Hg(II) Exposure Exacerbates UV-Induced DNA Damage in MRC5 Fibroblasts: A Comet Assay Study

Bradfield, Wendy; Pye, A. Kenneth; Clifford, Tim; Salter, Leo; Gould, David; Campbell, Sandra J.; Curnow, Alison

doi:10.1080/10934520500349243

Cited by 3 publications

(4 citation statements)

References 16 publications

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“…Our data support findings from previous studies, that nonlethal mercury exposure alone does not induce substantial DNA damage in either genome (Cebulska-Wasiewska et al 2005, Bradfield et al 2006). nDNA damage has been observed in some studies, but the weight of the evidence so far seems to support the hypothesis that compromising genetic damage may only occur at cytotoxic exposures (Cantoni and Costa 1983, Pieper et al 2014).…”

Section: Discussionsupporting

confidence: 93%

“…We did not observe increased damage in conjunction with UVC exposure, confirming a previous report (Cebulska-Wasiewska et al 2005), though elevated damage has been noted with UVA and also X-ray co-exposures (Cantoni and Costa 1983, Bradfield et al 2006). Collectively, these findings are consistent with one of mercury’s major proposed mechanisms of action, creating an environment sensitive to oxidative stress due to reduced antioxidant capabilities: H 2 O 2 , UVA, and X-ray exposures induce ROS generation, but UVC-induced ROS is very minor (Godar et al 1993, Agarwal and Sohal 1994, Hao et al 2004, Manda et al 2007).…”

Section: Discussionsupporting

confidence: 92%

“…Until recently studies had primarily focused on nuclear genome impacts following mercury exposure, because the methods used in many studies (e.g. the comet assay) predominantly evaluated nDNA (Cebulska-Wasiewska et al 2005, Bradfield et al 2006, Ondovcik et al 2012, Ryu et al 2014). mtDNA impacts have been addressed in only a few studies.…”

Section: Discussionmentioning

confidence: 99%

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Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

et al. 2017

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Mercury toxicity mechanisms have the potential to induce DNA damage and disrupt cellular processes, like mitochondrial function. Proper mitochondrial function is important for cellular bioenergetics and immune signaling and function. Impacts of mercury on the nuclear genome (nDNA) are conflicting and inconclusive, and mitochondrial DNA (mtDNA) impacts are relatively unknown. In this study, we assessed genotoxic (mtDNA and nDNA), metabolic, and innate immune impacts of inorganic and organic mercury exposure in Caenorhabditis elegans. Genotoxic outcomes measured included DNA damage, DNA damage repair (nucleotide excision repair, NER; base excision repair, BER), and genomic copy number following MeHg and HgCl2 exposure alone and in combination with known DNA damage-inducing agents ultraviolet C radiation (UVC) and hydrogen peroxide (H2O2), which cause bulky DNA lesions and oxidative DNA damage, respectively. Following exposure to both MeHg and HgCl2, low-level DNA damage (~0.25 lesions/10 kb mtDNA and nDNA) was observed. Unexpectedly, a higher MeHg concentration reduced damage in both genomes compared to controls. However, this observation was likely the result of developmental delay. In co-exposure treatments, both mercury compounds increased initial DNA damage (mtDNA and nDNA) in combination with H2O2 exposure, but had no impact in combination with UVC exposure. Mercury exposure both increased and decreased DNA damage removal via BER. DNA repair after H2O2 exposure in mercury-exposed nematodes resulted in damage levels lower than measured in controls. Impacts to NER were not detected. mtDNA copy number was significantly decreased in the MeHg-UVC and MeHg-H2O2 co-exposure treatments. Mercury exposure had metabolic impacts (steady-state ATP levels) that differed between the compounds; HgCl2 exposure decreased these levels, while MeHg slightly increased levels or had no impact. Both mercury species reduced mRNA levels for immune signaling-related genes, but had mild or no effects on survival on pathogenic bacteria. Overall, mercury exposure disrupted mitochondrial endpoints in a mercury-compound dependent fashion.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

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Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

et al. 2017

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“…by competing with ROSscavenging thiols (reviewed by Lo ´pez- Barea and Go ´mez-Ariza, 2006). Other authors have found genotoxicity induced by UV light to be enhanced by mercury (Bradfield et al, 2006). The link between genotoxicity and ROS led to many toxicological studies involving genotoxicity and oxidative stress-related biomarkers, such as lipid peroxidation (e.g.…”

Section: Introductionmentioning

confidence: 99%

Assessment of the genotoxic potential of contaminated estuarine sediments in fish peripheral blood: Laboratory versus in situ studies

Costa

Neuparth

Caeiro

et al. 2011

Environmental Research

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Juvenile Senegalese soles (Solea senegalensis) were exposed to estuarine sediments through 28-day laboratory and in situ (field) bioassays. The sediments, collected from three distinct sites (a reference plus two contaminated) of the Sado Estuary (W Portugal) were characterized for total organic matter, redox potential, fine fraction and for the levels of metals, polycyclic aromatic hydrocarbons (PAHs) and organochlorines, namely polychlorinated biphenyls (PCBs) and dichloro diphenyl tricholoethane plus its main metabolites (DDTs). Genotoxicity was determined in whole peripheral blood by the single-cell gel electrophoresis (SCGE or "comet") assay and by scoring erythrocytic nuclear abnormalities (ENA). Analysis was complemented with the determination of lipid peroxidation in blood plasma by the thiobarbituric acid reactive substances (TBARS) protocol and cell type sorting. The results showed that exposure to contaminated sediments induced DNA fragmentation and clastogenesis. Still, laboratory exposure to the most contaminated sediment revealed a possible antagonistic effect between metallic and organic contaminants that might have been enhanced by increased bioavailability. The laboratory assay caused a more pronounced increase in ENA whereas a very significant increase in DNA fragmentation was observed in field-tested fish exposed to the reference sediment, which is likely linked to increased lipid peroxidation that probably occurred due to impaired access to food. Influence of natural pathogens was ruled out by unaltered leukocyte counts. The statistical integration of data correlated lipid peroxidation with biological variables such as fish length and weight, whereas the genotoxicity biomarkers were more correlated to sediment contamination. It was demonstrated that laboratory and field bioassays for the risk assessment of sediment contamination may yield different genotoxicity profiles although both provided results that are in overall accordance with sediment contamination levels. While field assays may provide more ecologically relevant data, the multiple environmental variables may produce sufficient background noise to mask the true effects of contamination.

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Mercury and cancer: Where are we now after two decades of research?

Skalny

Aschner

Sekacheva

et al. 2022

Food and Chemical Toxicology

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Hg(II) Exposure Exacerbates UV-Induced DNA Damage in MRC5 Fibroblasts: A Comet Assay Study

Cited by 3 publications

References 16 publications

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

Assessment of the genotoxic potential of contaminated estuarine sediments in fish peripheral blood: Laboratory versus in situ studies

Mercury and cancer: Where are we now after two decades of research?

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