Metabolic breakdown

Glutamic acid is formed m most organisms from ammonia and a ketoglutaric acid a Ketoglutaric acid is one of the intermediates m the tricarboxylic acid cycle (also called the Krebs cycle) and arises via metabolic breakdown of food sources carbohy drates fats and proteins... 

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

Biochemistry is carbonyl chemistiy. Almost all metabolic pathways used by living organisms involve one or more of the four fundamental carbonvl-group reactions we ve seen in Chapters 19 through 23. The digestion and metabolic breakdown of all the major classes of food molecules—fats, carbohydrates, and proteins—take place by nucleophilic addition reactions, nucleophilic acyl substitutions, a substitutions, and carbonyl condensations. Similarly, hormones and other crucial biological molecules are built up from smaller precursors by these same carbonyl-group reactions. 

The metabolic breakdown of triacylglycerols begins with their hydrolysis to yield glycerol plus fatty acids. The reaction is catalyzed by a lipase, whose mechanism of action is shown in Figure 29.2. The active site of the enzyme contains a catalytic triad of aspartic acid, histidine, and serine residues, which act cooperatively to provide the necessary acid and base catalysis for the individual steps. Hydrolysis is accomplished by two sequential nucleophilic acyl substitution reactions, one that covalently binds an acyl group to the side chain -OH of a serine residue on the enzyme and a second that frees the fatty acid from the enzyme. 

One of the most striking features of the common fatty adds is that they have an even number of carbon atoms (Table 27.1, p. 1062). This even number results because all fatty acids are derived biosynthelically from acetyl CoA by sequential addition of two-carbon units to a growing chain. The acetyl CoA, in turn, arises primarily from the metabolic breakdown of carbohydrates in the glycolysis pathway that weTl see in Section 29.5. Thus, dietary carbohydrates consumed in excess of immediate energy needs are turned into fats for storage. 

Redox reactions can proceed by direct transfer of electrons between chemical species. Examples include the rusting of iron and the metabolic breakdown of carbohydrates. Redox processes also can take place by indirect electron transfer from one chemical species to another via an electrical circuit. When a chemical reaction is coupled with electron flow through a circuit, the process is electrochemical. Flashlight batteries and aluminum smelters involve electrochemical processes. 

Metabolism converts a lipophilic molecule into a more hydrophilic (water-loving) metabolite that can be excreted in urine by the kidneys. In the majority of cases the drug is detoxified, or made pharmacologically inactive by this metabolic breakdown. However, a few drugs need to be metabolised to become psychoactive for instance, the sedative-hypnotic chloral hydrate is converted to the active metabolite trichloroethanol. In this case the parent molecule is referred to as a prodrug. With many drugs, both the parent compound and its metabolites are psychoactive. An example of this is the tricyclic antidepressant imipramine which is metabolised to desipramine, with... 

Work has also been done on the absorption and inactivation of organomercurials by micro-organisms that tolerate and even thrive on mercurials [26, 27]. It has been postulated that inactivation occurred by the uptake of fungicide by micro-organisms, followed by metabolic breakdown and by possible utilization of portions of the byproducts. However, whether or not biological inactivation and mercury evolution occur together has not been determined. 

Creatinine is a metabolic breakdown product of muscle and usually has a constant value in an individual. Its value ranges from 0.6 mg/100 mL of serum to 1.2 mg/100 mL of serum. Creatinine is almost exclusively eliminated by the kidneys. Therefore, if the level of creatinine increases in the serum, it is likely that the capability of kidneys to eliminate the drugs is reduced. As a general rule, if the serum creatinine level (Ccr) is doubled, the kidney function is one-half. If the Ccr is quadrupled, the renal (kidney) function is one-fourth or 25%. 

Endrin and endrin aldehyde can enter your body when you eat foods or drink beverages or breathe air that contain this substance, or when it comes in contact with your skin. When endrin enters your body in any of these ways, it is rapidly changed into other substances. Endrin and its metabolic breakdown products are rapidly removed from the body, usually within a few days, through the urine and feces. There is some evidence that small amounts of endrin may remain in the fatty tissue of your body when you are exposed to high levels. No information is known about how endrin aldehyde or endrin ketone leaves the body. 

Other drugs, like GHB and Rohypnol , can interact directly with the neurotransmitter receptors to either enhance or block the effects of the brain s own neurotransmitters. Still other drugs can alter the metabolic breakdown or clearance of certain neurotransmitters after they are released from the synaptic terminal, thereby altering how long the neurotransmitter affects the activity of other nearby neurons. 

The mechanism of bromomethane-induced neurotoxicity is not known. It is generally agreed that effects are not the result of metabolic breakdown products such as methanol or bromide, since neither the characteristic effects nor the dose dependency correspond to those of the metabolites (Clarke et al. 1945 Honma et al. 1985). Rather, it is more likely that bromomethane acts by alkylating key cellular components such as enzymes (Lewis 1948 Rathus and Landy 1961). 

Drug molecules that have traversed the physieal and enzymatic barriers of the colonic mucosa may enter the blood-eapillary bed or the lymphatic sinuses. Intact drug that reaches the venous capillaries from the submucosa is transported to the liver via the hepatic-portal system where they may undergo significant metabolism. On the other hand, uptake into the lymphatie sinuses of the colon results in direct delivery into the systemic circulation that causes less metabolic breakdown of the absorbed drug [3]. 

Exposure Levels in Humans. Cresols are naturally occurring substances that are present in human urine (Fiege and Bayer 1987), and data on this are available. Cresols may also be present as a result of the metabolic breakdown of other organic compounds, such as toluene (Needham et al. 1984). As such positive monitoring for cresols in humans does not necessarily mean exposure to them. The ability to rigorously establish cresol exposure levels in humans has yet to be demonstrated. 

Together, the chemistry of codeine and the drug s absorption into the bloodstream, distribution to various compartments and tissues in the body, metabolism (breakdown of the parent compound into smaller molecules, or metabolites), and excretion are intimately related to how codeine exerts its medicinal or therapeutic effects. Codeine s chemical properties and pharmacologic characteristics explain how, figuratively speaking, a spoonful of codeine can relieve pain, suppress cough, or act as an antidiarrheal. 

Local anesthetics are frequently coadministered with vasoconstrictor molecules such as epinephrine. Normally, they are applied or injected locally and then taken up by local blood vessels into the systemic circulation, ultimately leading to their metabolic breakdown. The co-administration of a vasoconstrictor decreases the systemic absorption of the local anesthetic, thereby increasing its effective half-life in the area of administration and decreasing the probability of systemic toxicity (i.e., cardiac toxicity) secondary to systemic distribution. 

Alanine occupies a central role in intermediary metabolism, primarily as the metabolic breakdown product of pyrimidine (uracil, cytidine) metabolism [7]. Increases in /1-alanine may also be detected in hyper-/ -alaninemia, GABA-T deficiency (see above), and putative combined semialdehyde dehydrogenase deficiency... 

Furukawa, K., Tomizuka, N. Kamibayashi, A. (1983). Metabolic breakdown of kaneclors (polychlorobiphenyls) and their products by Acinetobacter sp. Applied and Environmental Microbiology, 46, 140-5. 

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