DNA damage table

The observation that bile acids cause DNA damage (Table 3.4) suggests that bile acids should increase the frequency of mutation since unrepaired DNA damage causes replication errors. Table 3.5 lists the studies showing that bile acids cause an increase in mutant cells in the GI tract. In vitro, DOC treatment... 

The number and diversity of repair systems reflect both the importance of DNA repair to cell survival and the diverse sources of DNA damage (Table 25-5). Some common types of lesions, such as pyrimidine dimers (see Fig. 8-34), can be repaired by several distinct systems. Many DNA repair processes also appear to be extraordinarily inefficient energetically—an exception to... 

It has been shown above that there is a marked effect of the charge of the thiol and its efficiency to protect against OH attack but also to repair DNA damage (for thiol binding to DNA see Smoluk et al. 1986). An extension to GSH-deficient cells in combination with the oxygen explosion technique allowed to determine the rate constants of various thiols with radiation-induced DNA damage (Table 12.21 Prise et al. 1995). 

Table 13.2 Methods used to subject cells to oxidative stress that has produced increased intracellular DNA damage (see Halil well and Aruoma, 1991)...

Free-radical generation occurs normally in the human body, and rates of free-radical generation are probably increased in most diseases (see Table 13.1). Their importance as a mechanism of tissue injury is still uncertain, largely because the assays used to measure them have, until recently, been primitive. The development of new assays applicable to humans (such as the assays of oxidative DNA damage described above) should allow rapid evaluation of the role of free radicals in disease pathology and provide a logical basis for the therapeutic use of antioxidants. A rationale is presented in Fig. 13.3. Attempts to use antioxidants in the treatment of human disease can be divided into three main areas ... 

No results indicating genotoxicity were observed in in vitro studies that examined six organophosphate ester hydraulic fluids for gene mutation, deoxyribonucleic acid (DNA) damage, or chromosomal aberrations in eukaryotes (see summarized data in Table 2-11). 

Note THF = tetrahydrofuran BHT = butylated hydroxytoluene, an antioxidant Camptothecin (CM) = causes inhibition of the DNA enzyme topoisomerase (Top 1) which induces DNA damage and apoptosis DHT = dihydrotestosterone PrEC = normal prostate stromal cells LNCaP, PC-3, DU-145 = neoplastic prostate epithelial cells (See Table 21.1). 

Table 6.1 DNA damaging assay against three yeasts" (dose 100 gg/mL)...

Among Lamiaceae family plants, except 4/wg postii, none of the species gave hit in the yeast based assay. However, a few Salvia species (S. triloba, S. blepharo-chlaena, S. syriaca), and a few Sideritis species (S. aytachii, S. lycia) showed high inhibition against at least one or two tested yeasts among the three yeasts nsed in DNA damaging microtiter assay (Table 6.1). 

Since DNA damaging activity resnlts didn t give almost no hit except a few extracts Ajuga and Juniperus) (Table 6.4) we directed onr bioactivity assay to ovarian cytotoxic activity search. 

Table 6.4 Yeast based DNA damaging mierotiter assay (% inhibition)...

Reactive oxygen species (ROS) are a common mediator of apoptosis. Induction of apoptosis by bile acids appears to be caused, at least in part, by oxidative stress and consequent DNA damage. Unrepaired DNA damage can trigger apoptosis. Table 3.3 lists studies indicating that bile acids induce production of ROS and reactive nitrogen species (RNS) in cells of the GI tract. Table 3.4... 

Table 3.4 Bile acids induce DNA damage in cells of the GI tract. ...

TNB. All concentrations produced bacterial toxicity, but it was unclear whether DNA damage occurred (McGregor et al. 1980). 1,3,5-TNB did not affect mitotic recombination or produce any other observable genotoxic effect in S. cerevisiae (McGregor et al. 1980). Refer to Table 2-3 for a further summary of the genotoxic effects of 1,3,5-TNB exposure. 

The fitted means and standard errors for log-transformed comet tail moments, as well as the percentage of cells exhibiting extensive DNA damage (e.g., cells labeled 3 and 4) are reported in Table 2 [see p. 137]. An adjusted p value indicated no differences existed between cells treated with extracts from exposed filters or with hydrogen peroxide. Cellular responses were significantly different (P < 0.05) between unloaded PMj 5 filter extracts and loaded PM2 5 extracts as well as extracts containing deferoxamine. 

For example, Plaper et al. (2002) state that three Cr + compounds were examined (work done In the past) but that the hydroxyl radical is a known mediator of DNA damage (knowledge that exists in the present). Similarly, the present-tense, active-voice combination Is used in the Discussion section to state scientific truths (knowledge expected to be true over time), just as it was in the Results section. Note that Interpretations and/or mechanisms put forth in a Discussion section are often considered to be truths and therefore are stated in present-tense active voice. Table 5.1 summarizes common verb tense—voice combinations and their functions, with example sentences. 

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