Metabolic compensation temperature

There is a large and somewhat contentious literature dealing with the question of how fully the respiratory rates of ectotherms can be adjusted to offset g10 effects on metabolic reactions, a process known as temperature compensation of metabolism. Metabolic compensation... 

Metabolic acidosis follows, and an increased anion gap results from accumulation of lactate as well as excretion of bicarbonate by the kidney to compensate for respiratory alkalosis. Arterial blood gas testing often reveals this mixed respiratory alkalosis and metabolic acidosis. Body temperature may be elevated owing to uncoupling of oxidative phosphorylation. Severe hyperthermia may occur in serious cases. Vomiting and hyperpnea as well as hyperthermia contribute to fluid loss and dehydration. With very severe poisoning, profound metabolic acidosis, seizures, coma. 

Corrrect answer = E. When phosphorylation is partially uncoupled from electron flow, one would expect a decrease in the proton gradient across the inner mitochondrial membrane and, hence, impaired ATP synthesis. In an attempt to compensate for this delect in energy capture, metabolism and electron flow to oxygen is increased. This hypermetabolism will be accompanied by elevated body temperature because the energy in fuels is largely wasted, appearing as heat. The electron transport chain will still be inhibited by cyanide. 

The concept of temperature compensation of metabolism at the whole animal level in poikilotherms has been subject to strong criticism by Holeton (1974, 1980) and especially by I.V. Ivleva (1981), who believed that such compensation was an artefact arising from inadequate acclimation. However, Ivleva s own experiments were carried out on aquatic invertebrates, not fish, and the data referred to standard metabolism rather than total or active. Note that total metabolism is that taking place in an animal in nature, active metabolism is that which supplies locomotory activity, standard metabolism is that observed in experiments, and basal metabolism is that in the resting state. Ivlev (1959) found that apparent adaptive reactions of animals are seen mostly in active, not standard or basal, metabolism. However, more recent work (Karamushko and Shatunovsky, 1993 Musatov, 1993) appears rather to favour the concept of I.V. Ivleva, that standard, not active, metabolism illustrates the adaptive reactions. 

The results of studies using a wide range of oxidizable substrates showed that, in fact, there was a modicum of temperature compensation, but that it was nothing like the metabolic cold adaptation originally envisaged. Some thermal compensation was also achieved by increasing the density of cristae within the mitochondria, but this was of less importance than actual mitochondrial density. 

Bullock, T.H. (1955). Compensation for temperature in the metabolism and activity of poikilotherms. Biological Reviews of the Cambridge Philosophical Society 30, 311-342. 

Microorganisms have been found growing at depths of 2.8-4.2 km beneath the land surface (Pedersen 1993 Fyfe 1996 Kerr 1997). Microbes at 4.2 km grow at a temperature of 110°C. Temperature, rather than pressure, is probably the most important growth-limiting factor for deep-earth microbes (Pedersen 1993 Fyfe 1996). Organic biopolymers and complex cellular structures tend to be destroyed at elevated temperatures, and apparently elevated metabolism and cellular repair activity does not compensate for the rates at which critical bonds are broken hence, cells cannot repair thermal damage beyond a point. 

Metabolic Effects. The characteristic effects of 2,4-DNP are elevation of the basal metabolic rate (often easured indirectly as oxygen consumption), elevation of body temperature and increased perspiration (humans). The body compensates for these effects by increasing the respiratory rate to deliver more oxygen to the tissues. As body temperature rises, peripheral vasodilation occurs as a cooling mechanism and the pulse rate rises to maintain the circulation. 

Examination of metabolic pathways in extreme thermophiles has provided interesting insights into the necessary adaptations for life at high temperatures and possible explanations for the mechanisms used by early life. These pathways include enzymes not found in mesophiles and that can perform unique reactions which often bypass steps found in conventional pathways characterized in mesophilic organisms (e.g., [33]). These shortened metabolic pathways presumably compensate for changes in equilibrium or instability of intermediates at higher temperatures. Thus, these shortcuts may be of some use in construction of synthetic metabolic pathways. 

The human body maintains an appropriate balance between the metabolic heat that it produces and the environmental heat to which it is exposed. Sweating and the evaporation of the sweat are the body s primary way of trying to maintain an acceptable temperature balance. As sweat (water) evaporates it carries away latent heat, a large amount of heat removed when sweat goes from a liquid phase to a gas phase. However, when heat gain from the environment is more than the body can compensate for by sweating, the result is heat stress. 

The function of psychrophilic enzymes at low temperatures has studied to understand more about biocatalysis. These enzymes have up to 10-fold higher activity than mesophilic enzymes at biologically low temperatures, presumably to compensate for the reduction of chemical reaction rates. Nevertheless, this activity is still lower than that of mesophilic enzymes at 37°C. Psychrophiles maintain catalytic efficiency, kcat/Km, necessary for cellular metabolism, by increased turnover rates, kcat, and increased substrate affinity (lower K i). For instance, a chitobiase from an Antarctic bacterium has a cat of eight times higher than that of a related mesophilic chitobiase at 5°C. Similarly, Km for the substrate is 25 times lower at this temperature, such that the kcat/Km is 200 times that of the mesophilic chitobiase at low temperatures (66). Active site structure also... 

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