Zinc and the gene

Dreosti, Ivor E.

doi:10.1016/s0027-5107(01)00067-7

Cited by 143 publications

(69 citation statements)

References 46 publications

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“…In this study, the levels of metallothionein (MT) expression were measured to test whether this is one of the possible induced mechanisms that may exert a genomeprotective effect (Ho 2004). Zn can modulate the expression of metallothionein that is involved in cellular defence against free radicals and oxidative stress (Dreosti 2001). Our results showed that Zn-depleted cells have a lower MT expression indicating that MT is not involved in protecting against Zn deficiency-induced oxidative stress.…”

Section: Discussionmentioning

confidence: 90%

“…To date, there are no studies on the effect of Zn on genomic stability in primary HOK cells even though Zn is recognised as one of the key minerals that are essential in maintaining DNA integrity (Ho 2004;Dreosti 2001). The Cytokinesis Block Micronucleus Cytome (CBMN-Cyt) assay has been identified as currently the best validated biomarker of DNA damage and cytotoxicity that is sensitive to nutritional status as well as being associated with and predictive of degenerative diseases (Fenech 2010).…”

Section: Introductionmentioning

confidence: 99%

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Zinc deficiency or excess within the physiological range increases genome instability and cytotoxicity, respectively, in human oral keratinocyte cells

et al. 2011

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Zinc (Zn) is an essential component of Zn-finger proteins and acts as a cofactor for enzymes required for cellular metabolism and in the maintenance of DNA integrity. The study investigated the genotoxic and cytotoxic effects of Zn deficiency or excess in a primary human oral keratinocyte cell line and determined the optimal concentration of two Zn compounds (Zn Sulphate (ZnSO 4 ) and Zn Carnosine (ZnC)) to minimise DNA damage. Zn-deficient medium (0 lM) was produced using Chelex treatment, and the two Zn compounds ZnSO 4 and ZnC were tested at concentrations of 0.0, 0.4, 4.0, 16.0, 32.0 and 100.0 lM. Cell viability was decreased in Zndepleted cells (0 lM) as well as at 32 lM and 100 lM for both Zn compounds (P \ 0.0001) as measured via the MTT assay. DNA strand breaks, as measured by the comet assay, were found to be increased in Zn-depleted cells compared with the other treatment groups (P \ 0.05). The Cytokinesis Block Micronucleus Cytome assay showed a significant increase in the frequency of both apoptotic and necrotic cells under Zn-deficient conditions (P \ 0.05). Furthermore, elevated frequencies of micronuclei (MNi), nucleoplasmic bridges (NPBs) and nuclear buds (NBuds) were observed at 0 and 0.4 lM Zn, whereas these biomarkers were minimised for both Zn compounds at 4 and 16 lM Zn (P \ 0.05), suggesting these concentrations are optimal to maintain genome stability. Expression of PARP, p53 and OGG1 measured by western blotting was increased in Zn-depleted cells indicating that DNA repair mechanisms are activated. These results suggest that maintaining Zn concentrations within the range of 4-16 lM is essential for DNA damage prevention in cultured human oral keratinocytes.

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Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Zinc deficiency or excess within the physiological range increases genome instability and cytotoxicity, respectively, in human oral keratinocyte cells

et al. 2011

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“…This association is plausible: zinc can physically displace DNA-bound iron and reduce the extent of iron-catalyzed hydroxyl radical production (OH.) and OH.-driven DNA damage [41]. Others have also reported dietary effects with the OGG1 common allele: Le Marchand and colleagues [7] observed a 50% lower risk (95% CI, 0.3-0.8) of lung cancer among homozygous or heterozygous carriers of the common C allele with higher compared to lower vegetable intake.…”

Section: Discussionmentioning

confidence: 99%

Vegetables- and antioxidant-related nutrients, genetic susceptibility, and non-Hodgkin lymphoma risk

Kelemen

Wang

Lim

et al. 2008

Cancer Causes Control

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Genetic susceptibility to DNA oxidation, carcinogen metabolism, and altered DNA repair may increase non-Hodgkin lymphoma (NHL) risk, whereas vegetables-and antioxidant-related nutrients may decrease risk. We evaluated the interaction of a priori-defined dietary factors with 28 polymorphisms in these metabolic pathways. Incident cases (n = 1,141) were identified during 1998-2000 from four cancer registries and frequency-matched to population-based controls (n = 949). We estimated diet-gene joint effects using two-phase semi-parametric maximum-likelihood methods, which utilized genotype data from all subjects as well as 371 cases and 311 controls with available diet information. Adjusted odds ratios (95% confidence intervals) were lower among common allele carriers with higher dietary intakes. For the GSTM3 3-base insertion and higher total vegetable intake, the risk was 0.56 (0.35-0.92, p interaction = 0.03); for GSTP1 A114V and higher cruciferous vegetable intake, the risk was 0.52 (0.34-0.81, p interaction = 0.02); for OGG1 S326C and higher daily zinc intake, the risk was 0.71 (0.47-1.08, p interaction = 0.04) and for XRCC3 T241M and higher green leafy vegetable intake, the risk was 0.63 (0.41-0.97, p interaction = 0.03). Calculation of the false positive report probability determined a high likelihood of falsely positive associations. Although most associations have not been examined previously with NHL, our results suggest the examined polymorphisms are not modifiers of the association between vegetable and zinc intakes and NHL risk.

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“…Some metals are essential to life as they are involved in multiple functions, such as enzymes structure and activity, transport proteins, hormonal function and specific receptor sites, being crucial for the well functioning of the biological systems, if maintained at required levels (Apostoli, 2002). For example, Zn that is the most abundant intracellular component is involved in genetic stability and gene expression as well as in DNA repair and programmed cell death (Dreosti, 2001). Deficiency in Zn has been associated with growth retardation and increasing cancer risk, but in excess it can be neurotoxic (Cai et al, 2005;Dreosti, 2001).…”

Section: Introductionmentioning

confidence: 99%

Essential and non-essential trace metals in scalp hair of men chronically exposed to volcanogenic metals in the Azores, Portugal

Amaral

Arruda

Cabral

et al. 2008

Environment International

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This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. Volcanoes produce and release large amounts of toxicants, and the concentration of metals in hair can be used as a biomarker of exposure to trace metals. In order to investigate whether humans exposed to volcanic emissions demonstrate higher concentrations of essential and non-essential trace metals, scalp hair of men (3-89 years) living in two areas of the Azores, one exposed to volcanic emissions and the other not, was sampled, and their content in Cd, Cu, Pb, Rb, Se, and Zn was quantified by using High Resolution Inductively Coupled Plasma Mass Spectrometry. In average, men exposed to volcanic emissions presented higher concentrations of Cd (96.9 ppb), Cu (16.2 ppm), Pb (3417.6 ppb), Rb (216.3 ppb), and Zn (242.8 ppm), but not Se (469.6 ppb). Also, strong and significant correlations were found between Cd-Rb and Pb-Rb in the exposed men. In conclusion, humans living chronically exposed to volcanic emissions show high concentrations of essential and non-essential trace metals in scalp hair, and is suggested that this type of exposure may be as harmful as living close to industrial facilities. A B S T R A C T A R T I C L E I N F O

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Zinc and the gene

Cited by 143 publications

References 46 publications

Zinc deficiency or excess within the physiological range increases genome instability and cytotoxicity, respectively, in human oral keratinocyte cells

Zinc deficiency or excess within the physiological range increases genome instability and cytotoxicity, respectively, in human oral keratinocyte cells

Vegetables- and antioxidant-related nutrients, genetic susceptibility, and non-Hodgkin lymphoma risk

Essential and non-essential trace metals in scalp hair of men chronically exposed to volcanogenic metals in the Azores, Portugal

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