Effects of antioxidants on quercetin-induced nuclear DNA damage and lipid peroxidation

Sahu, Saura C.; Washington, Melissa

doi:10.1016/0304-3835(91)90122-x

Cited by 53 publications

(15 citation statements)

References 32 publications

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“…However, in other experimental models, quercetin at high doses has been seen to increase the development of certain tumors (benign renal neoplasms) (65). These results have been confirmed by the observation that quercetin is able to damage DNA, favoring the appearance of mutations (66) and incrementing lipid peroxidation in the rat liver-particularly in the presence of iron (67). Thus, the effect of quercetin as a pro-oxidant or antioxidant is dependent upon the corresponding redox status and prevalent biological environment (68).…”

Section: Effects Of Polyphenols In Alcoholic Beverages Upon Carcinogesupporting

confidence: 62%

The Effects of Alcohol Consumption Upon The Gastrointestinal Tract

Bujanda¹

2000

American Journal of Gastroenterology

271

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Regardless of the type and dose of beverage involved, alcohol facilitates the development of gastroesophageal reflux disease by reducing the pressure of the lower esophageal sphincter and esophageal motility. Fermented and nondistilled alcoholic beverages increase gastrin levels and acid secretion. Succinic and maleic acid contained in certain alcoholic drinks also stimulate acid secretion. Low alcohol doses accelerate gastric emptying, whereas high doses delay emptying and slow bowel motility. Alcohol facilitates the development of superficial gastritis and chronic atrophic gastritis--though it has not been shown to cause peptic ulcer. Alcoholic beverages, fundamentally wine, have important bactericidal effects upon Helicobacter pylori and enteropathogenic bacteria. The main alcohol-related intestinal alterations are diarrhea and malabsorption, with recovery after restoring a normal diet. Alcohol facilitates the development of oropharyngeal, esophageal, gastric, and colon cancer. Initial research suggests that wine may be comparatively less carcinogenic.

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Section: Effects Of Polyphenols In Alcoholic Beverages Upon Carcinogesupporting

confidence: 62%

The Effects of Alcohol Consumption Upon The Gastrointestinal Tract

Bujanda¹

2000

American Journal of Gastroenterology

271

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“…For instance, quercetin induced DNA damage in isolated rat liver nuclei in the presence of iron or copper [Sahu and Washington, 1991]. Both EGCG and quercetin induced strand breaks in plasmid DNA, but this damage was prevented when the metal chelator, diethylenetriamine pentaacetic acid, was present during incubation [Ohshima et al, 1998].…”

Section: ] Therefore It Seems That Onoomentioning

confidence: 99%

Epigallocatechin gallate protects U937 cells against nitric oxide‐induced cell cycle arrest and apoptosis

Kelly

Geigerman

Loo

2001

J of Cellular Biochemistry

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Ingesting phenolic phytochemicals in many plant products may promote health, but the effects of phenolic phytochemicals at the cellular level have not been fully examined. Thus, it was determined if the tea phenolic phytochemical, epigallocatechin gallate (EGCG), protects U937 human pro-monocytic cells against the nitrogen free radical, nitric oxide (*NO). Cells were incubated for 4-6 h with 500 microM S-nitrosoglutathione (GSNO), which generates *NO, but this did not induce single-strand breaks in DNA. Nevertheless, 82 +/- 4% of GSNO-treated cells, compared to only 39 +/- 1% of untreated cells, were arrested in the G(1)-phase of the cell cycle. However, dosing the GSNO-treated cells with 9, 14, or 18 microg/ml of EGCG resulted in only 74 +/- 8%, 66 +/- 1%, and 43 +/- 3% of the cells, respectively, in the G(1)-phase. Exposing cells to GSNO also resulted in the emergence of a sub-G(1) apoptotic cell population numbering 14 +/- 3%, but only 5 +/- 2%, 5 +/- 1%, and 2 +/- 0% upon dosing of the GSNO-treated cells with 9, 14, and 18 microg/ml of EGCG, respectively. Furthermore, exposing cells to GSNO resulted in greater cell surface binding of annexin V-FITC, but binding was 41-89% lower in GSNO-treated cells dosed with EGCG. Collectively, these data suggest that *NO or downstream products induced cell cycle arrest and apoptosis that was not due to single-strand breaks in DNA, and that EGCG scavenged cytotoxic *NO or downstream products, thus reducing the number of cells in a state of cell cycle arrest or apoptosis.

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“…One striking example reported in the literature is that of quercetin, which in the presence of transition metals acts as a pro-oxidant and has mutagenic activity [38, 39]. It was shown that some flavonoids are able to reduce transition metals, a process during which the highly oxidizing radical OH• is formed and could therefore damage DNA.…”

Section: Electrochemical Biosensors For Detection Of Dna Damagementioning

confidence: 99%

Electrochemical DNA Sensors for Detection of DNA Damage

Diculescu

Chiorcea-Paquim

Oliveira-Brett

2005

Sensors

121

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Electrochemical devices have received particular attention due to their rapid detection and great sensitivity for the evaluation of DNA-hazard compounds interaction mechanisms. Several types of bioanalytical method use nucleic acids probes to detect DNA damage. This article reviews current directions and strategies in the development and applications of electrochemical DNA sensors for the detection of DNA damage.

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Effects of antioxidants on quercetin-induced nuclear DNA damage and lipid peroxidation

Cited by 53 publications

References 32 publications

The Effects of Alcohol Consumption Upon The Gastrointestinal Tract

The Effects of Alcohol Consumption Upon The Gastrointestinal Tract

Epigallocatechin gallate protects U937 cells against nitric oxide‐induced cell cycle arrest and apoptosis

Electrochemical DNA Sensors for Detection of DNA Damage

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