Antagonistic Growth Effects of Mercury and Selenium in <i>Caenorhabditis elegans</i> Are Chemical-Species-Dependent and Do Not Depend on Internal Hg/Se Ratios

Wyatt, Lauren; Diringer, Sarah E.; Rogers, Laura; Hsu‐Kim, Heileen; Pan, William; Meyer, Joel N.

doi:10.1021/acs.est.5b06044

Cited by 22 publications

(12 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Considering diet as a factor that contributes to health status is not new; however, it is increasingly important to consider when determining mercury exposure impacts. Certain nutritional factors, like selenium, are hypothesized to alter mercury exposure by reducing bioavailable mercury and increasing antioxidant function [ 37 , 98 , 99 , 100 , 101 , 102 ], while others, such as omega-3 fatty acids and vitamin B, have been associated with modifying child neurological [ 67 , 68 , 74 , 103 ] and immunological outcomes [ 104 , 105 ].…”

Section: Discussionmentioning

confidence: 99%

Spatial, Temporal, and Dietary Variables Associated with Elevated Mercury Exposure in Peruvian Riverine Communities Upstream and Downstream of Artisanal and Small-Scale Gold Mining

Wyatt

Ortiz

Feingold

et al. 2017

IJERPH

Self Cite

View full text Add to dashboard Cite

Artisanal and small-scale gold mining (ASGM) is a primary contributor to global mercury and its rapid expansion raises concern for human exposure. Non-occupational exposure risks are presumed to be strongly tied to environmental contamination; however, the relationship between environmental and human mercury exposure, how exposure has changed over time, and risk factors beyond fish consumption are not well understood in ASGM settings. In Peruvian riverine communities (n = 12), where ASGM has increased 4–6 fold over the past decade, we provide a large-scale assessment of the connection between environmental and human mercury exposure by comparing total mercury contents in human hair (2-cm segment, n = 231) to locally caught fish tissue, analyzing temporal exposure in women of child bearing age (WCBA, 15–49 years, n = 46) over one year, and evaluating general mercury exposure risks including fish and non-fish dietary items through household surveys and linear mixed models. Calculations of an individual’s oral reference dose using the total mercury content in locally-sourced fish underestimated the observed mercury exposure for individuals in many communities. This discrepancy was particularly evident in communities upstream of ASGM, where mercury levels in river fish, water, and sediment measurements from a previous study were low, yet hair mercury was chronically elevated. Hair from 86% of individuals and 77% of children exceeded a USEPA (U.S. Environmental Protection Agency) provisional level (1.2 µg/g) that could result in child developmental impairment. Chronically elevated mercury exposure was observed in the temporal analysis in WCBA. If the most recent exposure exceeded the USEPA level, there was a 97% probability that the individual exceeded that level 8–10 months of the previous year. Frequent household consumption of some fruits (tomato, banana) and grains (quinoa) was significantly associated with 29–75% reductions in hair mercury. Collectively, these data demonstrate that communities located hundreds of kilometers from ASGM are vulnerable to chronically elevated mercury exposure. Furthermore, unexpected associations with fish mercury contents and non-fish dietary intake highlight the need for more in-depth analyses of exposure regimes to identify the most vulnerable populations and to establish potential interventions.

show abstract

Section: Discussionmentioning

confidence: 99%

Spatial, Temporal, and Dietary Variables Associated with Elevated Mercury Exposure in Peruvian Riverine Communities Upstream and Downstream of Artisanal and Small-Scale Gold Mining

Wyatt

Ortiz

Feingold

et al. 2017

IJERPH

Self Cite

View full text Add to dashboard Cite

show abstract

“…In C. elegans , MeHg and HgCl 2 behave differently in terms of uptake and interactions with other co-exposures (e.g. selenium compounds) (Wyatt et al 2016). …”

Section: Discussionmentioning

confidence: 99%

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

et al. 2017

Self Cite

View full text Add to dashboard Cite

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.

show abstract

“…Total Hg in fur and blood of wild bat was weakly associated with mtDNA damage in wing punches (Karouna‐Renier et al, ). Alterations in mtDNA damage and mtDNA CN resulted from inorganic Hg (iHg) and MeHg exposures in laboratory experiments with the nematode model C. elegans (Wyatt et al, , ). In these laboratory experiments, mtDNA damage increased with HgCl 2 exposure, as did nDNA damage.…”

Section: Introductionmentioning

confidence: 99%

Predictors of mitochondrial DNA copy number and damage in a mercury‐exposed rural Peruvian population near artisanal and small‐scale gold mining: An exploratory study

Berky

Ryde

Feingold

et al. 2018

Environ and Mol Mutagen

Self Cite

View full text Add to dashboard Cite

Mitochondrial DNA (mtDNA) copy number (CN) and damage in circulating white blood cells have been proposed as effect biomarkers for pollutant exposures. Studies have shown that mercury accumulates in mitochondria and affects mitochondrial function and integrity; however, these data are derived largely from experiments in model systems, rather than human population studies that evaluate the potential utility of mitochondrial exposure biomarkers. We measured mtDNA CN and damage in white blood cells (WBCs) from 83 residents of nine communities in the Madre de Dios region of the Peruvian Amazon that vary in proximity to artisanal and small‐scale gold mining. Prior research from this region reported high levels of mercury in fish and a significant association between food consumption and human total hair mercury level of residents. We observed that mtDNA CN and damage were both associated with consumption of fruit and vegetables, higher diversity of fruit consumed, residential location, and health characteristics, suggesting common environmental drivers. Surprisingly, we observed negative associations of mtDNA damage with both obesity and age. We did not observe any association between total hair mercury or, in contrast to previous results, age, with either mtDNA damage or CN. The results of this exploratory study highlight the importance of combining epidemiological and laboratory research in studying the effects of stressors on mitochondria, suggesting that future work should incorporate nutritional and social characteristics, and caution should be taken when applying conclusions from epidemiological studies conducted in the developed world to other regions, as results may not be easily translated. Environ. Mol. Mutagen. 60: 197–210, 2019. © 2018 Wiley Periodicals, Inc.

show abstract

Antagonistic Growth Effects of Mercury and Selenium in Caenorhabditis elegans Are Chemical-Species-Dependent and Do Not Depend on Internal Hg/Se Ratios

Cited by 22 publications

References 53 publications

Spatial, Temporal, and Dietary Variables Associated with Elevated Mercury Exposure in Peruvian Riverine Communities Upstream and Downstream of Artisanal and Small-Scale Gold Mining

Spatial, Temporal, and Dietary Variables Associated with Elevated Mercury Exposure in Peruvian Riverine Communities Upstream and Downstream of Artisanal and Small-Scale Gold Mining

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

Predictors of mitochondrial DNA copy number and damage in a mercury‐exposed rural Peruvian population near artisanal and small‐scale gold mining: An exploratory study

Contact Info

Product

Resources

About