Cancer genotoxicity

The effect of DNA toxicity such as cancer, genotoxic disease syndrome, modification of a genetic profile, and abnormalities in development generally appear after several years. 

Additional research on cadmium is recommended in three areas (1) effects on cancer, genotoxicity, and reproductive toxicity under conditions of acute, intermediate, and chronic durations of exposure, and administered by way of diet, iiflialation, and dermal routes of exposure (2) emphasis on studies with pregnant animals and (3) methods for reducing toxic effects. Finally, the issue of the significance of cadmium residues in various body parts requires resolution. At this time, it appears that cadmium residues in the vertebrate kidney or liver that exceed... 

In such circumstances, it is preferable to test the induced influence of a given set of structural parameters with established significance over the cancer genotoxicity correlation, see Eq. (3.139). Hypothetically, this shows the direct, scarce correlation with the observed activity. The residual correlation follows (Putz, 2011a) ... 

A further consensus developed within the scientific community regarding the relative carcinogenicity of the different types of asbestos fibers. There is strong evidence that the genotoxic and carcinogenic potentials of asbestos fibers are not identical in particular mesothelial cancer is mostiy, if not exclusively, associated with amphibole fibers (43). 

Genotoxicity studies are required to identify compounds that can induce genetic damage ranging from single point gene mutations to gross alterations of chromosomal structure. Such effects are taken as indicative of the potential to cause cancer or heritable defects in humans. A standard battery of three types of test is recommended ... 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer potency or perform cancer risk assessments. Minimal risk levels (MRLs) for noncancer end points (if derived) and the end points from which they were derived are indicated and discussed. 

This study, like that of Fisher and Allen (1993), incorporated a linear multistage model. However, the mechanism of trichloroethylene carcinogenicity appears to be non-genotoxic, and a non-linear model (as opposed to the linearized multistage model) has been proposed for use along with PBPK modeling for cancer risk assessment. The use of this non-linear model has resulted in a 100-fold increase in the virtually safe lifetime exposure estimates (Clewell et al. 1995). 

It is well known that excessive intake of P-carotene may lead to carotenodermia (yellow skin), and it is undoubtedly the case that some carotenoid is directly lost via the skin or through photo-oxidation in the skin. As far as is known the carotenoids are not cytotoxic or genotoxic even at concentrations up to 10 times the normal plasma concentration which may cause carotenodermia. However, they are associated with amenorrhoea in girls who may be consuming bizarre diets and, in long-term supplementation studies, with an increase in lung cancer (The Alpha-tocopherol, Beta-carotene Cancer Prevention Study Group, 1994). 

Cavalieri, E. Frenkel, K. Liehr, J. G. Rogan, E. Roy, D. Estrogens as endogenous genotoxic agents—DNA adducts and mutations. J. Natl. Cancer Inst. Monogr. 2000, 27, 75-93. 

Tobi SE, Gilbert M, Paul N and McMillan TJ. 2002. The green tea polyphenol, epigallocatechin-3-gallate, protects against the oxidative cellular and genotoxic damage of UVA radiation. Int J Cancer 102(5) 439-444. 

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