Metformin does not prevent DNA damage in lymphocytes despite its antioxidant properties against cumene hydroperoxide-induced oxidative stress

Onaran, İlhan; Güven, Gülgün S.; Ozdas, Sule; Kanigür, Gönül; Vehid, Suphi

doi:10.1016/j.mrgentox.2006.06.036

Cited by 29 publications

(18 citation statements)

References 42 publications

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“…The mechanisms responsible for metformin activation of antioxidant defences are unresolved. There are also studies showing reduced production of reactive oxygen species in cell cultures [68][69][70] reduced production of superoxide free radicals in platelets [71] and decreased lipid peroxidation [72].…”

Section: Glycation and Oxidative Stressmentioning

confidence: 99%

Metformin: Effects on Micro and Macrovascular Complications in Type 2 Diabetes

Bailey

2008

Cardiovasc Drugs Ther

108

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Metformin has long been known to reduce the development of atherosclerotic lesions in animal models, and clinical studies have shown the drug to reduce surrogate measures such as carotid intima-media thickness. The anti-atherogenic effects of metformin include reductions in insulin resistance, hyperinsulinaemia and obesity. There may be modest favourable effects against dyslipidaemia, reductions in pro-inflammatory cytokines and monocyte adhesion molecules, and improved glycation status, benefiting endothelial function in the macro- and micro-vasculature. Additionally metformin exerts anti-thrombotic effects, contributing to overall reductions in athero-thrombotic risk in type 2 diabetic patients.

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Section: Glycation and Oxidative Stressmentioning

confidence: 99%

Metformin: Effects on Micro and Macrovascular Complications in Type 2 Diabetes

Bailey

2008

Cardiovasc Drugs Ther

108

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“…Although widely used, metformin can cause minor incidents of gastrointestinal upsets such as dysphagia, early satiety, reflux, constipation, abdominal pain, nausea, vomiting, and diarrhea (Wolosin and Edelman, 2000) but no major side effects have been reported. However, it has been observed that metformin induces DNA damage either by increasing the levels of reactive oxygen species and reducing aconitase activity (http://www.ncbi.nlm.nih.gov/pmc/ articles/PMC3313505/ Anedda et al, 2008) or by increasing the cumene hydroperoxide (CumOOH) content which in turn induces fragmentation (Onaran et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Genotoxicity evaluation of metformin and glimepiride by micronucleus assay in exfoliated urothelial cells of type 2 diabetes mellitus patients

Harishankar

Logeshwaran

Sujeevan

et al. 2015

Food and Chemical Toxicology

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“…While some reports indicated no genotoxic effects (Attia et al , 2009), others (Janjetovic et al , 2011) have assumed that metformin can produce oxidative stress due to DNA fragmentation. Onaran et al (2006) proposed that high concentrations of metformin increased cumene hydroperoxide (CumOOH)-induced DNA damage. Furthermore, Anedda et al , (2008) showed that metformin induces oxidative stress in white adipocytes, by|through increasing the levels of reactive oxygen species, and reducing aconitase activity.…”

Section: Introductionmentioning

confidence: 99%

Metformin (dimethyl-biguanide) induced DNA damage in mammalian cells

et al. 2011

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Metformin (dimethyl-biguanide) is an insulin-sensitizing agent that lowers fasting plasma-insulin concentration, wherefore it’s wide use for patients with a variety of insulin-resistant and prediabetic states, including impaired glucose tolerance. During pregnancy it is a further resource for reducing first-trimester pregnancy loss in women with the polycystic ovary syndrome. We tested metformin genotoxicity in cells of Chinese hamster ovary, CHO-K1 (chromosome aberrations; comet assays) and in mice (micronucleus assays). Concentrations of 114.4 μg/mL and 572 μg/mL were used in in vitro tests, and 95.4 mg/kg, 190.8 mg/kg and 333.9 mg/kg in assaying. Although the in vitro tests revealed no chromosome aberrations in metaphase cells, DNA damage was detected by comet assaying after 24 h of incubation at both concentrations. The frequency of DNA damage was higher at concentrations of 114.4 μg/mL. Furthermore, although mortality was not observed in in vitro tests, the highest dose of metformin suppressed bone marrow cells. However, no statistically significant differences were noted in micronuclei frequencies between treatments. In vitro results indicate that chronic metformin exposure may be potentially genotoxic. Thus, pregnant woman undergoing treatment with metformin should be properly evaluated beforehand, as regards vulnerability to DNA damage.

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Metformin does not prevent DNA damage in lymphocytes despite its antioxidant properties against cumene hydroperoxide-induced oxidative stress

Cited by 29 publications

References 42 publications

Metformin: Effects on Micro and Macrovascular Complications in Type 2 Diabetes

Metformin: Effects on Micro and Macrovascular Complications in Type 2 Diabetes

Genotoxicity evaluation of metformin and glimepiride by micronucleus assay in exfoliated urothelial cells of type 2 diabetes mellitus patients

Metformin (dimethyl-biguanide) induced DNA damage in mammalian cells

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