Repair of iron-induced DNA oxidation by the flavonoid myricetin in primary rat hepatocyte cultures

Abalea, Valérie; Cillard, Josiane; Dubos, Marie-Pierre; Sergent, Odile; Cillard, P.; Morel, Isabelle

doi:10.1016/s0891-5849(99)00010-6

Cited by 86 publications

(42 citation statements)

References 62 publications

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“…74,75 Myricetin has been reported to increase the expression of DNA polymerase beta gene in a dose-dependent manner, an enzyme responsible for the error-free DNA repair. 66 Since SCE contains myricetin, the reduction in the radiation-induced micronuclei by SCE may be also due to the error-free DNA repair in the SCE + irradiation group.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Radiation-Induced DNA Damage by Jamun, Syzygium cumini, in the Cultured Splenocytes of Mice Exposed to Different Doses of γ-Radiation

2011

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The radioprotective property of 50 mg/kg body weight jamun (Syzygium cumini) extract was studied in the cultured splenocytes of mice exposed to 0, 0.5, 1, 2, 3, or 4 Gy of γ-radiation. The spleens of irradiated mice were removed aseptically and the splenocytes were extracted from the individual spleens and cultured. The micronuclei were prepared 72 hours after irradiation in binucleate splenocytes by blocking cytokinesis with cytochalasin-B. Irradiation of mice resulted in a dose-dependent elevation in the micronucleated splenocytes. The exposure of mice not only elevated splenocytes bearing one micronucleus but also cells bearing 2 and multiple (>2) micronuclei indicating induction of complex DNA damage after irradiation. Oral treatment of mice with 50 mg/kg body weight of jamun leaf extract protected against the radiation-induced micronuclei formation. Jamun extract also protected against the formation of 2 and multiple micronuclei indicating repair or inhibition of complex DNA damage. The assessment of lipid peroxidation in mice brain homogenate has indicated a concentration dependent inhibition of lipid peroxidation by jamun extract. Studies in a cell free system revealed that jamun extract inhibited the formation of OH, O 2 −, DPPH, and ABTS + free radicals in a concentration dependent manner. Our study demonstrates that jamun extract protected mice against the radiation-induced DNA damage and inhibition of radiation-induced free radical formation may be one of the mechanisms of radioprotection.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Radiation-Induced DNA Damage by Jamun, Syzygium cumini, in the Cultured Splenocytes of Mice Exposed to Different Doses of γ-Radiation

2011

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“…Curcumin has phenolic components, which provide protective effects against alkylating agents. Phenolic components in curcumin play a diverse role against DNA damage; either by stimulating detoxifying enzymes or by stimulating DNA repair pathways through transcription regulation or mRNA stabilization (Abalea et al 1999). Previous studies also showed the protective effect of phenolic components against the alkylating agents (Franke et al 2005, Corona et al 2007).…”

Section: Discussionmentioning

confidence: 97%

Effect of Curcumin On the Genotoxicity Induced By Alkylating Agents

Isitez¹,

Çiğerci²

2017

AKU-J. Sci. Eng.

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DNA damage due to genotoxic stress is an important type of stress which organisms are exposed during the their life. The direct-acting alkylating agent methyl methanesulfonate (MMS), is covalently linked to DNA and cause DNA damage, creating an indirect effect of the alkylating agent cyclophosphamide (CP) cause to DNA damage by changing the function of cellular proteins. In this study, the effects of curcumin on MMS and CP treated mice DNA damage, total antioxidant capacity, total oxidant capacity (oxidative stress index) and genotoxicity markers such as micronucleus index, cell growth arrest and induced DNA damage, which is Gadd45 and Gadd153 genes expression levels were investigated.Curcumin reduce DNA damage, the number of micronucleus and oxidative stres occurred by both MMS and CP induction. Curcumin's protective effect on DNA damage was provided by inducing Gadd45 and Gadd153 mRNA expression levels. We could state that curcumin, a phenolic compound show protective effects before the damage. In brief, curcumin has both antioxidant and antigenotoxic effects. Alkilleyici Ajanlar Tarafından Uyarılan Genotoksisite Üzerine Curcumin'in Etkisi Anahtar kelimelerCurcumin, Alkilleyici ajanlar, Genotoksisite, Comet assay, Gen ekspresyonu. ÖzetDNA hasarı organizmaların yaşamı boyunca maruz kaldığı önemli bir genotoksik stres türüdür. Doğrudan etkili alkilleyici ajanlardan olan metil metansülfonat (MMS), DNA'ya kovalent olarak bağlanarak DNA'da hasar oluştururken, dolaylı yoldan etkili alkilleyici ajanlardan olan siklofosfamid (SP) ise hücresel proteinlerin fonksiyonlarını değiştirerek DNA hasarına sebep olur. Bu araştırmada, deneysel olarak MMS ve SP uygulanan farelerde DNA hasarı, total antioksidan kapasite, total oksidan kapasite (oksidatif stres indeksi) ile genotoksisite belirteci mikronukleus indeksi ve hücre büyümesini durduran ve indüklenmiş DNA hasarının belirteci olan genlerden Gadd45 ve Gadd153'ün ifadelerindeki değişiklikler ile bunlara curcumin'in etkileri araştırıldı. Önce curcumin, sonra MMS ve SP'in uygulandığı gruplarda, curcumin'in DNA hasar derecesini mononükleer lökositlerde azalttığı, kemik iliğinde oluşan mikronukleus sayısını azalttığı, plazmada oksidatif stresi azalttığı ve indüklenmiş DNA hasarının belirteci olan Gadd45 ve Gadd153'ün mRNA ekspresyon düzeylerinin uyarılmasını sağlayarak koruyucu özellik gösterdiği bulundu. Sonuç olarak, fenolik bir bileşik olan curcumin'in, hasar oluştuktan sonra değil de, hasar oluşmadan önce koruyucu özellik göstererek antioksidan ve antigenotoksik özelliğe sahip olduğu bulundu.

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“…There are additional compounds which afforded protection against induced oxidative stress, most probably by means of an iron-chelating mechanism. These include a phenolic compound (o-phenanthroline) (104), a novel metal chelator (Tachpyr, N,N'N''-tris(2-pyridylmethyl)-cis,cis-1,3,5-triaminocyclohexane) (105), flavonoid (106), which offer a possibility for overcoming oxidative stress and subsequent carcinogenesis. Since iron-induced oxidative stress and inefficient repair could be related to DNA damage and probably to carcinogenesis, modulation of these processes by antioxidants might be relevant in further prevention of cEOC.…”

Section: Discussionmentioning

confidence: 99%

Clear cell carcinoma of the ovary: Potential pathogenic mechanisms (Review)

Kajihara

Yamada²,

Kanayama³

et al. 2010

Oncol Rep

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Abstract. Epithelial ovarian cancer (EOC) is the most common cause of gynecological cancer-related mortality. Clear cell EOC (cEOC) has a number of clinical features distinguishing it from other EOC because of frequent concurrence of endometriosis and highly chemoresistant nature resulting in a poor prognosis. Recent biochemical studies based on genomewide expression analysis technology have noted specific expression of a transcription factor, hepatocyte nuclear factor-1ß (HNF-1ß), in cEOC and genetic alteration may be involved in oxidative stress. We describe the HNF-1ß-dependent pathophysiology of cEOC and discuss its role in oxidative stress-induced carcinogenesis. A systematic search was performed in the electronic databases PubMed and ScienceDirect up to July 2009, combining the keywords, genome-wide, microarray, epithelial ovarian cancer, clear cell carcinoma, oxidative stress, and detoxification, with specific expression profiles of genes. The catalog of cEOC-specificity might be a manifestation of six essential alterations in cell physiology: oxidative stress and detoxification, proteases, signal transduction, adhesion, transcription, and metabolism. Among 54 genes highly upregulated in cEOC, 47 genes (87.0%) were associated with the redox-related genes. Several important cEOC-related genes overlap with those known to be regulated by HNF-1ß. Twenty-two (40.7%) of the 54 genes predominantly identified in cEOC were involved in downstream targets of HNF-1ß. The HNF-1ß-dependent pathway might provide new insights into regulation of glycogen synthesis, detoxification and resistance to anticancer agents. This review summarizes recent advances in the understanding of oxidative stress and antioxidant mechanisms in pathogenesis of cEOC. A redox-sensitive subset of cEOC genes linked to oxidative and detoxification pathways was identified and associated with HNF-1ß-specific downstream targets.

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Repair of iron-induced DNA oxidation by the flavonoid myricetin in primary rat hepatocyte cultures

Cited by 86 publications

References 62 publications

Inhibition of Radiation-Induced DNA Damage by Jamun, Syzygium cumini, in the Cultured Splenocytes of Mice Exposed to Different Doses of γ-Radiation

Inhibition of Radiation-Induced DNA Damage by Jamun, Syzygium cumini, in the Cultured Splenocytes of Mice Exposed to Different Doses of γ-Radiation

Effect of Curcumin On the Genotoxicity Induced By Alkylating Agents

Clear cell carcinoma of the ovary: Potential pathogenic mechanisms (Review)

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