No abstract

Depression of metabolic rate has been recorded for virtually all major animal phyla in response to environmental stress. The extent of depression is usually measured as the ratio of the depressed metabolic rate to the normal resting metabolic rate. Metabolic rate is sometimes only depressed to approx. 80 % of the resting value (i.e. a depression of approx. 20 % of resting) ; it is more commonly 5-40 % of resting (i.e. a depression of approx. 60-95 % of resting) ; extreme depression is to 1 % or less of resting, or even to an unmeasurably low metabolic rate (i.e. a depression of approx. 99-100 % of resting). We have examined the resting and depressed metabolic rate of animals as a function of their body mass, corrected to a common temperature. This allometric approach allows ready comparison of the absolute level of both resting and depressed metabolic rate for various animals, and suggests three general patterns of metabolic depression.Firstly, metabolic depression to approx. 0.05-0.4 of rest is a common and remarkably consistent pattern for various non-cryptobiotic animals (e.g. molluscs, earthworms, crustaceans, fishes, amphibians, reptiles). This extent of metabolic depression is typical for dormant animals with ' intrinsic ' depression, i.e. reduction of metabolic rate in anticipation of adverse environmental conditions but without substantial changes to their ionic or osmotic status, or state of body water. Some of these types of animal are able to survive anoxia for limited periods, and their anaerobic metabolic depression is also to approx. 0.05-0.4 of resting. Metabolic depression to much less than 0.2 of resting is apparent for some ' resting ', ' over-wintering ' or diapaused eggs of these animals, but this can be due to early developmental arrest so that the egg has a low ' metabolic mass ' of developed tissue (compared to the overall mass of the egg) with no metabolic depression, rather than having metabolic depression of the entire cell mass. A profound decrease in metabolic rate occurs in hibernating (or aestivating) mammals and birds during torpor, e.g. to less than 0.01 of pre-torpor metabolic rate, but there is often no intrinsic metabolic depression in addition to that reduction in metabolic rate due to readjustment of thermoregulatory control and a decrease in body temperature with a concommitant Q "! effect. There may be a modest intrinsic metabolic depression for some species in shallow torpor (to approx. 0.86) and a more substantial metabolic depression for deep torpor (approx. 0.6), but any energy saving accruing from this intrinsic depression is small compared to the substantial savings accrued from the readjustment of thermoregulation and the Q "! effect. Secondly, a more extreme pattern of metabolic depression (to 0.05 of rest) is evident for cryptobiotic animals. For these animals there is a profound change in their internal environment -for anoxybiotic animals there is an absence of oxygen and for osmobiotic, anhydrobiotic or cryobiotic animals there is an alteration of the ionic\osmot...

Depression of metabolic rate has been recorded for virtually all major animal phyla in response to environmental stress. The extent of depression is usually measured as the ratio of the depressed metabolic rate to the normal resting metabolic rate. Metabolic rate is sometimes only depressed to approx. 80% of the resting value (i.e. a depression of approx. 20% of resting); it is more commonly 5-40% of resting (i.e. a depression of approx. 60-95% of resting); extreme depression is to 1% or less of resting, or even to an unmeasurably low metabolic rate (i.e. a depression of approx. 99-100% of resting). We have examined the resting and depressed metabolic rate of animals as a function of their body mass, corrected to a common temperature. This allometric approach allows ready comparison of the absolute level of both resting and depressed metabolic rate for various animals, and suggests three general patterns of metabolic depression. Firstly, metabolic depression to approx. 0.05-0.4 of rest is a common and remarkably consistent pattern for various non-cryptobiotic animals (e.g. molluscs, earthworms, crustaceans, fishes, amphibians, reptiles). This extent of metabolic depression is typical for dormant animals with 'intrinsic' depression, i.e. reduction of metabolic rate in anticipation of adverse environmental conditions but without substantial changes to their ionic or osmotic status, or state of body water. Some of these types of animal are able to survive anoxia for limited periods, and their anaerobic metabolic depression is also to approx. 0.05-0.4 of resting. Metabolic depression to much less than 0.2 of resting is apparent for some 'resting', 'over-wintering' or diapaused eggs of these animals, but this can be due to early developmental arrest so that the egg has a low 'metabolic mass' of developed tissue (compared to the overall mass of the egg) with no metabolic depression, rather than having metabolic depression of the entire cell mass. A profound decrease in metabolic rate occurs in hibernating (or aestivating) mammals and birds during torpor, e.g. to less than 0.01 of pre-torpor metabolic rate, but there is often no intrinsic metabolic depression in addition to that reduction in metabolic rate due to readjustment of thermoregulatory control and a decrease in body temperature with a concommitant Q10 effect. There may be a modest intrinsic metabolic depression for some species in shallow torpor (to approx. 0.86) and a more substantial metabolic depression for deep torpor (approx. 0.6), but any energy saving accruing from this intrinsic depression is small compared to the substantial savings accrued from the readjustment of thermoregulation and the Q10 effect. Secondly, a more extreme pattern of metabolic depression (to < 0.05 of rest) is evident for cryptobiotic animals. For these animals there is a profound change in their internal environment--for anoxybiotic animals there is an absence of oxygen and for osmobiotic, anhydrobiotic or cryobiotic animals there is an alteration of the ionic/osmotic balance or s...

For the past 70 years the dominant perception of cancer metabolism has been that it is fuelled mainly by glucose (via aerobic glycolysis) and glutamine. Consequently, investigations into the diagnosis, treatment and the basic metabolism of cancer cells have been directed by this perception. However, the data on cancer metabolism are equivocal, and in this study we have sought to clarify the issue. Using an innovative system we have measured the total ATP turnover of the MCF-7 breast cancer cell line, the contributions to this turnover by oxidative and glycolytic ATP production and the contributions to the oxidative component by glucose, lactate, glutamine, palmitate and oleate. The total ATP turnover over approx. 5days was 26.8μmol of ATP·107 cells−1·h−1. ATP production was 80% oxidative and 20% glycolytic. Contributions to the oxidative component were approx. 10% glucose, 14% glutamine, 7% palmitate, 4% oleate and 65% from unidentified sources. The contribution by glucose (glycolysis and oxidation) to total ATP turnover was 28.8%, glutamine contributed 10.7% and glucose and glutamine combined contributed 40%. Glucose and glutamine are significant fuels, but they account for less than half of the total ATP turnover. The contribution of aerobic glycolysis is not different from that in a variety of other non-transformed cell types.

Harvard University Press, 1987.) £23.95. appearance of an insect and the heart beating once more stimulated discussions of the meaning of life and whether Polypedilum should be the first interstellar traveller as its ancestors perhaps once were.Had we had this book it would have been a reminder that metabolic arrest is a continuum and that many organisms have been able to harness the necessary mechanisms to some extent or other. D. F. HOULIHAN Scientific Basis of Dermatology. A Physiological Approach. Edited by A. J. THODAY and P. S. FRIEDMANN. Pp 375. (Churchill Livingstone, 1986.) £40.00.An understanding of the processes occurring in diseased skin relies heavily on a prior knowledge of skin physiology. This book sets out, in one volume, to discuss normal skin function and to use this as a background for a consideration of selected types of skin disease.This book is divided into two sections of approximately equal length. The first section deals with normal cutaneous physiology. An introductory chapter, which provides a foundation in the form of an overview, is followed by eight others which discuss mechanical and physical functions, resistance to permeability, protection against ultraviolet radiation and the skin's immune, sensory, thermoregulatory, communicatory and endocrine roles. The authors are, in the main, concerned with human skin physiology but refer in a number of areas, notably with respect to thermoregulation and the communicatory role of skin, to other species. This sortie into comparative dermatology not only aids an understanding of skin function in man but also extends the potential readership of the book,

Rat thymocytes have been used to characterize the changes in energy metabolism that occur as cells undergo a resting/proliferation transition. In the resting state, anaerobic ATP production accounts for only 4% of ATP turnover. The remainder is fueled by the oxidation of a mixture of an unidentified endogenous fuel (62%), glucose (18%) and glutamine (16%). 48 h after mitogen stimulation, the ATP turnover has increased twofold. In these proliferating cells, glucose inhibits oxygen consumption by 58%, indicating a profound Crabtree effect which is not present in resting cells. Consequently, proliferating cells, in the presence of glucose and glutamine, fuel the majority (61%) of ATP turnover anaerobically, producing lactate from glucose. The development of a Crabtree effect may be the result of the 8-10-fold increase in glycolytic enzyme activities which occurs with proliferation. Possible advantages of such a proliferative metabolism are a sparing of endogenous fuel, and a minimizing of oxidative metabolism, with its concurrent production of free radicals.The Crabtree effect (the inhibition of oxygen consumption by the addition of glucose) was first described in tumor tissue (Crabtree, 1929). A Crabtree effect must by necessity result in aerobic glycolysis (the production of lactate despite the presence of mitochondria and oxygen), a phenomenon that was documented by Warburg in 1929. The Crabtree effect and/or aerobic glycolysis has been demonstrated in a variety of cancer cells (Nelson et al., 1984;Racker, 1965;Sener et al., 1988;Burk et al., 1967;Brand et al., 1986), as well as non-cancer tissues such as pig platelets, coronary epithelium, guinea pig sperm, hamster embryos, thymocytes and smooth muscle (Nishimura and Minakami, 1975; No11 et al., 1990; Mujica et al., 1991 ;Seshagiri and Bavister, 1991 ;Brand, 1985;Barron et al., 1991).The more general occurrence, of at least aerobic glycolysis, led to the suggestion that these processes are a characteristic of proliferative metabolism rather than cancer metabolism per se (for a compilation of pertinant literature, see Wang et al., 1976). Proliferative metabolism is of course an integral part of cancer metabolism. Data on proliferative metabolism are rare, but two very recent studies do not support such a link. In Ehrlich ascites tumor cells, ATP turnover increases by 1.5-fold with proliferation, the increase is fueled oxidatively, and the rate of aerobic lactate production is constant and high, accounting for 35 -50% of ATP turnover (Schmidt et al., 1991). In this case, aerobic glycolysis is evident, but there is no evidence of glycolysis assuming a greater role in ATP production with proliferation, and a possible correlation between proliferation and a Crabtree effect was not investigated. Data on proliferating and differentiating mouse erythroid cells, although very limited, again suggest limited glucose oxidation, but no correlation between glycolytic ATP production and proliferatioddifferentiation (Kim et al., 1991).Rat thymocytes provide a model system for...

Arterial blood gas tensions, pH, and hemoglobin concentrations were measured in four free-diving Weddell seals Leptonychotes weddelli. A microprocessor-controlled sampling system enabled us to obtain 24 single and 31 serial aortic blood samples. The arterial O2 tension (PaO2) at rest [78 +/- 13 (SD) Torr] increased with diving compression to a maximum measured value of 232 Torr and then rapidly decreased to 25-35 Torr. The lowest diving PaO2 we measured was 18 Torr just before the seal surfaced from a 27-min dive. A consistent increase of arterial hemoglobin concentrations from 15.1 +/- 1.10 to 22.4 +/- 1.41 g/100 ml (dives less than 17 min) and to 25.4 +/- 0.79 g/100 ml (dives greater than 17 min) occurred during each dive. We suggest that an extension of the sympathetic outflow of the diving reflex possibly caused profound contraction of the Weddell seal's very large spleen (0.89% of body wt at autopsy), although we have no direct evidence. This contraction may have injected large quantities of red blood cells (2/3 of the total) into the seal's central circulation during diving and allowed arterial O2 content to remain constant for the first 15-18 min of long dives. The increase of arterial CO2 tensions during the dive and the compression increase of arterial N2 tensions were also moderated by injecting red blood cells sequestered at ambient pressure. After each dive circulating red blood cells are oxygenated and rapidly sequestered, possibly in the spleen during the first 15 min of recovery.

Arterial blood nitrogen tensions of free-diving Weddell seals (Leptonychotes weddelli) were measured by attaching a microprocessor-controlled blood pump and drawing samples at depth to determine how these marine mammals dive to great depths and ascend rapidly without developing decompression sickness. Forty-seven samples of arterial blood were obtained from four Weddell seals during free dives lasting up to 23 minutes to depths of 230 meters beneath the sea ice of McMurdo Sound, Antarctica. Peak arterial blood nitrogen tensions of between 2000 and 2500 millimeters of mercury were recorded at depths of 40 to 80 meters during descent, indicating that the seal's lung collapses by 25 to 50 meters. Then arterial blood nitrogen tensions slowly decreased to about 1500 millimeters of mercury at the surface. In a single dive, alveolar collapse and redistribution of blood nitrogen allow the seal to avoid nitrogen narcosis and decompression sickness.