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Cells exposure

On the other hand, comparative analysis of Fi variables gave the relative reduction of SOS-response in preincubated with AR bacterial cells (Table 3). So, repression SOS-response was proportionally to the length of the AR alkyl radical and was Fi = 3.7 (for Ce-AR) and Fi = 7.0 (for C12-AR) that 76.43-40.40 fold lower than the SOS-system activation level in cells exposured only by UV radiation. With reduction of the AR concentration to lO- M is still observed statistically significant differences in the values of induction index (Fi) of the control and experimental samples, although the repression of SOS-response was less expressed. An increase of the AR concentration up to 1(>3 M in the case of Ci-AR and C3-AR led to some suppression, and for the C5-, Ca- and C12-AR to increase the values of R. [Pg.195]

Living cells are delicately balanced chemical machines. The ionization track generated by a nuclear particle upsets this balance, almost always destroying the cell in the process. Although the body has a remarkable ability to repair and replace damaged cells, exposure to radiation can overload these control mechanisms, causing weakness, illness, and even death. [Pg.1599]

Elevated O2 concentrations Exposure to activated phagocytic cells Exposure to redox cycling drugs (e.g. alloxan, paraquat, menadione)... [Pg.201]

With regard to the design of the test, mice are mated when 7-8 weeks old. By this age all germ cell stages are present. The test compound is normally administered by the IP route to maximize the likelihood of germ cell exposure. The preferred dose is just below the toxic level so long as fertility is not compromised. One lower dose should also be included. [Pg.216]

Oxidized, denatured hemoglobin forms aggregates, which can become attached to the inner surface of the red cell, known as Heinz bodies. This leads to damage to the red cell, which may result in direct destruction of the cell, which can be shown in vitro, or removal from the circulation by the spleen in vivo. When caused by Fava beans, the syndrome is known as Favism. As the deficient enzyme (glucose-6-phosphate dehydrogenase) is intrinsic to the red cell, exposure of such cells in vitro to suitable drugs will lead to cell damage and death. [Pg.150]

On the other hand, there is strong evidence that the effects of flavonoids on cultured cells are not merely toxic but via induction of apoptosis or inhibition of proliferation. Thus signs of apoptosis, such as induction of caspase-3, fragmentation of DNA and chromatin condensation, are frequently detected upon cell exposure to flavonoids [213, 217-221]. In addition, the effects of flavonoids are generally reversible upon removal or addition of serum [222-224]. [Pg.632]

Keith WG, Powell RE (1969) Kinetics of decomposition of peroxynitrous acid. J Chem Soc (A) 90 Keyer K, Imlay JA (1997) Inactivation of dehytratase [4F3-4S] clusters and disruprion of iron home-stasis upon cell exposure to peroxynitrite. J Biol Chem 272 27652-27659 Khaikin Gl, Alfassi ZB, Huie RE, Neta P (1996) Oxidation of ferrous and ferrocyanide ions by peroxyl radicals. J Phys Chem 100 7072-7077... [Pg.42]

Qaddoumi et al. [65] studied the uptake of PLGA nanoparticles in rabbit conjunctival epithelial cell culture. The highest uptake by cultured conjunctival cells was achieved for the smallest particles (100 nm), compared to larger 800 nm and 10 pm particles. A study of the fate of the tiny 100-nm particles following 2 h of cultured cells exposure to a 0.5 mg/mL dose showed that 6% was internalized by conjunctival epithelial cells, 1.5% was surface-bound, whereas the remainder of the dose was found in the donor medium. In an in vivo rabbit eye study [66] on the uptake of poly(hexyl cyanoacrylate) nanoparticles, 6 h postinstillation into the conjunctival sac, it was found that the fraction that was internalized by conjunctival epithelial cells was only 1% of the dose reflecting in vivo precorneal elimination... [Pg.503]

Work from our laboratory has provided single-channel evidence for a redox control of the KCa3.1 channel in bovine aortic endothelial cells (Cai and Sauve 1997). In these cells, exposure to the reactive oxygen species (ROS) generating system... [Pg.363]

Faist et al.292 have also examined the effect of dietary CML on the expression of GST in the rat kidney. In their Study 1, casein-linked CML was administered at two pharmacological doses [110 and 300 mg CML per kg body weight (b.w.) per day] for 10 d. In Study 2, supplementary breadcrust was used to give a daily intake of 11 mg (kg b.w.) 1 d for 42 d. In Study 1, the glutathione level in the kidneys increased 43 and 65%, respectively, and Phase II GST activity increased 12 and 96%, respectively, over the control. In Study 2, the protein content of the isoenzyme GST In- increased, but that of lji- and la-1 remained the same as in the control. Both studies were supported by experiments on Caco-2 cells. Exposure to purified CML... [Pg.90]

Kll. Keyer, K., andlmlay, J. A., Inactivation of dehydratase [4Fe-4S] clusters and disruption of iron homeostasis upon cell exposure to peroxynitrite. J. Biol. Chem. 272,27652—27659 (1997). [Pg.240]

Khan SR, Thamiselvan S. Nephrolithiasis a consequence of renal epithelial cell exposure to oxalate and calcium oxalate. Mol. Urol.2000 4(4) 305-11. [Pg.755]

Two trisulfated tetraoside glycosides isolated from the Antarctic sea cucumber Staurocucumis liouvillei, liouvillosides A (88) and B (89) showed little or no cytotoxicity at concentration ranging from 6.25 to 50 ig/ml against Vero cells within 8 h of cell exposure to the compounds but both saponins were cytotoxic following prolonged incubation periods [73]. [Pg.160]

One consequence of NK cell exposure to OT that occurs quickly (within 10 minutes) is an increase in the activation of mitogen-activated protein kinases (MAPK). These enzymes are critical to the function of the NK cells, as well as nearly all other cell types. TBTC can significantly activate MAPKs within 10 min of exposure and this activation can be accounted for by TBTC-induced activation of the immediate upstream activators of MAPKs, referred to as MAPK kinases (MAP2Ks). Activation of MAPKs by TBTC would leave the NK cell unable to respond to target cells when they were encountered. The activation of the MAPK pathway by OT exposure occurs within a timeframe that could account for the loss of lytic function seen at exposures of less than 48 h, while the other alterations such as ATP decreases and binding decreases take longer to occur. We have unpublished data indicating that DBTC is also able to increase MAPK activity in NK cells within 10 min. Thus, it will be important to examine the other OTs to determine if this is a common mechanism in the OT-induced inhibition of NK lytic function. [Pg.479]

Lenz AG, Karg E, Lentner B et al (2009) A dose-controlled system for air-liquid interface cell exposure and application to zinc oxide nanoparticles. Part Fibre Toxicol 6 32... [Pg.120]


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See also in sourсe #XX -- [ Pg.509 ]




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