt-dependent LPO. Due to the combination of weak metal chelating (abolished by EDTA), OH. and lipid peroxyl radicals scavenging, reducing activities to liberated fatty acid and phospholipid hydroperoxides, carnosine and carcinine appear to be physiological antioxidants able to efficiently protect the lipid phase of biological membranes and aqueous environments.

[The regulatory role of silicon in cell division]. / Le rôle régulateur du silicium dans la division cellulaire.

Several reports have suggested that silicon has an activating effect on cell proliferation. In order to test this hypothesis, both peripheral human lymphocytes and LDV/7 lymphoblast cells were cultured in the presence of a compound composed of monomethylsilanetriol (silanol), a soluble organic form of silicon, and serine. This molecule stimulates peripheral lymphocyte proliferation at an optimal concentration of 10 mg of silicon per liter of culture medium; in identical conditions, it inhibits the growth of lymphoblastoïd cells (p less than 0.001). Silanol-serine also inhibits the growth of PHA stimulated lymphocytes. The effect of silicon on cell growth has a negative correlation (p less than 0.001) with the mitotic activity of cultured cells: the more intense the latter, the stronger is the inhibitory effect of silanol-serine. This would suggest a regulatory role of this compound on the cell cycle.