Human urine enzyme hydrolyzed

Figure 9. Computer output for Auto-Assay of silylated weakly polar weak acids (E-U) fraction of enzyme-hydrolyzed human urine. ( Report is read as, e.g. A9-THC, positively identified, at a level of 5.84 X 10"2 ng, with a Confidence Index of 24 and a retention time of 86 sec. Chromatographic conditions same as Figure 4.

Mice and humans possess a gene that encodes a membrane-bound gluzincin metalloen-dopeptidase (Chapter 8, Table 8.2). This enzyme hydrolyzes small peptides (<3 kDa) on the amino-terminal side of aspartate residues on various proteins. If this gluzincin loses its proteolytic activity due to mutation, BSP and DMP-1 fragments are absent and the osteoid matrix fails to mineralize. There is also an excessive excretion of phosphate into urine (phosphaturia) and a low content of phosphate in the blood (hypophosphatemia). Rickets... 

Hydrolyzable tannins are comparatively restricted in the human diet and there are no human metabolic data. Studies in rats have indicated that some 63% of a dose of 1 g/kg commercial tannic acid is excreted unchanged in the feces accompanied by small amounts of gallic acid, pyrogallol, and resorcinol. Plasma after enzymic hydrolysis was found to contain 4-O-methylgallic acid, pyrogallol, and resorcinol. Urine also contained a small amount of gallic acid after enzymic hydrolysis. The most notable observation from this study is the failure of the gut microflora to metabolize the galloylglucoses efficiently, at least at this substantial dose. The viability or composition of the gut microflora was not reported. ... 

Azo-based dyes, known to be carcinogenic, contain easily hydrolyzed azo bonds. In the GI tract, these bonds are cleaved to yield the free aromatic amine(s) [20]. Azo reduction may also take place in the liver of humans and other mammals by reductase enzymes, but it is likely that hydrolysis in the GI tract is predominant [21]. The resultant aromatic amines are easily absorbed in the intestines. It was found that inclusion of sulfonate moieties on the aromatic amine feedstocks mitigates the toxicity, as illustrated with the azo dye Brilliant Black BN (Cl Food Black 1) in Figure 13.6. The sulfonate moieties are highly ionized in the GI tract and at environmental pHs (5-9), and their reduction products cannot penetrate the GI endothelial membranes following oral exposure. Consequently, the chemicals are poorly absorbed, and any portion that is absorbed is rapidly excreted in the urine [22, 23]. 

PAH metabolites and their conjugates are excreted predominantly through the feces and to a lesser extent in the urine. Conjugates excreted in the bile can be hydrolyzed by enzymes of the gut flora and reabsorbed. It can be inferred from available data on total body burdens in humans that PAHs do not persist for long periods in the body and that turnover is rapid. This excludes those PAH moieties that become covalently bound to tissue constituents, in particular to nucleic acids, and are not removed by repair. The excretion of urinary metabolites is a method used to assess internal human exposure of PAHs [16]. 

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