Acid exposure

Oridation. This is caused by contact with oxidising acids, exposure to u-v, prolonged application of excessive heat, or exposure to weathering. It results in a deterioration of mechanical properties (embrittlement and possibly stress cracking), increase in power factor, and loss of clarity. It affects most thermoplastics to varying degrees, in particular polyolefins, PVC, nylons, and cellulose derivatives. 

Recently the Bohlmann-Rahtz synthesis has received greater attention. Baldwin has employed this method for the construction of heterocyclic substituted a-amino acids. Exposure of alkynyl ketone 39 to 3-aminocrotoyl ester 40 resulted in the Michael product 41. Thermolysis then gave rise to the desired pyridyl-P-alanines 42. 

Scheme 21 presents the successful sequence of reactions that solved the remaining two problems and led to the completion of the synthesis of cobyric acid. Exposure of 96 to concentrated sulfuric acid for one hour brings about a clean conversion of the nitrile grouping to the corresponding primary amide grouping. The stability of die corrin nucleus under these rather severe conditions is noteworthy. This new substance, intermediate 97, is identified as cobyrinic acid abcdeg hexamethylester f amide and it is produced along with a very similar substance which is epimeric to 97 at C-13. The action of sulfuric acid on 96 produces a diastereomeric... 

S.B. des Varannes, F. Mion, P. Ducrotte, F. Zerbib, P. Denis, T. Ponchon, R. Thibault, and J.P. Galmiche, Simultaneous recordings of oesophageal acid exposure with conventional pH monitoring and a wireless system (Bravo). Gut 54, 1682-1686 (2005). 

Fire retardant treatment, for wood, 26 348 Fire science, 11 450 Fire test methods, 11 449—450 Fire test terminology, 19 588 Fire-tube furnaces, 12 319—320, 327 Firing, of ferrites, 11 73 Firming agents, 12 32 as food additives, 12 57 First aid and rescue, 21 858 First aid, for nitric acid exposure, 17 192 First failure, time to, 26 987 First falling rate period, 23 67 First-generation ionic liquids, 26 837-838, 841, 865... 

Hydrogen cyanide (HCN) is a colorless, highly poisonous gas or liquid (below 26.7 °C) having an odor of bitter almonds (Hartung 1994 Pesce 1994). It is a weak acid. Exposures may occur in industrial situations as well as from cigarette smoke and combustion products and from naturally occurring cyanide compounds in foods. There is a potential for exposure when any acid is mixed with a cyanide salt. Intravenously administered sodium nitroprusside (Na2[Fe(CN)5N0]-2H20) has been used clinically to lower blood pressure (Schulz et al. 1982). Chemical and physical properties are listed in Table 5-2. 

Various membrane materials are to be compared for corrosion resistance in hydrochloric acid. Membrane samples are ultrasonically cleaned with Freon for 5 minutes and dried at 200°C for 2 hours followed by similar steps of ultrasonic cleaning with demineralized water and drying. The conditioned membrane samples are then immersed in 35% HG solution, making sure that no air bubbles are trapped in pores. The acid exposure at the test temperature (e.g. 25°C) continues for a given period (e.g. one week). The tested samples are ultrasonically washed with demineralized water for 5 minutes and dried at 200°C for 2 hours. The weights of the cleaned membrane samples before and after the acid exposure are compared to assess the relative corrosion resistance of various membrane materials. 

Although small proportions of other products are formed when D-xylose is exposed to rather high acid concentrations, arabinose, lyxose, and ribose form considerably more of alternative products (generally reductic acid) than of 2-furaldehyde under these conditions. Reductic acid (2,3-dihydroxy-2-cyclopenten-l-one, 47) has been detected as a product after acid exposure of D-xylose or its major dehydration product, 2-furalde-hyde. Further work performed with D-[l- C]xylose and [a- C]2-fural-dehyde showed that reductic acid having identical label distribution was obtained from both starting materials. This indicated that a common primary source was involved, probably 2-furaldehyde, as it is readily formed from D-xylose under acidic conditions. 

Other studies (Table 3.2) indicate that exposure to high physiological concentrations of bile acids, if repeated over a long period, increases the risk of GI cancer. A reasonable hypothesis is that bile acids act by a common underlying mechanism at various sites within the GI tract. Nevertheless, conditions vary widely from site to site within the GI tract, and it is certainly possible that at any particular site some factor(s) other than bile-acid exposure, or in combination with bile-acid exposure, is more important in carcinogenesis at that site. 

There are three main sources of evidence for pro-tumorigenic activity of bile acids in the lower gastro-intestinal tract (activity in rodent CRC models, human observational data and mechanistic studies using CRC cells in vitro), which together create a strong case for a role for colorectal mucosal bile acid exposure during human colorectal carcinogenesis. 

It is well recognised that the faecal bile acid content of random stool samples is highly variable with marked daily variation.Therefore, studies testing the association between luminal bile acid exposure and the presence of colorectal neoplasia have usually measured serum bile acid levels, which demonstrate less variability and are believed to reflect the total bile acid pool more accurately. Serum DCA levels have been shown to be higher in individuals with a colorectal adenoma compared with individuals without a neoplasm. Only one study has assessed future risk of CRC in a prospective study of serum bile-acid levels. The study was hampered by the small sample size (46 CRC cases). There were no significant differences in the absolute concentrations of primary and secondary bile acids or DCA/CA ratio between cases and controls although there was a trend towards increased CRC risk for those with a DCA/ CA ratio in the top third of values (relative risk 3.9 [95% confidence interval 0.9-17.0 = 0.1]). It will be important to test the possible utility of the DCA/ CA ratio as a CRC risk biomarker in larger, adequately powered studies. A recent study has demonstrated increased levels of allo-DCA and allo-LCA metabolites in the stool of CRC patients compared with healthy controls. ... 

Figure 5.2 Therapeutic interventions for decreasing colorectal mucosal bile acid exposure as a CRC chemoprevention strategy. 1) Lifestyle modifications including reduction in dietary animal fat and increased fibre intake may, at least partly, be explained by reduction in luminal primary (cholic acid [CA] and chenodeoxycholic acid [CDCA]) and secondary (deoxycholic acid [DCA] and lithocholic acid [LCA]) bile acids. 2) Reduction of secondary bile acids, which are believed to have pro-carcinogenic activity could be obtained by decreased bacterial conversion from primary bile acids. 3) Alternatively, bile acids could be sequestered by chemical binding agents, e.g. aluminium hydroxide (Al(OH)3) or probiotic bacteria. 4) Exogenous ursodeoxycholic acid (UDCA) can reduce the luminal proportion of secondary bile acids and also has direct anti-neoplastic activity on colonocytes in vitro.

The mechanistic basis of the anti-neoplastic activity of UDCA and the explanation for the significant difference in bioactivity of UDCA compared with DCA despite marked similarity in chemical structure remain unresolved. UDCA administration in healthy volunteers and colorectal adenoma patients has been demonstrated to decrease the proportion of DCA in aqueous phase stool. Therefore, one possible mechanism of the chemopreventative activity of UDCA is reduction of mucosal secondary bile acid exposure. Consistent with this idea, UDCA administration has been demonstrated to reduce the incidence of K-ras mutations and decrease Cox-2 expression in AOM-induced tumors, which is the opposite of the reported effects of DCA in the same model. However, it is clear that exogenous administration of UDCA has direct anti-neoplastic activity on human CRC cells in vitro, either alone or in combination with DCA, including anti-proliferative and anti-apoptotic effects, as well as induction of cell senescence. " ... 

Other Agents Targeting Mucosal Bile Acid Exposure... 

Alternative potential strategies for reduction of mucosal secondary bile acid exposure are to target deconjugation of glycine/taurine bile salts by bacterial bile salt hydrolases and/or bacterial 7-dehydroxylation of primary bile acids to secondary bile acids. Sequestration of bile acids in the intestinal lumen using probiotic bacteria has also been proposed as an area for future research. ... 

Figure 2 summarizes the values obtained for the four measurements on the seven coatings after exposure to 0.1 M HoSO at 60°C for 1000 hours. The ordinate shows the values measurecf for each of the four techniques, and the abcissa represents the amount of corrosion observed on the steel under each of the coatings after the acid exposure, with the amount of observed corrosion decreasing from left to right. 

Erosion and discoloration of the teeth has been attributed to chromic acid exposure. Papillomas of the oral cavity and larynx were found in 15 of 77 chrome platers exposed for an average of 6.6 years to chromic acid mist at air concentrations of chromium of 0.4mg/mk ... 

---