ROS production

Under normal physiological conditions, therefore, antioxidant defences in the skin are able to modulate free-radical production. The initiation of an inflammatory event has the potential for increasing ROS production to such an extent that defence systems are overwhelmed and tissue damage occurs. This event results in the production of even more toxic oxidants and the development of overt disease requiring treatment. Section 4 of this chapter will describe the role of ROS in skin inflammation. 

Another factor responsible for regulating the levels of p53 by (3-carotene could be the dose employed. At high carotenoid concentrations, an increase in p53 expression was observed in SCC cells (Schwartz, 1993) and in HL-60 cells (Palozza et al 2002b). In HL-60 cells, the treatment with the carotenoid induced a remarkable increase in ROS production, accompanied by an enhanced expression of p21WAFl and by a concomitant arrest of cell cycle at the G0/G1 phase (Palozza et al., 2002b). An arrest of cell cycle, accompanied by apoptosis induction, was also observed following dietary supplementation with lutein (Chew et al., 2003). The inhibition of mouse mammary tumor growth by lutein was also supported by the observed increase in the expression of p53 and Bax induced by the carotenoid (Chew et al., 2003). 

A recent observation shows that P-carotene was able to counteract the dangerous effect of 7-ketocholesterol in human macrophages by limiting the apoptotic processes reducing the intracellular ROS production and inhibiting the phosphorylation of p38, JNK, and ERK1/2 induced by the oxysterol (Palozza et al., 2007b). 

SWNTs HiPCO HaCaT Oxidative stress (ROS production, NF-kB activation) [45]... 

Principle ROS production can be monitored by imaging the ROS-sensitive fluorescent dye dichlorofluorescein (DCF) in a confocal microscope. 

Brain antioxidant defenses modify ischemia-reperfusion injury. The high metabolic rate ofbrain cells implies a high baseline ROS production, and brain cells possess high concentrations of both enzymatic and small-molecule antioxidant defenses. SOD1 may represent as much as 1% of total protein in brain it converts 02 to H202, which is then further metabolized to water and oxygen by... 

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. 

Coteur, G. et al., Effects of PCBs on reactive oxygen species (ROS) production by the immune cells of Paracentrotus lividus (Echinodermata), Mar. Poll. Bull., 8, 667, 2001. 

The highly branched 1,1-dimethylcyclopentane (1,1-DMCP) not only has the highest ON among the four RC isomers, but also some of its RO products have exceptional ON (e.g. the RON of 1,1-dimethylpentane is 92). This product can be obtained by using metal catalysts which selectively open at secondary-secondary C-C bonds. As discussed earlier, Ir/Si02 is best suited for this reaction. 

ROS production by an extracellular agar oligosaccharide oxidase Appressoria formation in the specific pathogenic oomycete Pythium porpyrae... 

After irradiation of fullerenes C60 in the cell medium, ROS production has been detected, and this index increased as follow fullerene C60 < fullerene C60-compos-ite-1 < fullerene C -composite-2. As one may see from the data presented in Table 6.1, the rate of ROS generation elevated nearly twice after absorption of light in predetermined range by fullerenes C60, if fullerene C60 was bound to the surface of aminopropylaerosyl, and threefold, if anthracenal that absorbs at X = 357nm was introduced to the content of composite. 

Antonsson and Marinou 2000 Adams and Cory, 1998). Stress may also cause inaease, nitric oxide (NO), or reactive oxygen species (ROS) production which, in turn, triggers release of apoptotic proteins from the intermemhrane space (Kroemer and Reed, 2000 Vieira et at, 2000). Release of these proteins from mitochondria are required for stress induced killing hut are, with a few exceptions (Bergmann et al, 1994, Schulze- Osthoff et al, 1993), dispensible for CD95 and TNF-receptor transduced apoptosis. These other death processes require FADD and caspase-8 to be recruited into the death receptor complexes and cannot be blocked by Bcl-2 (Krammer, 2000 Scaffidi et al, 1998). 

---