Aminoacid toxicity

Other Examples of the Use of Principal Properties Characterization by principal properties has been reported for classes of compounds in applications other than organic synthesis Aminoacids, where principal properties have been used for quantitative structure-activity relations (QSAR) of peptides [64], Environmentally hazardous chemicals, for toxicity studies on homogeneous subgroups [65]. Eluents for chromatography, where principal properties of solvent mixtures have been used for optimization of chromatographic separations in HPLC and TLC [66],... 

Trace amounts of Se are necessary for animal life, since one of the key enzymes of glutathione metabolism, namely glutathione peroxidase, contains 4 g-atoms of Se. The borderline between life and death, however, is fairly narrow. Thus, the minimum desiderable pasture content of Se for liverstock is 0.03 ppm, while continual ingestion of fodder contain 1-5 ppm will induce toxicity [112]. Se excretion occurs via urine (in the form of trimethyl selenium, selenates and Se-aminoacids), through the feces (in the form of Se-aminoacids) or sweat (as selenates and di- and trimethyl... 

As said above, plant root chemistry may also influence deeply alpine soil microorganism s biomass. It turns out that the particular chemical composition of exudates is a strong selective force in favour of bacteria that can catabolize particular compounds. Plants support heterotrophic microorganisms by way of rhizodeposition of root exudates and litter from dead tissue that include phenolic acids, flavonoids, terpenoids, carbohydrates, hydroxamic acids, aminoacids, denatured protein from dying root cells, CO2, and ethylene (Wardle, 1992). In certain plants, as much as 20-30% of fixed carbon may be lost as rhizodeposition (Lynch and Whipps, 1990). Most of these compounds enter the soil nutrient cycle by way of the soil microbiota, giving rise to competition between the myriad species living there, from microarthropods and nematodes to mycorrhiza and bacteria, for these resources (e.g. Hoover and Crossley, 1995). There is evidence that root phenolic exudates are metabolized preferentially by some soil microbes, while the same compounds are toxic to others. Phenolic acids usually occur in small concentration in soil chiefly because of soil metabolism while adsorption in clay and other soil particles plays a minor role (Bliun et al., 1999). However, their phytotoxicity is compounded by synergism between particular mixtures (Blum, 1996). 

It all works much better if we consider some simpler cases that are less obvious in ordinary life but still have greater importance for medicine than skin or eye color. Take, for example, the disease phenylketonuria, which 1 mentioned briefly in Chapter 8. If left untreated it produces severe mental retardation and, in many cases, death before the age of 25. It is caused by an incapacity to convert the aminoacid phenylalanine into another aminoacid, tyrosine. It is not, however, a deficiency disease, because its harmful effects are not caused by a shortage of tyrosine, and cannot be avoided by adding tyrosine to the diet. Instead they are caused by the toxic effects on the brain of a substance called phenylpyruvate, which the body produces in its efforts to remove the excess of phenylalanine. The name of the disease reflects the fact that phenylpyravate, which belongs to a general class of chemical substances known as phenylketones, is excreted in the urine of affected people. This provides a simple method of diagnosis, and the disease is treated by carefully controlling the diet so that it provides no more phenylalanine than is needed for normal health. There is then no surplus to be converted into phenylpyruvate. 

In insects, kynureninase is much less important than in mammals, so nearly no HA arises from tryptophan metabolism, but rather HK which is (auto)oxidised to ommochromes. The ommochrome pathway could be a defensive strategy against tryptophan toxicity, developed by organisms that have lost the ability to completely degrade this aminoacid. 

A number of natural products contain the azepine framework, e.g. the nonproteinogenic aminoacid muscaflavine 35, a yellow pigment of the fly agaric, the 2i/-azepine chalciporon 36, a pungent substance of the peppery bolete [22], and the ethano-bridged tetrahydroazepine ( )-anatoxin 37, a toxic principle of blue-green algae. 

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