Cytotoxic effects, lipid peroxides

Susa N, Ueno S, Furukawa Y, et al. 1997a. Potent protective effect of melatonin on chromium(VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes. Toxicol Appl Pharmacol 144 377-384. [Pg.465]

In 2006, Cnlcasi et al. (27A22) also reported on the free radical-related cytotoxicity of the vapor phase of MSS and the paradoxical temporary inhibition of cytotoxicity of vapor-phase free radicals by the MSS particulate phase. In their ESR stndies, the spin trap 5-(diethoxyphosphoryl)-5-methyl-l-pyrroline-iV-oxide (DEPMPO) was employed. They experimented with cigarettes made with cellulose acetate hl-ters, empty cavity hlters, and cavity hlters containing carbon (charcoal). In their stndy, hlters containing carbon were effective in redncing vapor-phase free radical formation, cytotoxicity, and lipid peroxidation in three cell lines. The... [Pg.1249]

However, peroxidation can also occur in extracellular lipid transport proteins, such as low-density lipoprotein (LDL), that are protected from oxidation only by antioxidants present in the lipoprotein itself or the exttacellular environment of the artery wall. It appeats that these antioxidants are not always adequate to protect LDL from oxidation in vivo, and extensive lipid peroxidation can occur in the artery wall and contribute to the pathogenesis of atherosclerosis (Palinski et al., 1989 Ester-bauer et al., 1990, 1993 Yla-Herttuala et al., 1990 Salonen et al., 1992). Once initiation occurs the formation of the peroxyl radical results in a chain reaction, which, in effect, greatly amplifies the severity of the initial oxidative insult. In this situation it is likely that the peroxidation reaction can proceed unchecked resulting in the formation of toxic lipid decomposition products such as aldehydes and the F2 isoprostanes (Esterbauer et al., 1991 Morrow et al., 1990). In support of this hypothesis, cytotoxic aldehydes such as 4-... [Pg.24]

On the other hand, microsomes may also directly oxidize or reduce various substrates. As already mentioned, microsomal oxidation of carbon tetrachloride results in the formation of trichloromethyl free radical and the initiation of lipid peroxidation. The effect of carbon tetrachloride on microsomes has been widely studied in connection with its cytotoxic activity in humans and animals. It has been shown that CCI4 is reduced by cytochrome P-450. For example, by the use of spin-trapping technique, Albani et al. [38] demonstrated the formation of the CCI3 radical in rat liver microsomal fractions and in vivo in rats. McCay et al. [39] found that carbon tetrachloride metabolism to CC13 by rat liver accompanied by the formation of lipid dienyl and lipid peroxydienyl radicals. The incubation of carbon tetrachloride with liver cells resulted in the formation of the C02 free radical (identified as the PBN-CO2 radical spin adduct) in addition to trichoromethyl radical [40]. It was found that glutathione rather than dioxygen is needed for the formation of this additional free radical. The formation of trichloromethyl radical caused the inactivation of hepatic microsomal calcium pump [41]. [Pg.768]

The superoxide anion (O2 ) exhibits numerous physiological toxic effects including endothelial cell damage, increased microvascular permeability, formation of chemotactic factors such as leukotriene B4, recruitment of neutrophils at sites of inflammation, lipid peroxidation and oxidation, release of cytokines, DNA singlestrand damage, and formation of peroxynitrite anion (ONOO-), a potent cytotoxic and proinflammatory molecule generated according to equation 7.210 ... [Pg.270]

Molsidomine and pirsidomine, are both stable as solids at room temperature in the absence oflight [137]. However the ring opened metabolites SIN-1A and C87-3786 are both photo labile and sensitive to an oxidising environment resulting ultimately in the release of superoxide and NO in stoichiometric quantities [138]. Generation of these two species is an obvious problem due to the resulting formation of peroxynitrite and the generation of OH, which may initiate lipid peroxidation [139-141] (see Eq. (19)). Such concerns over the formation of peroxynitrite from SIN-1A or C87-3786 are warranted since their cytotoxic effects show close consistency with cellular studies doped with neat peroxynitrite [142, 143]. [Pg.223]

Studies carried out with complete cells in vivo, cell membranes and other cell fractions point to the selective oxidation of phosphatidylserine (26) to a hydroperoxide (PS-OOH) on oxidative stress caused by toxic agents such as H2O2, t-BuOOH and cumyl hydroperoxide (27). Formation of PS-OOH is observed during apoptosis. These phenomena are important because of the cytotoxic effects of various peroxides used in commercial products coming into direct contact with the human body, as is the case of epidermal keratinocytes in contact with cosmetic formulations" ". The toxic effects of f-BuOOH are associated with vasoconstriction and damage to the vascular smooth muscles ". Global determination methods for primary lipid oxidation products are discussed in Section IV.B. [Pg.613]

Rabinovitch, A., Suarez, W. L., Thomas, P. D., Strynadka, K., and Simpson, 1. (1992). Cytotoxic effects of cytokines on rat islets Evidence for involvement of free radicals and lipid peroxidation. Diabetohgia 33, 409-413. [Pg.214]

EGb 761 might also directly scavenge peroxynitrites and inhibit lipid peroxidation because it has been reported both to block the cytotoxicity induced by peroxynitrites and inhibit cyclosporine-A-induced peroxidation. This hypothesis is supported by the finding that the purported anti-ischemic agent ebselen completely protected and rescued hippocampal cells against SNP-induced toxicity. In contrast, the hydroxyl radical scavenging properties of EGb 761 do not seem able to account for its protective effects because catalase failed to display any neuroprotective properties in this model. [Pg.370]

There are few reports on the inhibitory effect of conjugated polyenes on the growth of cancer cell lines. Begin et al. (1988) reported the toxic effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on several kinds of tumor cells other polyunsaturated fatty acids, i.e., arachidonic acid (22 4n-6), a-linolenic acid (18 3n-3), and y-linolenic acid (18 3n-6) have cytotoxic action on several tumor cell lines at concentrations above 50 pM. Further, Tsuzuki et al. (2004) demonstrated that the anticarcinogenic effect of CLN are directly associated with lipid peroxidation. They transplanted human colon cancer cells (DLD-1) into nude mice, and CLA (9c, lit and lOt, 12c-18 2) and CLN (9c, lit, 13t-18 3) were administered to animals. Tumor growth was suppressed by the supplementation of CLA and CLN, and the extent of suppression was CLN >9c, llt-CLA.>10t, 12c-CLA, in that order. Furthermore, DNA fragmentation was enhanced and lipid peroxidation increased in tumor cells of the CLN-fed mouse. Thus this study indicates the possibility of seaweeds as potential sources of anticancer substances. [Pg.476]

The potential consequences of the peroxidation of membrane lipids include loss of polyunsaturated fatty acids, decreased lipid fluidity, altered membrane permeability, effects on membrane-associated enzymes, altered ion transport, release of material from subcellular compartments, and the generation of cytotoxic metabolites of lipid hydroperoxides. The physiological significance of lipid peroxidation products is shown in Table 1. [Pg.136]

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