Carcinogen synthetic

Aftertreatment The wetfastness of dyeings produced with acid dyes is often unsatisfactory. Formerly, tannic acid and tartar emetic were used, which form a 1 1 adduct on the material by hydrogen bonding. This process is expensive and said to be carcinogenic. Synthetic tanning agents (Synthanes) are preferred. They are condensation products of aromatic sulfonic acids with formaldehyde [106] or of phenols with formaldehyde, which are made water-soluble by reaction with bisulfite. These products deposit on the fiber surface and form an electrostatic barrier... 

There are more natural carcinogens by weight in a cup of coffee than potentially carcinogenic synthetic pesticide residues in the average US diet in a year, and there are still a thousand known chemicals in roasted coffee that have not been tested. 

Acroleiu, iu lARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans. Some Monomers, Plastics and Synthetic Elastomers andMcrolein, Vol. 19, International Agency for Research on Cancer, Lyon, France, 1979, pp. 479—494. 

The formation of nitrosamines, e.g. n-nitrosodiedianolamine, which are possible human carcinogens, can occur in synthetic or semi-synthetic fluids which contain a nitrite salt and diethanolamine or triethanolamine. 

Liver cancer can also be a consequence of exposure to hepatotoxic chemicals. Natural hepatocarcinogens include fungal aflatoxins. Synthetic hepato-carcinogens include nitrosoamines, certain chlorinated hydrocarbons, polychlorinated biphenyls (PCBs), chloroform, carbon tetrachloride, dimethyl-benzanthracene, and vinyl chloride.Table 5.15 lists the chemical compounds that induce liver cancer or cirrhosis in experimental animals or... 

Antioxidants are not important only to the health conscious food manufacturers also rely on these chemicals to maintain the shelf life of their products. Synthetic antioxidants such as butylated hydroxyanisole, butylated hydroxytoluene, propyl gallate and tert-butyl hydroquinone were widely used in food processing to control oxidation and maintain food quality. However, as these synthetic antioxidants are suspected to be carcinogenic they now have restricted use in food (Madahavi and Salunkhe, 1995). Therefore, natural antioxidant sources, especially of plant origin, are of great interest to the food industry. 

Methods for the synthesis of the biologically active dihydrodiol and diol epoxide metabolites of both carcinogenic and noncarcinogenic polycyclic aromatic hydrocarbons are reviewed. Four general synthetic routes to the trans-dihydrodiol precursors of the bay region anti and syn diol epoxide derivatives have been developed. Syntheses of the oxidized metabolites of the following hydrocarbons via these methods are described benzo(a)pyrene, benz(a)anthracene, benzo-(e)pyrene, dibenz(a,h)anthracene, triphenylene, phen-anthrene, anthracene, chrysene, benzo(c)phenanthrene, dibenzo(a,i)pyrene, dibenzo(a,h)pyrene, 7-methyl-benz(a)anthracene, 7,12-dimethylbenz(a)anthracene, 3-methylcholanthrene, 5-methylchrysene, fluoranthene, benzo(b)fluoranthene, benzo(j)fluoranthene, benzo(k)-fluoranthene, and dibenzo(a,e)fluoranthene. 

Although benz(a)anthracene (BA) is generally considered noncarcino-genic (27), it is a weak tumor initiator when administered with a phorbol ester promoter (28). More importantly, BA is a convenient model for the highly potent carcinogenic PAH 7,12-dimethylbenz(a)-anthracene and 3-methylcholanthrene (27), both of which are BA derivatives but which offer more serious synthetic problems. 

The role of N-acetoxy arylamides as metabolically formed ultimate carcinogens jji vivo also appears to be limited. Their enzymatic formation via peroxidation of N-hydroxy arylamides can be excluded since tissues containing high levels of peroxidases such as the rat mammary gland (83) and the dog urinary bladder (84) do not form acetylated carcinogen-DNA adducts in vivo (63). Their non-enzymatic formation by reaction of acetyl coenzyme A with N-hydroxy arylamides (6 ) cannot be excluded however, even if formed, their direct reaction with cellular DNA appears unlikely as treatment of cultured cells with synthetic N-acetoxy AAF (85,86) results primarily in deacetylated arylamine-DNA adducts, apparently due to rapid N-deacetylation to form the reactive N-acetoxy arylamine (V). 

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