Search PubMed⌕ Search

Biomedical subjects

A C Economos

Publications and source records attributed to A C Economos.

30 records · Page 2Linked to original sources
PubMed1982

Is cell aging caused by respiration-dependent injury to the mitochondrial genome?

Though intrinsic mitochondrial aging has been considered before as a possible cause of cellular senescence, the mechanisms of such mitochondrial aging have remained obscure. In this article we expand on our hypothesis of free-radical-induced inhibition of mitochondrial replenishment in fixed postmitotic cells. We maintain that the respiration-dependent production of superoxide and hydroxyl radicals may not be fully counteracted, leading to a continuous production of lipoperoxides and malonaldehyde in actively respiring mitochondria. These compounds, in turn, can easily react with the mitochondrial DNA which is in close spatial relationship with the inner mitochondrial membrane, producing an injury that the mitochondria may be unable to counteract because of their apparent lack of adequate repair mechanisms. Mitochondrial division may thus be inhibited leading to age-related reduction of mitochondrial numbers, a deficit in energy production with a concomitant decrease in protein synthesis, deterioration of physiological performance, and therefore, of organismic performance.

Animals↗
PubMed1981

Beyond rate of living.

The validity of the rate of living theory of aging in mammals has been seriously questioned over the last two decades because it does not account for the life span of many mammalian species. However, though this concept is an oversimplification and inapplicable in general, this does not mean that aging is unrelated to cellular metabolic processes. In general agreement with previous discussions, it can be stated that the rate of aging is proportional to the difference between the rate of cellular entropy production (which is by necessity roughly proportional to the rate of cellular biochemical processes and thus specific metabolic rate) and the cellular "counterentropic' mechanisms (such as cellular repair, antioxidant protection, etc.). These counterentropic mechanisms may have evolved to a different degree in some mammals. This could be effected indirectly by natural selection of certain traits, particularly those expressed in differences in the rates of embryonic and postnatal development. These rates, relatively to basal metabolic rate, determine a species' rate of becoming, which is proposed to be a predictor of mammalian life span. Data from 22 species, from shrew to elephant, with representatives from the main mammalian orders (including many exceptions to the rate of living concept), agree with this hypothesis. A mechanism underlying such natural selection, proposed elsewhere, is based on differential selection pressures among orders for which the different life-styles (particularly with respect to the birth of young) are responsible.

Aging↗
PubMed1980

Usefulness of stochastic analysis of body weight as a tool in experimental aging research.

The statistical characteristics of body weight in a number of longitudinally studied mouse populations were examined. Frequency distribution of body weights appears to be rather "fluid" (though within a strict range), changing from symmetric to positively skewed to symmetric and finally to negatively skewed as the mice pass through the stages of early maturity, middle age, and senescence. Because body weight is a highly integrated physiological variable, it is postulated that various diets which affect survivorship would affect body weight frequency distribution similarly. The data from studies with an antioxidant diet and two toxic diets support this hypothesis. In general, the effects on body weight can be assessed in a relatively short time (6-9 months) after initiation of the experiment and 4-6 months before the effect of the experimental diet is manifested in the population's survivorship, thus offering an analytical tool for considerable shortening of the duration of such studies.

Adult↗
PubMed1980

Brain-life span conjecture: a reevaluation of the evidence.

Empirical evidence for the conjecture that brain weight of mammals is a better predictor of life span than is body weight, is reexamined and evaluated in this paper. The original evidence was that for 63 mammalian species, log brain weight explained 79% of the log life span variance, whereas log body weight explained only 60%; thus, the correlation coefficient rbr for the linear regression of the log life span on log brain weight was 0.88, whereas the correlation coefficient rb for the regression of log life span on log body weight was 0.77. From data on 40 mammalian species (including three primates), we found rbr = 0.81 and rb = 0.75; from data on 35 primate species, we found rbr = 0.68 and rb = 0.65. Correlation coefficients rliv, radr for the regression of log life span on log liver weight or log adrenal weight, respectively, were rliv = 0.78 and radr = 0.81 for the same 40 mammalian species. We conclude that brain weight appears to be a slightly better predictor of life span than body weight but not better than adrenal weight. One primary reason why body weight is a poorer predictor of life span may be a result of its wider range of values compared with brain and adrenal weights.

Adrenal Glands↗
PubMed1980

Taxonomic differences in the mammalian life span-body weight relationship and the problem of brain weight.

Despite the highly significant correlation between brain and body weight throughout the entire mammalian class, there are consistent differences between rodents, higher primates, carnivores, and ungulates. Primates have larger brains than carnivores of equal size, while rodents have smaller brains, and ungulates have similar-sized brains as carnivores with the same body weight. Further, life span correlates well with body weight for all mammals together (over 150 species), although there are large and consistent interorder differences. For a given body weight, carnivores have a shorter life span than primates, one as long as rodent, and one longer than ungulates. These differences in life span are not matched by the differences in brain weight. Therefore, the conjecture that brain size is a determinant of life span is not valid.

Animals↗
PubMed1979

Quantitative analysis of mating behavior in aging male Drosophila melanogaster.

Dynamic changes in quantitative aspects of mating behavior of the male fruit fly as its life unfolds, from eclosion through maturity (peak performance) and "physiological death" (loss of fertility followed by complete loss of ability to mate), towards actual death, have been identified in this work by observations and measurements on 28 male fruit flies of the Oregon R strain studied individually. At weekly sessions from the first day of their imaginal life until their natural death, each fly was given the opportunity to mate with up to three virgin females during a one-hour period. Length of the latency period of each accomplished mating and duration of copulation were recorded. After mating the females were allowed to lay eggs for 24 hours and the number of offspring was counted 26 days later. The period between 1 and 4 weeks of age is characterized by peak and fairly constant performance: multiple matings, short latencies, long durations of copulation, and high degree of fertility (number of offspring); then a decline sets in, in some measures slower than in others, as the flies age. Large intra- and inter-individual variabilities were, however, found which obscure possible correlations between individual measures of mating ability and length of life. At the individual level, a preliminary analysis showed a good correlation (r = 0.80 and 0.79) between life span and week of last mating (onset of impotence) or week of last fertile mating (onset of sterility). At the population level it was found that a number of measures, i.e. number of remaining maters at each age, number of remaining fertile maters and total number of matings, had an age-course similar to survivorship but anticipated it by 4--6 weeks. Other measures, such as number of multiple matings and number of offspring declined with age faster than survivorship.

Aging↗