Interaction of lipid peroxidation products with DNA. A review

Vaca, Carlos E.; Wilhelm, J.; Harms‐Ringdahl, Mats

doi:10.1016/0165-1110(88)90022-x

Cited by 438 publications

(228 citation statements)

References 50 publications

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“…33,34 Increased accumulation of LPO byproducts such as 4-HNE and oxidized proteins are critical features in ethanol-induced liver injury. Although malondialdehyde forms a pyrimidopurinone with the N-1 and N 2-position of guanine, 4-HNE induces DNA damage through its putative epoxidation product, 2,3-epoxy-4-hydroxynonanal.…”

Section: Discussionmentioning

confidence: 99%

Ethanol‐induced cytochrome P4502E1 causes carcinogenic etheno‐DNA lesions in alcoholic liver disease†‡

et al. 2009

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Oxidative stress is thought to play a major role in the pathogenesis of hepatocellular cancer (HCC), a frequent complication of alcoholic liver disease (ALD). However, the underlying mechanisms are poorly understood. In hepatocytes of ALD patients, we recently detected by immunohistochemistry significantly increased levels of carcinogenic etheno-DNA adducts that are formed by the reaction of the major lipid peroxidation product, 4-hydroxynonenal (4-HNE) with nucleobases. In the current study, we show that protein-bound 4-HNE and etheno-DNA adducts both strongly correlate with cytochrome P450 2E1 (CYP2E1) expression in patients with ALD (r ‫؍‬ 0.9, P < 0.01). Increased levels of etheno-DNA adducts were also detected in the liver of alcohol-fed lean ( E xcess consumption of alcohol is widespread inWestern countries and, in the United States, alcohol abuse affects approximately 18 million adults. 1 The consumption of more than 80 g ethanol per day for more than 10 years increases the risk for hepatocellular carcinoma (HCC) by approximately fivefold. 2 Worldwide, HCC is one of the most common malignant tumors, ranking as the seventh most prevalent in men and the ninth in women. The risk for HCC in decompensated alcohol-induced cirrhosis is approximately 1% to 2% per year. 2 Although the evolution of alcohol-related HCC involves several factors, 3,4 including the presence of cirrhosis, oxidative stress, disturbed DNA methylation, and defective retinoic acid signaling, the precise mechanisms at a molecular level by which alcohol causes HCC are poorly understood. Recently, the International Agency for Research on Cancer has classified ethanol as a human (group 1) carcinogen, because it induces HCC (among other tumors) in animals and increases the risk for developing HCC in humans. 3,5,6

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Section: Discussionmentioning

confidence: 99%

Ethanol‐induced cytochrome P4502E1 causes carcinogenic etheno‐DNA lesions in alcoholic liver disease†‡

et al. 2009

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“…Membrane lipid peroxidation is an important pathophysiological event in a variety of diseases and stress conditions. MDA is a major reactive aldehyde produced from the peroxidation of polyunsaturated fatty acid present in the biological membranes [25]. It was hypothesized that CCl 4 - induced hepatotoxicity is mainly due to the lipid peroxidation of hepatocyte membranes by free radical derivatives of CCl 4 [26].…”

Section: Discussionmentioning

confidence: 99%

Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver

et al. 2010

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BackgroundCarbon tetra chloride (CCl4), an industrial solvent, is a hepatotoxic agent and it is the well established animal model for free radical-induced liver injury. The present investigation was carried out to establish the protective effect of natansnin, a novel dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver.ResultsCCl4 significantly increased the levels of lipid peroxides, oxidized glutathione and decreased the levels of reduced glutathione, SOD and CAT. CCl4 induce marked histopathological changes and increase in the levels of apoptotic proteins. CCl4 treatment significantly increased the levels of apoptotic proteins such as caspases-3, PARP, Bax, Bid and cytochrome C and also increased the levels of inflammatory mediators iNos and Cox-2. Natansnin treatment significantly decreased the levels of CCl4 induced apoptotic proteins and inflammatory mediators. Further natansinin treatment significantly inhibited the CCl4 induced apoptosis which was evident form the reduced TUNEL positive cells.ConclusionsIn conclusion, our study demonstrated the protective effect of natansnin against CCl4 induced oxidative stress and cellular degeneration in rat liver tissue. This protective effect of natansnin can be correlated to its direct antioxidant effect.

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“…MA formed from two king-size cigarettes N and O were 27.9 and 36.0 g/cigarette À1 , respectively. MA, formaldehyde, acrolein, acetaldehyde, and glyoxal are major reactive carbonyl compounds resulting from the oxidation of biological membranes (Vaca et al, 1988) and animal blood plasma (Miyake and Shibamoto, 1998). Also, these reactive carbonyl compounds directly cross-link to proteins and bind covalently to nucleic acids (Lam et al, 1986) and consequently cause biological complications, including carcinogenesis (Furihata et al, 1989), aging, and atherosclerosis (Halliwell and Gutteridge, 1989).…”

Section: Discussionmentioning

confidence: 99%

Determination of toxic carbonyl compounds in cigarette smoke

2006

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Toxic carbonyl compounds, including formaldehyde, malonaldehyde, and glyoxal, formed in mainstream cigarette smoke were quantified by derivatization-solid phase extraction-gas chromatography methods. Cigarette smoke from 14 commercial brands and one reference (2R1F) was drawn into a separatory funnel containing aqueous phosphate-buffered saline. Reactive carbonyl compounds trapped in the buffer solution were derivatized into stable nitrogen containing compounds (pyrazoles for -dicarbonyl and , -unsaturated aldehyde; quinoxalines for -dicarbonyls; and thiazolidines for alkanals). After derivatives were recovered using C 18 solid phase extraction cartridges, they were analyzed quantitatively by a gas chromatograph with a nitrogen phosphorus detector. The total carbonyl compounds recovered from regular size cigarettes ranged from 1.92 mg/cigarette À1 to 3.14 mg/cigarette À1 . The total carbonyl compounds recovered from a reference cigarette and a king size cigarette were 3.23 mg/cigarette À1 and 3.39 mg/cigarette À1 , respectively. The general decreasing order of the carbonyl compounds yielded was acetaldehyde (1110-2101 g/cigarette À1 ) > diacetyl (301-433 g/cigarette À1 ), acrolein (238-468 g/cigarette À1 ) > formaldehyde (87.0-243 g/cigarette À1 ), propanal (87.0-176 g/cigarette À1 ) > malonaldehyde (18.9-36.0 g/cigarette À1 ), methylglyoxal (13.4-59.6 g/cigarette À1 ) > glyoxal (1.93-6.98 g/cigarette À1 ).

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Interaction of lipid peroxidation products with DNA. A review

Cited by 438 publications

References 50 publications

Ethanol‐induced cytochrome P4502E1 causes carcinogenic etheno‐DNA lesions in alcoholic liver disease†‡

Ethanol‐induced cytochrome P4502E1 causes carcinogenic etheno‐DNA lesions in alcoholic liver disease†‡

Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver

Determination of toxic carbonyl compounds in cigarette smoke

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