Destructive metabolism

Catabolism Destructive metabolism breakdown of complex chemical compounds into simpler ones. 

Metabolic reactions are of two general kinds. Catabolism includes all reactions that break down large molecules into smaller ones with a release of energy, as in the breakdown of carbohydrates. Catabolic reactions are also called destructive metabolism. 

Much of the current work is based on the fact that the side chain can be replaced by an alternative functionality, which contains sulfur. Metabolic destruction presumably involves the readily oxidized thioether groups. 

Spoilage is a biological process. Molds, bacteria, and vermin eat foodstuffs, rendering them unfit for human consumption. To stop spoilage, processors treat food to kill microorganisms, chill it to slow the metabolism of destruction, and keep it sealed to ward off pests. Even in fully developed societies, these procedures are only partially successful, and in economically developing countries, up to 50% of crops may be lost to spoilage. 

The mechanism of action for liver toxicity and carcinogenicity may involve the formation of reactive products (Bonse and Henschler 1976 Bonse et al. 1975 Fisher et al. 1991 Larson and Bull 1992b). Methods for reducing the destructive damage caused by these intermediates, or for blocking their formation through inhibition of metabolic pathways may prove effective in reducing hepatic toxicity but are not currently available for clinical use. 

Reduce destruction. This may be achieved by blocking the neuronal or glial uptake (3a) of the NT or its extra- (3b) or intraneuronal metabolism (3c). Its success depends on there still being an adequate, even if reduced, release of the NT, and the protected NT being able to work postsynaptically and not stimulate autoreceptors to reduce the synaptic release of the endogenous NT even further. If the uptake sites are outside the synapse then the protected NT may not easily gain access to the receptors located postsynaptically. 

A second explanation of the ability of oxidative stress to cause DNA damage is that the stress tri ers a series of metabolic events within the cell that lead to activation of nuclease enzymes, which cleave the DNA backbone. Oxidative stress causes rises in intracellular free Ca, which can fiagment DNA by activating Ca -dependent endonucleases (Orrenius etal., 1989 Farber, 1990 Ueda and Shah, 1992) in a mechanism with some of the features of apoptosis (see Wyllie, 1980). An example of apoptosis is the killing of immature thymocytes by glucocorticoid hormones, which activate a cell-destructive process that apparently involves DNA fragmentation by a Ca -dependent nuclease. 

Effects In Humans. Neither postmortem nor functional cerebrospinal fluid (CSF) studies in humans provide firm evidence for similar, long-term damages or alterations to monoaminergic neurons in chronic stimulant abusers. In part, the lack of demonstrable neurochemical changes may well be due to the obvious preclusion of well-controlled prospective experimentation in humans, as well as to variability in critical variables (e.g., individual sensitivity or pattern of abuse) encountered in clinical research. Possible relationship of the various complications of stimulant abuse including hyperpyrexia, seizure, anoxia, and metabolic exhaustion to neuronal chromatolysis, terminal destruction, and monoamine and enzymatic depletion have not been systematically explored in human autopsy eases. It should be also noted that, under nonperturbed conditions, overt behavioral deficits are rare in... 

Subchondral bone undergoes metabolic changes, including increased bone turnover, that appear to be precursors to tissue destruction. The normally contiguous bony surface becomes fissured. Persistent use of the joint eventually results in loss of cartilage, permitting bone-to-bone contact that ultimately promotes thickening and eburnation of exposed bone. Microfractures may appear in subchondral bone, and osteonecrosis may develop beneath the surface. 

OA is often divided into primary (idiopathic) and secondary disease (Table 55-1). Primary OA is the predominant form and occurs in the absence of a precipitating event. It may assume a localized, generalized, or erosive pattern. Localized OA is distinguished from generalized disease by the number of sites involved, whereas erosive disease is characterized by an erosive pattern of bone destruction and marked proliferation of interphalangeal joints of the hands. Secondary OA occurs when the disease is caused by congenital or developmental disorders or inflammatory, metabolic, or endocrine diseases. 

Gout A group of disorders of purine metabolism, manifested by various combinations of hyperuricemia recurrent acute inflammatory arthritis induced by crystals of monosodium urate monohydrate tophaceous deposits of monosodium urate monohydrate crystals in and around the joints of the extremities, which may lead to crippling destruction of joints and uric acid urolithiasis. 

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