CiteULike: Zman's library [30 articles]

The stress response in fish

SE Wendelaar-Bonga — 2008-07-17T06:20:52-00:00

Physiological Review, Vol. 77, No. 3. (1 July 1997), pp. 591-625.

The stress response in teleost fish shows many similarities to that of the terrestrial vertebrates. These concern the principal messengers of the brain-sympathetic-chromaffin cell axis (equivalent of the brain-sympathetic-adrenal medulla axis) and the brain-pituitary-interrenal axis (equivalent of the brain-pituitary-adrenal axis), as well as their functions, involving stimulation of oxygen uptake and transfer, mobilization of energy substrates, reallocation of energy away from growth and reproduction, and mainly suppressive effects on immune functions. There is also growing evidence for intensive interaction between the neuroendocrine system and the immune system in fish. Conspicuous differences, however, are present, and these are primarily related to the aquatic environment of fishes. For example, stressors increase the permeability of the surface epithelia, including the gills, to water and ions, and thus induce systemic hydromineral disturbances. High circulating catecholamine levels as well as structural damage to the gills and perhaps the skin are prime causal factors. This is associated with increased cellular turnover in these organs. In fish, cortisol combines glucocorticoid and mineralocorticoid actions, with the latter being essential for the restoration of hydromineral homeostasis, in concert with hormones such as prolactin (in freshwater) and growth hormone (in seawater). Toxic stressors are part of the stress literature in fish more so than in mammals. This is mainly related to the fact that fish are exposed to aquatic pollutants via the extensive and delicate respiratory surface of the gills and, in seawater, also via drinking. The high bioavailability of many chemicals in water is an additional factor. Together with the variety of highly sensitive perceptive mechanisms in the integument, this may explain why so many pollutants evoke an integrated stress response in fish in addition to their toxic effects at the cell and tissue levels. Exposure to chemicals may also directly compromise the stress response by interfering with specific neuroendocrine control mechanisms. Because hydromineral disturbance is inherent to stress in fish, external factors such as water pH, mineral composition, and ionic calcium levels have a significant impact on stressor intensity. Although the species studied comprise a small and nonrepresentative sample of the almost 20,000 known teleost species, there are many indications that the stress response is variable and flexible in fish, in line with the great diversity of adaptations that enable these animals to live in a large variety of aquatic habitats.

Tradeoffs and the evolution of thermal reaction norms

Michael Angilletta — 2008-01-25T19:31:44-00:00

Trends in Ecology & Evolution, Vol. 18, No. 5. (May 2003), pp. 234-240.

Tradeoffs have played a prominent role in the development of theories describing the evolution of reaction norms. Different classes of tradeoffs are known to constrain the evolution of phenotypes, but current theories incorporate only a subset of these tradeoffs. Consequently, these theories cannot account for some of the variation in reaction norms that has been observed within and among species. Empirical studies of thermal reaction norms for physiological and life historical traits have shown that different proximate mechanisms can produce similar reaction norms. As a consequence, certain tradeoffs can be circumvented when the fitness costs imposed by these tradeoffs are severe. We argue that a unified theory that includes all classes of tradeoffs would provide a better understanding of the mechanisms that drive the evolution of reaction norms.

Pathogen survival in the external environment and the evolution of virulence

Bruno Walther — 2008-04-22T00:43:41-00:00

Biological Reviews, Vol. 79, No. 4. (2004), pp. 849-869.

ABSTRACT Recent studies have provided evolutionary explanations for much of the variation in mortality among human infectious diseases. One gap in this knowledge concerns respiratory tract pathogens transmitted from person to person by direct contact or through environmental contamination. The sit-and-wait hypothesis predicts that virulence should be positively correlated with durability in the external environment because high durability reduces the dependence of transmission on host mobility. Reviewing the epidemiological and medical literature, we confirm this prediction for respiratory tract pathogens of humans. Our results clearly distinguish a high-virulence high-survival group of variola (smallpox) virus, Mycobacterium tuberculosis, Corynebacterium diphtheriae, Bordetella pertussis, Streptococcus pneumoniae, and influenza virus (where all pathogens have a mean percent mortality 0.01% and mean survival time >10 days) from a low-virulence low-survival group containing ten other pathogens. The correlation between virulence and durability explains three to four times of magnitude of difference in mean percent mortality and mean survival time, using both across-species and phylogenetically controlled analyses. Our findings bear on several areas of active research and public health policy: (1) many pathogens used in the biological control of insects are potential sit-and-wait pathogens as they combine three attributes that are advantageous for pest control: high virulence, long durability after application, and host specificity; (2) emerging pathogens such as the'hospital superbug'methicillin-resistant Staphylococcus aureus (MRSA) and potential bioweapons pathogens such as smallpox virus and anthrax that are particularly dangerous can be discerned by quantifying their durability; (3) hospital settings and the AIDS pandemic may provide footholds for emerging sit-and-wait pathogens; and (4) studies on food-borne and insect pathogens point to future research considering the potential evolutionary trade-offs and genetic linkages between virulence and durability.

Evolutionary Health Promotion

Boyd Eaton — 2008-04-22T00:40:58-00:00

Preventive Medicine, Vol. 34, No. 2. (February 2002), pp. 109-118.

Health promotion's promise is enormous, but its potential is, as yet, unmatched by accomplishment. Life expectancy increases track more closely with economic prosperity and sanitary engineering than with strictly medical advances. Notable achievements in the past century--the decreased incidences of epidemic infections, dental caries, and stomach cancer--are owed to virologists, dentists, and (probably) refrigeration more than to physicians. Prevention speaks against tobacco abuse with a single voice, but in many other areas contradictory research findings have generated skepticism and even indifference among the general public for whom recommendations are targeted. Health promotion's shortcomings may reflect lack of an overall conceptual framework, a deficiency that might be corrected by adopting evolutionary premises: (1) The human genome was selected in past environments far different from those of the present. (2) Cultural evolution now proceeds too rapidly for genetic accomodation--resulting in dissociation between our genes and our lives. (3) This mismatch between biology and lifestyle fosters development of degenerative diseases. These principles could inform a research agenda and, ultimately, public policy: (1) Better characterize differences between ancient and modern life patterns. (2) Identify which of these affect the development of disease. (3) Integrate epidemiological, mechanistic, and genetic data with evolutionary principles to create an overarching formulation upon which to base persuasive, consistent, and effective recommendations.

Host-Parasite Relations, Vectors, and the Evolution of Disease Severity

PW Ewald — 2008-04-21T05:15:24-00:00

Annual Review of Ecology and Systematics, Vol. 14, No. 1. (1983), pp. 465-485.

Evolutionary biology and the treatment of signs and symptoms of infectious disease

Paul Ewald — 2008-04-21T05:11:30-00:00

Journal of Theoretical Biology, Vol. 86, No. 1. (7 September 1980), pp. 169-176.

When viewed from an evolutionary perspective, manifestations of infectious diseases can be classified as (1) adaptations of the host to counteract harmful aspects of the disease, (2) adaptations of the pathogen to manipulate the host, or (3) "side effects" of the disease that do not serve adaptive functions for either the host or the pathogen. Although the functions of most manifestations are not known, support or rejection of these hypotheses should be readily derivable in many cases from analyses of existing data and relatively simple experiments. This approach should lead to improved medical treatment because preferred treatment depends on assessment of the validity of the three explanations. As an illustration, this perspective and its consequences for therapy are analyzed for fever, rhinorrhea and diarrhea.

Widespread amphibian extinctions from epidemic disease driven by global warming

Alan Pounds — 2006-01-12T03:44:31-00:00

Nature, Vol. 439, No. 7073., pp. 161-167.

An ecological and evolutionary perspective on humanâmicrobe mutualism and disease

Les Dethlefsen — 2007-10-20T17:10:38-00:00

Nature, Vol. 449, No. 7164. (17 October 2007), pp. 811-818.

Global trends in emerging infectious diseases

Kate Jones — 2008-02-21T13:23:19-00:00

Nature, Vol. 451, No. 7181., pp. 990-993.

Urbanization and the ecology of wildlife diseases

Catherine Bradley — 2008-03-24T06:38:11-00:00

Trends in Ecology & Evolution, Vol. 22, No. 2. (February 2007), pp. 95-102.

Urbanization is intensifying worldwide, with two-thirds of the human population expected to reside in cities within 30 years. The role of cities in human infectious disease is well established, but less is known about how urban landscapes influence wildlife-pathogen interactions. Here, we draw on recent advances in wildlife epidemiology to consider how environmental changes linked with urbanization can alter the biology of hosts, pathogens and vectors. Although urbanization reduces the abundance of many wildlife parasites, transmission can, in some cases, increase among urban-adapted hosts, with effects on rarer wildlife or those living beyond city limits. Continued rapid urbanization, together with risks posed by multi-host pathogens for humans and vulnerable wildlife populations, emphasize the need for future research on wildlife diseases in urban landscapes.

Seasonality and the dynamics of infectious diseases

Sonia Altizer — 2006-03-30T14:33:32-00:00

Ecology Letters, Vol. 9, No. 4. (April 2006), pp. 467-484.

On the Adaptive Significance of Stress-Induced Immunosuppression

Lars Raberg — 2008-03-24T06:29:37-00:00

Proceedings: Biological Sciences, Vol. 265, No. 1406. (1998), pp. 1637-1641.

We approach the field of stress immunology from an ecological point of view and ask: why should a heavy physical workload, for example as a result of a high reproductive effort, compromise immune function? We argue that immunosuppression by neuroendocrine mechanisms, such as stress hormones, during heavy physical workload is adaptive, and consider two different ultimate explanations of such immunosuppression. First, several authors have suggested that the immune system is suppressed to reallocate resources to other metabolic demands. In our view, this hypothesis assumes that considerable amounts of energy or nutrients can be saved by suppressing the immune system; however, this assumption requires further investigation. Second, we suggest an alternative explanation based on the idea that the immune system is tightly regulated by neuroendocrine mechanisms to avoid hyperactivation and ensuing autoimmune responses. We hypothesize that the risk of autoimmune responses increases during heavy physical workload and that the immune system is suppressed to counteract this.

Energy metabolism of fish brain

Jose Soengas — 2008-03-13T07:26:48-00:00

Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology, Vol. 131, No. 3. (March 2002), pp. 271-296.

This review focuses on recent research on the metabolic function of fish brain. Fish brain is isolated from the systemic circulation by a blood-brain barrier that allows the transport of glucose, monocarboxylates and amino acids. The limited information available in fishes suggests that oxidation of exogenous glucose and oxidative phosphorylation provide most of the ATP required for brain function in teleosts, whereas oxidation of ketones and amino acids occurs preferentially in elasmobranchs. In several agnathans and benthic teleosts brain glycogen levels rather than exogenous glucose may be the proximate glucose source for oxidation. In situations when glucose is in limited supply, teleost brains utilize other fuels such as lactate or ketones. Information on use of lipids and amino acids as fuels in fish brain is scarce. The main pathways of brain energy metabolism are changed by several effectors. Thus, several parameters of brain energy metabolism have been demonstrated to change post-prandially in teleostean fishes. The absence of food in teleosts elicits profound changes in brain energy metabolism (increased glycogenolysis and use of ketones) in a way similar to that demonstrated in mammals though delayed in time. Environmental factors induce changes in brain energy parameters in teleosts such as the enhancement of glycogenolysis elicited by pollutants, increased capacity for anaerobic glycolysis under hypoxia/anoxia or changes in substrate utilization elicited by adaptation to cold. Furthermore, several studies demonstrate effects of melatonin, insulin, glucagon, GLP-1, cortisol or catecholamines on energy parameters of teleost brain, although in most cases the results are quite preliminary being difficult to relate the effects of those hormones to physiological situations. The few studies performed with the different cell types available in the nervous system of fish allow us to hypothesize few functional relationships among those cells. Future research perspectives are also outlined.

Reduction of stress response in carp,Cyprinus carpioL., held under deteriorating environmental conditions, by oral administration of bovine lactoferrin

Kakuta — 2008-03-13T07:21:10-00:00

Journal of Fish Diseases, Vol. 21, No. 3. (1998), pp. 161-167.

Abstract Bovine lactoferrin (LF) was evaluated for its ability to suppress stress reactions in carp, Cyprinus carpio L., held under deteriorating environmental conditions. Three test diets containing different levels of LF (0.01, 0.1 and 1%) were fed at 2% of fish body weight per day, i.e. LF at 2, 20 and 200 mg kg-1 body weight day-1 was administered orally to carp for 14 days at 20 oC. In the fish reared at a density of 2 individuals 10 l-1, plasma cortisol, adrenaline and noradrenaline decreased in the groups fed with 0.1 and 1% LF content diets. In the fish held at a density of 10 individuals 10 l-1 for 3 days, plasma cortisol, adrenaline, noradrenaline, dopamine and glucose were higher than those at 2 individuals 10 l-1 in both the control and LF-treated groups. The extent to which these parameters were elevated in the fish held at the same density was reduced with increasing LF content of the diet. Twenty-four hours after exposure to hypoxic conditions (dissolved oxygen level, 2.5 mg l-1), haemoglobin, haematocrit, plasma cortisol, adrenaline, noradrenaline and dopamine increased significantly in all groups. The responses of hypoxic fish fed with 0.1 and 1% LF diets for 14 days were smaller than those of the controls. These results suggest that LF has an ability to reduce the stress response of carp held under deteriorating environmental conditions.

The response of Atlantic cod, Gadus morhua , to progressive hypoxia: fish swimming speed and physiological stress

N Herbert — 2008-03-13T07:17:24-00:00

Marine Biology, Vol. 147, No. 6. (25 October 2005), pp. 1403-1412.

Abstract Atlantic cod, Gadus morhua, were exposed to a progressive stepwise decline in water oxygen pressure $$(19.9, 13.2, 10.5, 8.4, 6.2\,\,\textand\,\,4.3\,\textkPa\; P_ O_2 ).$$ Fish swimming speed and indicators of primary and secondary stress (e.g. blood cortisol and lactate) were measured to assess whether a severe shift in physiological homeostasis (i.e. stress) preceded any change in behaviour or vice versa. Swimming speed increased by 18% when $$P_ O_2 $$ was reduced rapidly from 19.9 kPa to 13.2 kPa and was interpreted as an initial avoidance response. However, swimming speed was reduced by 21% at a moderate level of steady $$P_ O_2$$ (8.4 kPa) and continued to drop by 41% under progressively deep hypoxia (4.3 kPa). Elevations in plasma cortisol and blood lactate indicated major physiological stress but only at 4.3 kPa, which corresponds to the critical oxygen tension of this species. We propose that the drop in speed during hypoxia aids to offset major stress and is adaptive for the survival of cod in extensive areas of low oxygen.

Biochemical indicators of thermal stress in Tilapia aurea (Steindachner)

KR Kindle — 2008-03-13T07:15:44-00:00

Journal of Fish Biology, Vol. 29, No. 2. (1986), pp. 243-255.

Tilapia aurea muscle and liver adenylate nucleotides, the adenylate energy charge (EC), plasma glucose, cortisol and chloride were monitored during acute and chronic temperature stress. Muscle EC is unaffected during acute cold water exposure but decreases significantly when tilapia are exposed to chronic, sublethal, low temperature stress. The decrease in EC is primarily the result of a decrease in ATP concentration. Plasma glucose and cortisol increase when tilapia are exposed to 11-12o C for 60 min, 11 days, and a 5-week period. Incomplete compensation is evident in 5-week acclimated fish since glucose and cortisol levels are intermediate between controls and acutely stressed fish. Acclimation to 35o C does not significantly affect plasma glucose and cortisol compared to controls (22o C). Plasma chloride is relatively unaffected by acute and chronic temperature stress. Liver adenylates are not significantly affected when tilapia are subjected to a sudden drop in water temperature (22o down to 11o C). EC is a useful indicator of chronic low temperature stress in T. aurea, while plasma glucose and cortisol are sensitive to both acute and chronic temperature stress.

Changes in selected blood component concentrations of rainbow trout, Salmo gairdneri Richardson, exposed to hypoxia or sublethal concentrations of phenol or ammonia

DJ Swift — 2008-03-13T07:12:20-00:00

Journal of Fish Biology, Vol. 19, No. 1. (1981), pp. 45-61.

Rainbow trout were exposed to sublethal phenol or non-ionized ammonia concentrations or to hypoxia. Blood samples were taken after various exposure periods and the packed cell volume (PCV) value, the whole blood glucose concentration and the plasma cortisol and chloride ion concentrations measured. At low pollutant concentrations there were no significant changes in the blood components compared to control fish values. At higher concentrations the general response to the stressors was significant increases in the PCV value and the glucose and cortisol concentrations during the first few hours of exposure, followed by a gradual return to normal values in the subsequent exposure time. The increases in glucose and cortisol concentrations were approximately proportional to the pollutant concentrations no such correlation was found for the PCV values. No clear pattern of plasma chloride ion changes was found in any experiment. Levels of no acute effect, in terms of toxic units (TU) based on the pollutants' 48 h LC50 values, were estimated for phenol as 0.3 TU and for un-ionized ammonia as 0.1 TU, using the plasma cortisol concentration measurements. The use of fish blood component measurements as general indicators of a stress response is discussed.

Substrate mobilization and hormonal changes in rainbow trout (Oncorhynchus mykiss, L.) and common carp (Cyprinus carpio, L.) during deep hypoxia and subsequent recovery

M Van Raaij — 2008-03-13T07:08:56-00:00

Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology, Vol. 166, No. 7. (10 November 1996), pp. 443-452.

Abstract Common carp (at 20C) and rainbow trout (at 15C) were fitted with an indwelling cannula in the dorsal aorta. The fish were exposed to a controlled decline of waterpO2 followed by 90 min deep hypoxia at 0.3 kPa (carp) or 4.8 kPa (trout). Thereafter, normoxic recovery was monitored in both species for 48 h. At regular intervals blood samples were analysed for glucose, lactate, free fatty acids, adrenaline, noradrenaline and cortisol. The oxygen restriction was maximal in both species and resulted in a significant increase of plasma lactate levels. In carp, adrenaline, noradrenaline and cortisol levels increased to 2, 50, and 753 ngml-1 respectively during anoxia, whereas in trout these hormones increased to 12, 8 and 735 ngml-1 respectively during hypoxia. In hypoxic trout, the plasma levels of glucose (3 moll-1) were increased modestly whereas levels of free fatty acids (0.25 mmoll-1) were decreased to 0.15 mmoll-1. In carp, however, a marked and prolonged hyperglycaemia (from 5 to 10 mmoll-1) and a significant continuous depression of plasma levels of free fatty acids (from 0.4 to 0.2 mmoll-1) were observed indicating a difference in metabolic organization. It is suggested that hyperglycaemia is likely to be the result of hepatic glycogenolysis, stimulated by circulating catecholamines and a stimulation of gluconeogenesis by cortisol during recovery. The mechanism for the decline of plasma levels of free fatty acids is most probably a reduction of lipolytic activity, which appears to be an adaptation to hypoxia.

Oxidative stress during stressful heat exposure and recovery in the North Sea eelpout Zoarces viviparus L.

Katja Heise — 2008-02-07T06:25:08-00:00

J Exp Biol, Vol. 209, No. 2. (15 January 2006), pp. 353-363.

The interplay between antioxidants, heat shock proteins and hypoxic signaling is supposed to be important for passive survival of critical temperature stress, e.g. during unfavorable conditions in hot summers. We investigated the effect of mild (18degreesC), critical (22degreesC) and severe (26degreesC) experimental heat stress, assumed to induce different degrees of functional hypoxia, as well as the effect of recovery following heat stress on these parameters in liver samples of the common eelpout Zoarces viviparus. Upon heat exposure to critical and higher temperatures we found an increase in oxidative damage markers such as TBARS (thiobarbituric reactive substances) and a more oxidized cellular redox potential, combined with reduced activities of the antioxidant enzyme superoxide dismutase at 26degreesC. Together, these point to higher oxidative stress levels during hyperthermia. In a recovery-time series, heat-induced hypoxia and subsequent reoxygenation upon return of the fishes to 12degreesC led to increased protein oxidation and chemiluminescence rates within the first 12 h of recovery, therein resembling ischemia/reperfusion injury in mammals. HSP70 levels were found to be only slightly elevated after recovery from sub-lethal heat stress, indicating minor importance of the heat shock response in this species. The DNA binding activity of the hypoxia-inducible transcription factor (HIF-1) was elevated only during mild heat exposure (18degreesC), but appeared impaired at more severe heat stress. We suppose that the more oxidized redox state during extreme heat may interfere with the hypoxic signaling response. 10.1242/jeb.01977

Climate Change Affects Marine Fishes Through the Oxygen Limitation of Thermal Tolerance

Hans Portner — 2008-02-07T06:17:51-00:00

Science, Vol. 315, No. 5808. (5 January 2007), pp. 95-97.

A cause-and-effect understanding of climate influences on ecosystems requires evaluation of thermal limits of member species and of their ability to cope with changing temperatures. Laboratory data available for marine fish and invertebrates from various climatic regions led to the hypothesis that, as a unifying principle, a mismatch between the demand for oxygen and the capacity of oxygen supply to tissues is the first mechanism to restrict whole-animal tolerance to thermal extremes. We show in the eelpout, Zoarces viviparus, a bioindicator fish species for environmental monitoring from North and Baltic Seas (Helcom), that thermally limited oxygen delivery closely matches environmental temperatures beyond which growth performance and abundance decrease. Decrements in aerobic performance in warming seas will thus be the first process to cause extinction or relocation to cooler waters. 10.1126/science.1135471

Living Fast, Dying When? The Link between Aging and Energetics

John Speakman — 2008-02-06T06:02:08-00:00

J. Nutr., Vol. 132, No. 6. (1 June 2002), pp. 1583S-1597.

The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die. Evidence supporting the "rate-of-living" theory was gleaned from the scaling of resting metabolism and life span as functions of body mass. The product of these factors yields a mass-invariant term, equivalent to the "amount of living." There are at least four problems with this evidence, which are summarized and reviewed in this communication: 1) life span is a poor measure of aging, 2) resting metabolism is a poor measure of energy expenditure, 3) the effects are confounded by body mass and 4) the comparisons made are not phylogenetically independent. We demonstrate that there is a poor association between resting metabolic rate (RMR) and daily energy expenditure (DEE) measured using the doubly labeled water (DLW) method at the level of species. Nevertheless, the scaling relation between DEE and body mass still has the same scaling exponent as the RMR and body mass relationship. Thus, if we use DEE rather than RMR in the analysis, the rate-of-living ideas are still supported. Data for 13 species of small mammal were obtained, where energy demands by DLW and longevity were reliably known. In these species, there was a strong negative relationship between residual longevity and residual DEE, both with the effects of body mass removed (r2 = 0.763, F = 32.1, P < 0.001). Hence, the association of energy demands and life span is not attributed to the confounding effects of body size. We subjected these latter data to an analysis that extracts phylogenetically independent contrasts, and the relationship remained significant (r2 = 0.815, F = 39.74, P < 0.001). Small mammals that live fast really do die young. However, there are very large differences between species in the amounts of living that each enjoy and these disparities are even greater when other taxa are included in the comparisons. Such differences are incompatible with the "rate-of-living" theory. However, the link between energetics and aging across species is reconcilable within the framework of the "free-radical damage hypothesis" and the "disposable soma hypothesis." Within species one might anticipate the rate-of-living model would be more appropriate. We reviewed data generated from three different sources to evaluate whether this were so, studies in which metabolic rate is experimentally increased and impacts on life span followed, studies of caloric restriction and studies where links between natural variation in metabolism and life span are sought. This review reveals that there might be contrasting effects of resting and nonresting energy expenditure on aging, with increases in the former being protective and increases in the latter being harmful.

Oxygen limited thermal tolerance in fish?: Answers obtained by nuclear magnetic resonance techniques

HO Portner — 2008-02-04T08:10:01-00:00

Respiratory Physiology & Neurobiology, Vol. 141, No. 3. (12 August 2004), pp. 243-260.

In various phyla of marine invertebrates limited capacities of both ventilatory and circulatory performance were found to set the borders of the thermal tolerance window with limitations in aerobic scope and onset of hypoxia as a first line of sensitivity to both cold and warm temperature extremes. The hypothesis of oxygen limited thermal tolerance has recently been investigated in fish using a combination of non-invasive nuclear magnetic resonance (NMR) methodology with invasive techniques. In contrast to observations in marine invertebrates arterial oxygen tensions in fish were independent of temperature, while venous oxygen tensions displayed a thermal optimum. As the fish heart relies on venous oxygen supply, limited cardio-circulatory capacity is concluded to set the first level of thermal intolerance in fish. Nonetheless, maximized ventilatory capacity is seen to support circulation in maintaining the width of thermal tolerance windows. The interdependent setting of low and high tolerance limits is interpreted to result from trade-offs between optimized tissue functional capacity and baseline oxygen demand and energy turnover co-determined by the adjustment of mitochondrial densities and functional properties to a species-specific temperature range. At temperature extremes, systemic hypoxia will elicit metabolic depression, thereby widening the thermal window transiently sustained especially in those species preadapted to hypoxic environments.

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2008-01-31T08:14:20-00:00

How to Review

2008-01-31T08:13:08-00:00

Stress and the evolution of condition-dependent signals

Katherine Buchanan — 2008-01-23T03:24:37-00:00

Trends in Ecology & Evolution, Vol. 15, No. 4. (1 April 2000), pp. 156-160.

Stressful events are known to initiate a cascade of physiological mechanisms that are potentially costly for metabolic processes. Although these mechanisms are well understood, the long-term costs and the potential implications for individual condition and behaviour have been considered only recently. Combining information from physiological, ecological and behavioural studies can help us to understand the implications of stress for individual life history strategies. Furthermore, the concept of individual variation in stress tolerance has implications for the immunocompetence handicap hypothesis and the evolution of secondary sexual signals.

The concept of allostasis in biology and biomedicine

Bruce Mcewen — 2008-01-23T03:13:03-00:00

Hormones and Behavior, Vol. 43, No. 1. (January 2003), pp. 2-15.

Living organisms have regular patterns and routines that involve obtaining food and carrying out life history stages such as breeding, migrating, molting, and hibernating. The acquisition, utilization, and storage of energy reserves (and other resources) are critical to lifetime reproductive success. There are also responses to predictable changes, e.g., seasonal, and unpredictable challenges, i.e., storms and natural disasters. Social organization in many populations provides advantages through cooperation in providing basic necessities and beneficial social support. But there are disadvantages owing to conflict in social hierarchies and competition for resources. Here we discuss the concept of allostasis, maintaining stability through change, as a fundamental process through which organisms actively adjust to both predictable and unpredictable events. Allostatic load refers to the cumulative cost to the body of allostasis, with allostatic overload being a state in which serious pathophysiology can occur. Using the balance between energy input and expenditure as the basis for applying the concept of allostasis, we propose two types of allostatic overload. Type 1 allostatic overload occurs when energy demand exceeds supply, resulting in activation of the emergency life history stage. This serves to direct the animal away from normal life history stages into a survival mode that decreases allostatic load and regains positive energy balance. The normal life cycle can be resumed when the perturbation passes. Type 2 allostatic overload begins when there is sufficient or even excess energy consumption accompanied by social conflict and other types of social dysfunction. The latter is the case in human society and certain situations affecting animals in captivity. In all cases, secretion of glucocorticosteroids and activity of other mediators of allostasis such as the autonomic nervous system, CNS neurotransmitters, and inflammatory cytokines wax and wane with allostatic load. If allostatic load is chronically high, then pathologies develop. Type 2 allostatic overload does not trigger an escape response, and can only be counteracted through learning and changes in the social structure.

Toxic oxygen: The radical life-giver

Doris Abele — 2008-01-23T02:18:52-00:00

Nature, Vol. 420, No. 6911. (7 November 2002), pp. 27-27.

Environmental Stress and Local Adaptation in Daphnia magna

Maarten Boersma — 2008-01-16T04:05:55-00:00

Limnology and Oceanography, Vol. 44, No. 2. (1999), pp. 393-402.

The effects of fish kairomones, crowding chemicals, and day length on the life-history traits of a set of 16 Daphnia magna clones, derived from four populations that differ in fish-predation pressure, were studied. Significant among-population differences were observed, the differences being in concordance with the hypothesis of local adaptation. The among-population genetic differences were not mediated through a change in response to fish kairomones, but through an overall smaller body size, smaller eggs, and a higher number of eggs in clones derived from habitats in which fish are present. Using a model, we show that the observed changes in life-history characteristics may lead to differences in fitness under different predation regimes, such that populations from habitats with fish have highest fitness under fish-predation regimes and populations without a fish background have higher fitness values under invertebrate predation regimes.

Plasticity of Daphnia magna life history traits in response to temperature and information about a predator

Olga Sakwinska — 2008-01-16T04:04:37-00:00

Freshwater Biology, Vol. 39, No. 4. (1998), pp. 681-687.

1. Exudates from predators often elicit early maturation in Daphnia, which may protect them from predation. Diel vertical migration (DVM) is also a predator-avoidance device and affects life history traits because of the variable temperature experienced during migration. This study asks, therefore, how do these two effects interact and what are the net costs and benefits of the two defences combined? 2. Key life history features were studied in a two factorial life table experiment in a monoclonal cohort of Daphnia magna to quantify the costs of predator-induced defences. 3. The costs of DVM, associated with low temperature, yielded a 30 decrease in the intrinsic rate of population increase. This was caused by later maturation and longer egg development time, despite a higher fecundity. 4. Chemical information that predators were present resulted in smaller, more numerous offspring, but had no significant effect on size and age at first reproduction. The costs of induction were therefore associated with smaller, and thus presumably lower quality, offspring. 5. Changes in life history induced by fish exudates were independent of the shifts caused by low temperature. 6. The measure of fitness chosen to assess the costs of induced defences is important because the costs often depend on the environment.

Mitochondrial uncoupling proteins--What is their physiological role?

Karim Echtay — 2007-11-05T19:26:54-00:00

Free Radical Biology and Medicine, Vol. 43, No. 10. (15 November 2007), pp. 1351-1371.

The physiological functions of the mitochondrial uncoupling proteins (UCP2 and UCP3) are still under debate. There is, however, ample evidence to indicate that, in contrast to UCP1, they are not crucial for nonshivering thermogenesis and do not catalyze the basal proton conductance of mitochondria. Rather, there is good evidence that they increase mitochondrial proton conductance when activated by superoxide, reactive oxygen species derivatives such as hydroxynonenal, and other alkenals or their analogues. This review critically examines the evidence of the different proposed mechanisms for UCPs functions, namely (a) to export fatty acid anions from mitochondria, (b) to regulate insulin secretion in pancreatic [beta]-cells, and (c) to cause mild uncoupling and so diminish mitochondrial superoxide production, hence protecting against oxidative damage. Beside, available scientific data on UCP4 and UCP5/BMCP1 will be reviewed. However, their physiological function has not yet been established.