Bimetallic reactivity. One-site addition two-metal oxidation reactions using a di-Co(II) complex of a binucleating ligand with 5- and 6-coordinate sites.

The preparation of an unsymmetrical binucleating ligand bearing a bridging oxadiazole ring flanked on one side by three ligands and on the other by four ligands is described. When bound to two metals, the ligand forms complexes where the metals are in 5- and 6-coordinate sites after the incorporation of an exogenous bridging ligand. A di-Co(2+) complex of this ligand has been prepared containing a hydroxide bridge. The complex is readily oxidized to the di-Co(3+) state by outer sphere electron transfer with ferrocenium ions. Addition of Br(2) or NO(2)(+) to the di-Co(2+) complex leads to the rapid formation of the di-Co(3+) bromo or nitro complexes, respectively. The ligand characteristics which allow for double oxidation with ferrocenium ions and for the one-site addition two-metal oxidations with Br(2) and NO(2)(+) are discussed in terms of mechanical coupling between the two metal sites.

Bimetallic reactivity. Preparation and properties of bimetallic complexes formed by binucleating ligands bearing 4- and 6-coordinate sites.

Four binucleating ligands bearing 4- and 6-coordinate sites employing phenolate bridges have been prepared. Bimetallic copper(II) and nickel(II) complexes of some of these ligands have been isolated and characterized. Crystal structures of two of the copper(II) complexes have been determined. A monometallic manganese(II) complex of one of these ligands was isolated. Upon exposure to dioxygen, acetonitrile solutions of the complex in the presence of chloride ions lead to the formation of a manganese(IV) complex. The crystal structure of this complex is reported, and it is shown that the metal is in the 4-coordinate ligand site and is bound to two chloride ions.

Bimetallic reactivity. On the use of oxadiazoles as binucleating ligands.

Two (1,3,4)-oxadiazole ligands have been prepared. In one case the oxadiazole ring is flanked by two o-aniline groups, and in the other case it is an extension of the first where the amines are condensed with 2-picolyl groups. A monometallic copper(II) complex of the former has been prepared, and its crystal structure was determined. A number of bimetallic copper(II), cobalt(II), and nickel(II) complexes of the di-deprotonated latter ligand were prepared and isolated. The crystal structure of the cobalt(II) complex bearing two acetate bridges is reported. The work demonstrates that the seldom-employed oxadiazole ring can be used effectively for generating bimetallic complexes.

Evolution, mutations, and human longevity: European royal and noble families.

The evolutionary theory of aging predicts that the equilibrium gene frequency for deleterious mutations should increase with age at onset of mutation action because of weaker (postponed) selection against later-acting mutations. According to this mutation accumulation hypothesis, one would expect the genetic variability for survival (additive genetic variance) to increase with age. The ratio of additive genetic variance to the observed phenotypic variance (the heritability of longevity) can be estimated most reliably as the doubled slope of the regression line for offspring life span on paternal age at death. Thus, if longevity is indeed determined by late-acting deleterious mutations, one would expect this slope to become steeper at higher paternal ages. To test this prediction of evolutionary theory of aging, we computerized and analyzed the most reliable and accurate genealogical data on longevity in European royal and noble families. Offspring longevity for each sex (8409 records for males and 3741 records for females) was considered as a dependent variable in the multiple regression model and as a function of three independent predictors: paternal age at death (for estimation of heritability of life span), paternal age at reproduction (control for parental age effects), and cohort life expectancy (control for cohort and secular trends and fluctuations). We found that the regression slope for offspring longevity as a function of paternal longevity increases with paternal longevity, as predicted by the evolutionary theory of aging and by the mutation accumulation hypothesis in particular.

Mutation load and human longevity.

Since paternal age at reproduction is considered to be the main factor determining human spontaneous mutation rate (Crow, J. (1993) Environ. Mol. Mutagenesis, 21, 122-129), the effect of paternal age on human longevity was studied on 8,518 adult persons (at age 30 and above) from European aristocratic families with well-known genealogy. The daughters born to old fathers (50-59 years) lose about 4.4 years of their life compared to daughters of young fathers (20-29 years) and these losses are highly statistically significant, while sons are not significantly affected. Since only daughters inherit the paternal X chromosome, this sex-specific decrease in daughters' longevity might indicate that human longevity genes (crucial, house-keeping genes) sensitive to mutational load might be located in this chromosome.