Stress metabolism

A variety of responses can be initiated by the direct interaction of metals with cellular components. Membrane damage and enzyme inhibition are examples of such a metal effect. Above a certain threshold concentration of metals in the cell, its physiological state is irreversibly changed (Van Assche et al., 1988). This response is reflected by an increase in capacity (activity under non-limiting substrate and coenzyme concentrations) of certain enzymes. This increase in capacity is generally called enzyme induction. These secondary, indirect effects of metals are considered to play an important role in the stress metabolism induced by toxic metal concentrations. 

This phenomenon is shown graphically in Figure 24. Under a normal range of temperatures, normal cellular protein synthesis proceeds. However, as the temperature rises, normal cellular metabolism decreases and heat stress metabolism increases until finally normal protein synthesis is stopped. Perhaps by understanding how to control the expression of normal cellular proteins, it may be possible to engineer plants that continue to express... 

In cirrhotic patients, a reduced synthesis rate of most proteins is found at an early stage, with albumin synthesis being the least compromised factor at first. Fat storage, muscle mass and protein turnover are reduced. This ultimately leads to catabolism (so-called stress metabolism) and increasing muscular atrophy (so-called wasting syndrome). The latter condition can also result from sympathicotonia with elevated catecholamine values similarly, decreased values of IGFl inhibit the formation of muscle tissue. 

Oxidative stress can be caused by a wide variety of factors, including inflammatory responses to infections or immune activation, exposure to heavy metals or toxic substances (Carpenter et al., 2002), and oxidative stress increases during the natural course of aging (Junqueira et al., 2007). When oxidative stress is induced by environmental exposures it represents a significant component of the toxicity syndrome, and most xenobiotics share the ability to cause oxidative stress. As a consequence, the effects of multiple exposures are additive at the level of oxidative stress. Metabolic changes associated with oxidative stress can be considered to be adaptive responses that increase prospects for survival during these stressful episodes. 

Shangari N et al., Toxicity of glyoxals-role of oxidative stress, metabolic detoxification and thiamine deficiency, Biochem. Soc. Trans., 31, 1390, 2003. 

Vemuganti, R., Kalluri, H., Yi, J.-H., Bowen, K.K., and Hazell, A.S., 2006. Gene expression changes in thalamus and inferior colliculus associated with inflammation, cellular stress, metabolism, and structural damage in thiamine deficiency. European Journal of Neuroscience. 23 1172-1188. 

Kuc J. Phytoalexins, stress metabolism, and disease resistance in plants. Annu Rev Phytopathol 1995 33 275-297. 

Hoffm. and Usnea longissima Ach. Lichen species. Turk J Oiem 35 647-661 Behera BC, Verma N, Sonone A et al (2005) Antimicrobial activity of Various solvent extracts of Lichen Usnea ghattensis. Agarkar Research Institute, Pune, India. Biotechnol Lett 27 991-995 Benzie IFF, Strain JJ (1996) The ferric reducing ability of plasma (FRAP) as a measure of antioxidant power the FRAP assay. Anal Biochem 239 70-76 Benzie IFF, Szeto YT (1999) Total antioxidant capacity of teas by the ferric reducing/antioxidant power assay. J Agric Food Chem 47 633-636 Betteridge DJ (2000) What is oxidative stress Metabolism 49 3-8... 

Stress response (Immune system) Osmoregulation Metabolism... 

In addition to reproductive effects, fish exposed to endocrine disrupters may have a decreased response to stress or decreased growth and metabolism which can affect their ability to survive, or to defend themselves against predators. All of these factors can affect the ability of the species to survive and to reproduce itself in sufficient numbers to maintain the stocks on which our commercial and sport fisheries are based. Not all fish species will be equally susceptible to the effects of endocrine disrupters. Selective sensitivity to such effects, especially those affecting reproduction, may well lead to major changes in the flora and fauna of some of our major aquatic ecosystems as the balance between fish, mammals, invertebrates and plants, and between predators and prey, is destabilised... 

The second method is by use of the heart rate. The total heart rate is regarded as a sum of several components and, in general, is linearly related to the metabolic heat production for heart rates above 120 beats per minute. Heat stress will, however, also increase the heat rate. The third method is to calculate the metabolic heat production from measures of oxygen consumption, and carbon dioxide production during activity and recovery. 

The primary fate of acetyl CoA under normal metabolic conditions is degradation in the citric acid cycle to yield C02. When the body is stressed by prolonged starvation, however, acetyl CoA is converted into compounds called ketone bodies, which can be used by the brain as a temporary fuel. Fill in the missing information indicated by the four question marks in the following biochemical pathway for the synthesis of ketone bodies from acetyl CoA ... 

Adrenaline (epinephrine) is a catecholamine, which is released as a neurotransmitter from neurons in the central nervous system and as a hormone from chromaffin cells of the adrenal gland. Adrenaline is required for increased metabolic and cardiovascular demand during stress. Its cellular actions are mediated via plasma membrane bound G-protein-coupled receptors. 

A principle glucocorticoid produced in the zona glometulosa of the adrenal cortex. It is involved in modulating stress responses, immune reactions and food metabolism. 

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