Cell damage bacterial

Williams, G.M., Mori, H. McQueen, C.A. (1989) Stracture-activity relationships in the rat hepatocyte DNA-repair test for 300 chemicals. Mutat. Res., 221, 263-286 Zimmer, D., Mazurek, J., Petzold, G. Bhuyan, B.K. (1980) Bacterial mutagenicity and mammalian cell damage by several substituted anilines. Mutat Res., 77, 317-326... 

Holme, J.A., Soderlund, E.J., Brunborg, G, Omichinski, J.G, Bekkedal, K., Trygg, B., Nelson, S.D. Dybing, E. (1989) Different mechanisms are involved in DNA damage, bacterial mutagenicity and cytotoxicity induced by l,2-dibromo-3-chloropropane in suspensions of rat liver cells. Carcinogenesis, 10, 49-54... 

Control of transcription initiation permits the synchronized regulation of multiple genes encoding products with interdependent activities. For example, when their DNA is heavily damaged, bacterial cells require a coordinated increase in the levels of the many DNA repair enzymes. And perhaps the most sophisticated form... 

Antibacterial antibiotics normally act by either making the plasma membrane of bacteria more permeable to essential ions and other small molecules by iono-phoric action or by inhibiting cell wall synthesis (see section 7.2.2). Those compounds that act on the plasma membrane also have the ability to penetrate the cell wall structure (Appendix 3). In both cases, the net result is a loss in the integrity of the bacterial cell envelope, which leads to irreversible cell damage and death. 

FIGURE 11.4 Passage of bacterial cells through membrane pores. Cell damage occurs at critical pore radius/cell radius ratio. (From Goosen, M.F.A., Sablani, S.S., Al-Hinai, H., Al-Obeidani, S., Al-Belushi, R., and Jackson, D., Sep. Sci. TechnoL, 39, 2261, 2004.)... 

In recent years, a new mode of operation has been suggested in which permeate flow is controlled at a constant rate, while transmembrane pressure is kept low. This approach was developed and tested for mammalian cells (23), where concern about cell damage due to compression on the membrane surface prompted an interest in controlling TMP and flux rate. The data reported in this paper demonstrate that the controlled permeate flow operating scheme also works well for bacterial systems, yielding more stable and improved flux as well as high protein passage. 

The well-known AMES test is a similar technique in principle. This widely used, simple, and rapid bacterial mutagenicity test detects carcinogenic effects of chemicals. It is based on two assumptions. First, cancer is commonly caused by damage to the cell DNA resulting in somatic mutations. Second, chemicals that damage bacterial DNA and induce mutations are also likely to induce mutations in mammalian cells. 

The oral cavity is lined with delicate mucus membranes that allow rapid absorption of harmful chemicals present in food, drinks, tobacco products and dental materials across its surface. The oral tissues are also vulnerable to cell damage through trauma, bacterial onslaught and other disease-causing agents. The oral cavity is therefore uniquely susceptible to oxidative stress that can be responsible for a number of oral diseases such as periodontitis [6], aphthous ulcers [14], lichen planus [15,13] and oral submucous fibrosis [16], some of which may develop into oral cancers [15,17]. 

Urobilinogen is a product of bilirubin metabolism, formed as a result of bacterial action in the gut (faecal urobilinogen is referred to as stercobilinogen). It is absorbed into the blood and the greater part is re-excreted by the liver while a small part is excreted in the urine where it can be oxidized to urobilin. Decreased faecal and urinary urobilinogen excretion occurs in biliary obstruction. Increased urinary excretion of urobilinogen occurs when there is liver cell damage, as in hepatitis. 

Figure 10 shows that with the addition of urea at pH 7.4, there is no change in medium pH or cellular calcium or pH. At pH 6.5, there is a slight increase in medium pH and cell pH with a slow rise in cell calcium. However, at pH 5.8, where internal bacterial urease is activated, there is a rapid rise in medium pH, cell pH and cell calcium. These data are consistent with the expectation that internal bacterial urease is responsible for elevation of medium pH by activation of a urea transporter. Further, the increase of medium NH3 results in cell alkalinization and elevation of cell calcium, which may eventually result in cell damage or apoptosis. 

The DNA strand breakage induced by the endogenous oxidant ONOO has been prevented by canolol and it followed in a dose-dependent manner. Antioxidative effect or terminations of oxy radical-induced strand breaks are responsible to this. The capacity of canolol to suppress ONOO-induced cell damage, killing of bacteria and mammalian cells and bacterial mutation as well as plasmid DNA strand breakage have been established with this study (Kuwahara et al., 2004). Canolol prevented oxidative stress-induced cellular apoptosis to a significant extent in SW480 cells. 

The sensitivity of a test can be a problem. Every test for toxic chemicals has some chemicals that the test is very sensitive to. And every test has some toxic chemicals that it is not sensitive to. Often several tests will be run and the median value for toxicity is judged to be representative for the toxicity of that chemical. It can be argued that if a test system is extremely sensitive to a chemical, than it must be concluded that this chemical could be toxic for humans at this very low level. If it damages one life form, it could very well damage another. Tests with live animals, LD50 tests, are usually not as sensitive as tests with Daphnia, with animal cells, with bacterial tests. Tests with live animals usually... 

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