The phenomenon of growth, decline and death—aging—has been the source of considerable speculation (1, 8, 10). This cycle seems to be a more or less direct function of the metabolic rate and this in turn depends on the species (animal or plant) on which are superimposed the factors of heredity and the effects of the stresses and strains of life—which alter the metabolic activity. The universality of this phenomenon suggests that the reactions which cause it are basically the same in all living things. Viewing this process in the light of present day free radical and radiation chemistry and of radiobiology, it seems possible that one factor in aging may be related to deleterious side attacks of free radicals (which are normally produced in the course of cellular metabolism) on cell constituents.* Irradiation of living things induces mutation, cancer, and aging (9). Inasmuch as these also arise spontaneously in nature, it is natural to inquire if the processes might not be similar. It is believed that one mechanism of irradiation effect is through liberation of OH and HO 2 radicals (12). There is evidence, although indirect, that these two highly active free radicals are produced normally in living systems. In the first place, free radicals are present in living cells; this was recently demonstrated in vivo by a paramagnetic resonance absorption method (3). Further, it was shown that the concentration of free radicals increased with increasing metabolic activity in conformity with the postulates set forth some years ago that free radicals were involved in biologic oxidation-reduction reactions (11, 13). Are some of these free radicals OH and/or HO2, or radicals of a similar high order of reactivity, and where might they arise in the cell? The most likely source of OH and HO2 radicals, at least in the animal cell, would be the interaction of the respiratory enzymes involved

/pdf/aging-a-theory-based-on-free-radical-and-radiation-chemistry-2cbm9l3kiz.pdf

Aging: A Theory Based on Free Radical and Radiation Chemistry

1. Energetics of reproduction in birds is reviewed with the question in mind how the parent adjusts its effort in relation to prevailing environmental conditions in order to maximize the output of young in its lifetime. Emphasis is on proximate controls, rather than ultimate factors measurable in terms of adult survival and recruitment of young. 2. The decision to breed or not to breed is clearly related to body condition of the female, presumably because of the implications this has for survival. 3. Laying date and clutch size are likewise under the influence of female condition and can hence be modified by experiments involving supplementary feeding. Natural variation in these features may often be related to territory quality. 4. How the bird decides whether or not to commence a second brood is not clear, but in the Great Tit the habitat-related difference in incidence of second broods is functionally understandable when survival probabilities of birds at different times are considered. 5. A distinction is made between a "capital" and "income" model for translatting rates of change of female body condition into appropriate decisions on laying date and clutch size and experiments are suggested that discriminate between the two. 6. Lack's view that brood size is in an evolutionary sense adjusted in order to balance food requirement and foraging capacity of the parents is accepted, and growth rates in nidicolous birds are analysed to ascertain if a finer adjustment exists superimposed on the integer steps of brood adjustment. Critical for this analysis are groups of birds where broods of one are common, since only in these circumstances is growth adjustment the only strategy open to the parents. In common with other animals, growth rate is related to mature body size but within a category of adult weight clear examples can be found for retardation of growth rate in pelecaniform and charadriiform species with singleton broods. 7. Since daily energy requirement is related to nestling size and growth rate, retardation of growth is explicable as a strategy only in terms of reducing the daily commitment of the parents, not reducing the total cost of producing a nestling. 8. An additional economy in growth is to reduce the contribution of fat to the nestling body. 9. Implied in Lack's view of brood size is a limitation of parental foraging capacity, and the last section of the paper is devoted to exploration of the proximate factors delimiting what Royama terms the optimal working capacity of parents feeding young. Observations of parent starlings confronted with manipulated brood size suggest a limit on the time that can be devoted to energetically extravagant flight activity, rather than a shortage of absolute time. Beyond the limit to which stressed parents can be made to fly, body weight declines. 10. Preliminary data on energy metabolized daily by parents confronted with large broods conforms to the simplified view that parental effort on a sustained basis equates to energy mobilization equivalent to 4 B.M.R. units and it is suggested that this level of energy expenditure represents a proximal decision substrate for determining the optimal working capacity of the parent. 11. The paper ends with a plea for more research on the proximate controls of avian reproduction, and calls attention to the central importance of the protein bank to parental body condition.

/pdf/the-prudent-parent-energetic-adjustments-in-avian-breeding-413z510qhu.pdf

The prudent parent: Energetic adjustments in avian breeding

The molecular origin of standard metabolic rate and thermogenesis in mammals is examined. It is pointed out that there are important differences and distinctions between the cellular reactions that 1) couple to oxygen consumption, 2) uncouple metabolism, 3) hydrolyze ATP, 4) control metabolic rate, 5) regulate metabolic rate, 6) produce heat, and 7) dissipate free energy. The quantitative contribution of different cellular reactions to these processes is assessed in mammals. We estimate that approximately 90% of mammalian oxygen consumption in the standard state is mitochondrial, of which approximately 20% is uncoupled by the mitochondrial proton leak and 80% is coupled to ATP synthesis. The consequences of the significant contribution of proton leak to standard metabolic rate for tissue P-to-O ratio, heat production, and free energy dissipation by oxidative phosphorylation and the estimated contribution of ATP-consuming processes to tissue oxygen consumption rate are discussed. Of the 80% of oxygen consumption coupled to ATP synthesis, approximately 25-30% is used by protein synthesis, 19-28% by the Na(+)-K(+)-ATPase, 4-8% by the Ca2(+)-ATPase, 2-8% by the actinomyosin ATPase, 7-10% by gluconeogenesis, and 3% by ureagenesis, with mRNA synthesis and substrate cycling also making significant contributions. The main cellular reactions that uncouple standard energy metabolism are the Na+, K+, H+, and Ca2+ channels and leaks of cell membranes and protein breakdown. Cellular metabolic rate is controlled by a number of processes including metabolic demand and substrate supply. The differences in standard metabolic rate between animals of different body mass and phylogeny appear to be due to proportionate changes in the whole of energy metabolism. Heat is produced by some reactions and taken up by others but is mainly produced by the reactions of mitochondrial respiration, oxidative phosphorylation, and proton leak on the inner mitochondrial membrane. Free energy is dissipated by all cellular reactions, but the major contributions are by the ATP-utilizing reactions and the uncoupling reactions. The functions and evolutionary significance of standard metabolic rate are discussed.

Cellular energy utilization and molecular origin of standard metabolic rate in mammals

T _ HE work reviewed in this paper is aimed at establishing connections between two fundamental aspects of living organisms, their metabolism and growth. What we call growth of even a simple organism is a tremendously complex phenomenon from the biochemical, physiological, cytological, and morphological viewpoints. There are, however, certain aspects that are amenable to quantitative analysis, and such an approach appears to lead to some insight into the connections between metabolism and growth, and to some answer to the seemingly trivial, but in fact hardly explored question, \"Why does an organism grow at all, and why, after a certain time, does its growth come to a stop?\

Quantitative Laws in Metabolism and Growth

Fish, like other living systems, must conform to the laws of thermodynamics. Fish gain matter and energy in food, and they lose absorbed matter and energy as a result of catabolism—which provides energy for maintenance and activity—and the elaboration of reproductive products. Physiological energetics, or animal bioenergetics, concerns the rates of energy expenditure, the losses and gains, and the efficiencies of energy transformation, as functional relations of the whole organism. The majority of such presentations commence with an energy-flow diagram indicating the main steps that the energy of food intake follows through the organism, and the paths of energy distribution. Each of these steps with their appropriate values is subject to quantitative change, depending on many biotic and abiotic factors. With the thought that the basis of these energy exchanges needs to be elaborated first, it was deemed more fitting to conclude with a quantitatively expressed flow diagram. An understanding of the physical, chemical, and biological basis on which the energetics is built, and the equivalents employed, constitutes the opening section of this chapter. Some necessary distinctions between mammalian and nonmammalian systems are made. An adequately nutritious diet is assumed; the basic source of fuel for the fire of life is solely derived from the food.

Samuel Brody

Papers

Bioenergetics and growth