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2151 Tumour formation There is a substantial body of literature linking ROS-induced DNA damage with tumourigenesis in a variety of experimental models One of the best established models is the English sole (Parophrys vetulus/Pleuronectes vetulus) carcinogenesis model Several studies have demonstrated a good correlation between the occurrence of liver tumours and related liver lesions in English sole and environmental or laboratory exposure to certain pollutants such as PAHs (Malins et al, 1988; Myers et al, 1990, 1998; Schiewe et al, 1991) The PAH benzo[a]pyrene is also carcinogenic to rainbow trout (Hendricks et al, 1985) Although indirect, there is evidence indicating that oxidative damage to DNA associated to environmental contaminant exposure is linked to tumourigenesis in English sole.

Occasionally, in a patient with a highly localized epileptogenic focus, which is producing intractable epileptic attacks, the focal area of the brain may be removed with bene t. Identi cation of the small percentage of patients with epilepsy who are likely to bene t from such surgery has improved very signi cantly in the last decade. It is more common in patients with focal pathology which has been clearly demonstrated on the medial side of the temporal lobe by sophisticated EEG and imaging techniques (MR scan). Outcomes are best in children and young adults; older patients may have dif culty in picking up the threads of a life disrupted by epilepsy even if the seizures themselves are abolished.

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Thus, Malins and Haimanot (1991) have found that concentrations of DNA modi cation caused by hydroxyl radicals are higher in apparently healthy sh from contaminated areas with respect to healthy uncontaminated sh, and in contaminated sh with hepatic tumours when compared to contaminated apparently healthy sh An additional relevant factor in contaminant-induced tumourigenesis is DNA adduct formation and mutagenesis, as discussed in section 22 Another well-studied model linking oxidative stress with tumour formation is the peroxisome proliferation model in responsive or sensitive species Peroxisome proliferators are non-genotoxic and non-mutagenic compounds that do not bind covalently to DNA However, chronic treatment of mice and rats with peroxisome proliferators leads to a higher liver tumour incidence (Reddy et al, 1980; Reddy & Lalwani, 1983; Stott, 1988; Lake, 1995).

Reddy and co-workers have proposed that the overproduction of H2O2 derived from increased activities of peroxisomal -oxidation and microsomal -oxidation enzymes could not be detoxi ed by catalase, whose activity is induced only slightly (Reddy et al, 1980; Reddy & Lalwani, 1983; Reddy & Rao, 1989) Then, the excess H2O2 could diffuse outside peroxisomes and react, directly or after conversion into hydroxyl radicals, with cellular macromolecules including DNA This would eventually cause DNA damage and ultimately tumour formation (Fig 26) Additionally, the administration of peroxisome proliferators in responsive species leads to a reduction in the activity of antioxidant and GSH-requiring enzymes (SOD, GPX and GST) and in the amount of oxyradical scavengers (reduced glutathione and vitamin E), thus facilitating the process of oxyradical-mediated hepatocarcinogenesis (Cattley et al, 1987; James & Ahokas, 1992; Demoz et al, 1993; Grasso, 1993; Lake, 1995).

a high maintenance overhead and livelock where the communication overhead (control token messages) is so high that the system cannot make any useful progress, ie communicate data among stations The results presented cannot be taken as representative of a realistic IVC network scenario Only four nodes were used in the simulation model where far more moving nodes would be expected to simulated increased topology changes with announced joins and leaves Also, the protocol is implemented on top of an 80211/DCF mode Thus, it is dif cult to assimilate the real performance of this protocol when compared to the 80211 based approaches However, a token ring is more robust to collisions compared to the 80211 The cost to pay is the maintenance of the ring MAC for DSRC Qing Xu et al.

It has been demonstrated that the administration of peroxisome proliferators leads to an increased H2O2 formation (Demoz et al, 1993; Lores Arnaiz et al, 1995), which is followed by oxidative DNA damage (Takagi et al, 1990) and an increased lipid peroxidation and lipofuscin deposition (Cattley et al, 1987; Demoz et al, 1993; Grasso, 1993) However, according to Demoz et al (1993) and Lake (1995), the magnitude of effects described is not enough to account for the tumour promotion ability of peroxisome proliferators Thus, James and Roberts (1995) have concluded that oxidative damage cannot cause the early stages of tumour formation and expansion although it could increase the number of cells initiated and these could be later on promoted by peroxisome proliferators.

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