The DNA and RNA content of the fruit fly, Drosophila melanogaster under goes two cycles of synthesis and loss during the larval and pupal stages of development. The adult stages show little or no change with age in DNA content. Thermal melting curves, sedimentation velocities and CsC1 buoyant density measurements have been used to show that the molecular weight of larval DNA is of the order of 10-4 daltons. However, a fraction of the larval DNA (about 25%) is of a molecular weight greater than 10-6. Molecular weights increase during the later larval and pupal stages until a maximum of greater than 10-6 is reached during the adult stages. The molecular weight of embryonic DNA is greater than 10-6 but is rapidly degraded after hatching during early first instar larval development. Several interpretations of these data are offered. Buoyant densities in cesium salts showed no developmental or age-related changes.

Aging↗

PubMedDate not supplied

Catalase levels in Drosophila and the lack of induction by hypolipidemic compounds. A brief note.

Catalase (EC 1.11.1.6) activity levels were found to decrease in the fruit fly, Drosophila melanogaster, from 1 to 5 days of age and to increase from 5 to 8 days of age, followed by a second decline in old age. Feeding the hypolipidemic compounds, beta-diethylaminoethyl-alpha-p-chlorophenoxyisobutyrate hydrochloride, Nafenopin and Clofenapate did not significantly alter catalase levels. Median survival time was decreased 8.3% by feeding Clofenapate and increased up to 5.5% by beta-diethylamino-ethyl-alpha-p-chlorophenoxyisobutyrate hydrochloride.

Animals↗

PubMedDate not supplied

Effect of vitamin A on longevity.

Increasing the dietary content of Vitamin A from inadequate to adequate during the developmental stages of Drosophila increased the median life span by as much as 17.5%. The optimum dietary range of concentrations of Vitamin A for increasing the life span of Drosophila was found to be between 4 and 8 IU/g food. The maximum life span was reduced as dietary concentrations of Vitamin A exceeded this value. Vitamin A palmitate and retinal inhibited the peroxidation of linolenic acid induced by the generation of superoxide radicals from acetaldehyde. Other forms of Vitamin A, such as retinol and retinoic acid, moderately inhibited lipid peroxidation at low concentrations but stimulated peroxidation considerably when present at high concentrations. Based upon the ability of these retinoids to inhibit the reduction of cytochrome c by superoxide radicals, we propose that retinoids can inhibit and stimulate lipid peroxidation depending upon their concentration by reacting with superoxide radicals. We suggest that this reaction is the basis for the apparent ability of Vitamin A to prolong and shorten life span depending upon the dietary intake.

Animals↗