Genotoxicity products

Streisinger, G. Attainment of minimal biological variability and measurements of genotoxicity production of homozygous diploid zebra fish. Natl Cancer Inst. Monogr. 65 53—58, 1984. 

The protein was expressed in E. coli using an E. co//-optimized cDNA [2670]. The pmified enzyme, reconstituted with recombinant adreno-doxin and NADPH-adrenodoxin reductase, did not catalyze the oxidation of cholesterol, vitamin Dj, la-hydroxy vitamin D3, or 25-hydroxyvita-min D3. In other studies, none of a test set of pro-carcinogens [350] was activated to a genotoxic product. 

Literature reports iadicate that sodium sorbate causes weak genotoxic effects such as chromosomal aberrations and mutations ia mammalian cells (172,173). This effect is thought to be caused by oxidative products of sodium sorbate ia stored solutions (173—175). The main oxidation product of sodium sorbate, 4,5-oxohexenoate, is mutagenic ia a Salmonella mammahan-microsome test (176). Sorbic acid and potassium sorbate were not genotoxic under the same test procedures (167,172,174—177). 

Although trichloroethylene itself may not be genotoxic, several of its metabolites are reactive and potentially genotoxic compounds (Miller and Guengerich 1982). Several isomers of 1,2-dichlorovinyl-cysteine, a product of trichloroethylene metabolism in the kidney, are mutagenic in the in vitro Ames assay... 

Another study showed that a mixture of oxidative metabolites of P-carotene, but not P-carotene, was able to increase the binding of benzo[a]pyrene to DNA. Other mixtures of P-carotene cleavage products have been shown to induce oxidative stress in vitro,exert cytotoxic and genotoxic effects, and inhibit gap junction intercellular communications. It has been suggested that these detrimental effects could possibly occur in vivo following the intake of high doses of carotenoids. 

Sommerburg, O. et al.. Cytotoxic and genotoxic effects due to beta-carotene cleavage products possibly formed in inflamed lung tissue. Free Rad. Biol. Med., 36, S56, 2004. 

PAHs, more correctly known as polyaromatic compounds (PACs) are common in the human environment, e.g, the exhaust of diesel engines, bitumen and asphalt production. Some of the PAHs are genotoxic and carcinogenic (e.g benz(a)pyrene). 

Ethylene oxide is used in the manufacture of raw materials and can be used to sterilize the surface of finished products and containers. Unfortunately, ethylene oxide is a genotoxic carcinogen and its use is not accepted without justification. In any event, tight controls are required on residues of ethylene oxide and its halohydrin-related substances. For raw materials the amount of these residues is limited to 1 and 50 pig/g, respectively for finished products 1 and 50 pg/g, respectively (with any affected ingredients subject to the control limits for raw materials) and for containers, based on simulated use, 1 and 50 pg/mL container volume, respectively. 

Alija, AJ, Bresgen, N, Sommerburg, O, Siems, W, and Eckl, PM, 2004. Cytotoxic and genotoxic effects of beta-carotene breakdown products on primary rat hepatocytes. Carcinogenesis 25, 827-831. 

Jongen, W.M.F., J.M. Cardinaals, and RM.J. Bos. 1985. Genotoxicity testing of arsenobetaine, the predominant form of arsenic in marine fishery products. Food Chem. Toxicol. 23 669-673. 

Benhar, M. et al., Enhanced ROS production in oncogenically transformed cells potentiates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and sensitization to genotoxic stress, Mol. Cell. Biol., 21, 6913, 2001. 

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