N-Doped Carbon Dots and ZnO Conglomerated Electrodes for Optically Responsive Supercapacitor Applications.

The over-dependence of human society on fossil fuels for energy is exhausting the level of such non-renewable energy sources. Alternative energy storage systems have gained more popularity recently to counter this issue. In this context, we report the fabrication of N-doped carbon dot (N-CD)-decorated ZnO-based electrodes for supercapacitor applications. Due to the light-responsive nature of the N-CDs and ZnO, the electrode was also responsive under the influence of UV light. After the experimental tests, it was found that the areal capacitance value of the supercapacitor increased upto ∼58.9% when illuminated compared to that under the dark conditions. Moreover, the device showed a maximum areal capacitance of 2.6 mF/cm2 after photocharging and galvanostatically discharging at a current density value of 1.6 µA/cm2, which is quite comparable with the previously reported data. The doping of N-CDs with ZnO showed a significant improvement in the areal capacitance value under both illuminated (∼58.64%) and dark conditions (∼22.08%) compared to the case of pristine ZnO, which justifies the purpose of attaching N-CDs with ZnO. Therefore, in brief, we have fabricated a photoresponsive electrode material for supercapacitor application by combining N-CDs and ZnO. An explicit electrochemical characterization of the electrode was also done to identify the contribution from diffusion-controlled capacitance and double layer capacitance, and it was observed that the diffusion-controlled capacitance gets reduced from 59.1 to 33.6% when the scan rate is increased from 2 to 75 mV/s. Moreover, a detailed study has also been done to understand the reaction mechanism. It was confirmed that the defects in the electrode material played a vital role in the intercalation of K+ ions.

Ecological Insights, and Fin Fish Diversity in Carps Spawning Grounds: Case Studies from the Surma River and Tanguar Haor, Bangladesh.

This study aims to provide a thorough ecological understanding of fin fish diversity within carp spawning grounds in the Surma River and Tanguar haor. Over two spawning seasons, this research investigates ecological factors impacting fin fish diversity and abundance in carp spawning grounds of the Surma River and Tanguar haor, emphasizing water quality, habitat features, spawn availability, and environmental influences. Fish spawn samples were collected with eight "Savar nets" at chosen sites and reared in a fiberglass tank at the mini hatchery for species identification. The representative spawn samples were examined under a microscope for preliminary species identification before rearing. The study found that both the Surma River and Tanguar haor offer ideal conditions for carp spawning due to factors such as water quality, natural food availability, habitat suitability, and favorable climatic conditions. The study identified 39 fish species under the 10 fish groups from both locations, with a higher percentage of carp species (31.42%) in the Surma River in 2021 compared to 2022 (22.50%). In Tanguar haor, the percentage of carp species was 7.55% and 6.50% in 2021 and 2022, respectively. The Surma River's ecological indices (2021-2022) indicated decreased diversity, likely due to environmental degradation, while Tanguar haor showed lower diversity possibly attributable to multiple environmental stressors. The dominant carp species, Labeo calbasu, Labeo bata, and Labeo gonius, were identified in both the Surma River and Tanguar haor. The spawning distribution varied among different locations, with some sites showing a presence of carp species, such as Hajipur (T1) in the Surma River and Alam Duar (T2) in Tanguar haor. The findings highlight the importance of hydrological and environmental parameters in shaping carp spawning habitat distribution and abundance, contributing to aquatic biodiversity conservation and resource management.

Effects of Hudson River Stressors on Atlantic Tomcod: Contaminants and a Warming Environment.

The Hudson River (HR) Estuary has a long history of pollution with a variety of contaminants including PCBs, and dioxins. In fact, 200 miles of the mainstem HR is designated a U.S. federal Superfund site, the largest in the nation, because of PCB contamination. The tidal HR hosts the southernmost spawning population of Atlantic tomcod, and studies revealed a correlation between exposure of juveniles to warm water temperature during summer to abundance of spawning adults of the same cohort in the following winter. Further, a battery of mechanistically linked biomarkers, ranging from the molecular to the population levels, were significantly impacted from contaminant exposures of the HR tomcod population. In response to xenobiotic insult, the HR tomcod population developed resistance to PCB sand TCDD toxicity resulting from a deletion in the aryl hydrocarbon receptor2 (AHR2) gene. Furthermore, RNA-Seq analysis of global gene expression demonstrated that effects of the AHR2 polymorphism were far more pervasive than anticipated. The most highly PCB-contaminated sediments in the upper HR were dredged between 2009 and 2015 with the objective of lowering PCB concentrations in fishes in the lower HR. Success of the remediation project has been controversial. These observations suggest that tomcod provides an informative model to evaluate the efficacy of HR PCB remediation efforts on downriver fish populations and possible interactive effects between contaminant exposure and a warming environment.

Probing the strongly correlated magnetic state of Co2C nanoparticles at low temperatures usingµSR.

Co2C nanoparticles (NPs) are amongst transition metal carbides whose magnetic properties have not been well explored. An earlier study (Royet al2021J. Phys.: Condens. Matter33375804) showed that a pellet made from Co2C NPs exhibits exchange bias (EB) effect below a temperature,TEB= 50 K and a spin glass (SG) feature emerges belowTSG= 5 K. In the current study we use magnetic, electrical transport, specific heat, and muon spin rotation (µSR) measurements to explore further the magnetic properties of a pellet made with 40 nm diameter pure Co2C NPs. We uncover the onset of Kondo localization at Kondo temperatureTK(= 40.1 K), which is close to the onset temperature (TEB) of the EB effect. A crossover from the Kondo-screened scenario to the Ruderman-Kittel-Kasuya-Yosida interaction-dominated regime is also observed forT

The Chemistry and Health Outcomes of Electronic Waste (E-Waste) Leachate: Exposure to E-Waste Is Toxic to Atlantic Killifish (Fundulus heteroclitus) Embryos.

Although there is rising global concern over the environmental, ecological, and human health risks associated with the discharge of leachates from e-waste dumpsites into the aquatic ecosystems, little is known in this research area. Thus, for this study, we first defined the chemistry of the test leachate, followed by assessment of the leachate on the development of a model aquatic organism (Fundulus heteroclitus) used extensively as a bioassay organism in pollution studies. Chemical analyses revealed that levels of phosphate (20.03 mg/L), cadmium (Cd) (0.4 mg/L), lead (Pb) (0.2 mg/L), and chromium (Cr) (0.4 mg/L) were higher than the 2009 US EPA and the 2009 National Environmental Standards and Regulations Enforcement Agency (NESREA) permissible limits. Polycyclic aromatic hydrocarbon (PAH) burdens were dominated mainly by the high molecular weight congeners, specifically the ∑4rings (73 µg/L). Total polychlorinated biphenyls (PCB) levels ranged from 0.00 to 0.40 µg/L with the ∑deca PCBs reaching the highest concentration. For the biological studies, F. heteroclitus embryos (48-h post-fertilization) were divided randomly into groups and exposed to one of six e-waste leachate concentrations (10, 1, 0.1, 0.01, 0.001, 0.0001%). Significant differences (p ≤ 0.05) between treated and control groups were observed in standard and total length, and head size. Further analysis using Duncan's post-hoc test of multiple comparison also revealed specific differences within and between specific treatment groups. We conclude that e-waste leachate arising from indiscriminate dumping into aquatic ecosystems in Nigeria contains mixtures of toxic constituents that can threaten ecosystem and public health.

Induction of NUPR1 and AP­1 contributes to the carcinogenic potential of nickel.

Nickel (Ni) is carcinogenic to humans, and causes cancers of the lung, nasal cavity, and paranasal sinuses. The primary mechanisms of Ni­mediated carcinogenesis involve the epigenetic reprogramming of cells and the ability for Ni to mimic hypoxia. However, the exact mechanisms of carcinogenesis related to Ni are obscure. Nuclear protein 1 (NUPR1) is a stress­response gene overexpressed in cancers, and is capable of conferring chemotherapeutic resistance. Likewise, activator protein 1 (AP­1) is highly responsive to environmental signals, and has been associated with cancer development. In this study, NUPR1 was found to be rapidly and highly induced in human bronchial epithelial (BEAS­2B) cells exposed to Ni, and was overexpressed in Ni­transformed BEAS­2B cells. Similarly, AP­1 subunits, JUN and FOS, were induced in BEAS­2B cells following Ni exposure. Knockdown of JUN or FOS was found to significantly suppress NUPR1 induction following Ni exposure, demonstrating their importance in NUPR1 transactivation. Reactive oxygen species (ROS) are known to induce AP­1, and Ni has been shown to produce ROS. Treatment of BEAS­2B cells with antioxidants was unable to prevent NUPR1 induction by Ni, suggesting that NUPR1 induction by Ni relies on mechanisms other than oxidative stress. To determine how NUPR1 is transcriptionally regulated following Ni exposure, the NUPR1 promoter was cloned and inserted into a luciferase gene reporter vector. Multiple JUN binding sites reside within the NUPR1 promoter, and upon deleting a JUN binding site in the upstream most region within the NUPR1 promoter using site­directed mutagenesis, NUPR1 promoter activity was significantly reduced. This suggests that AP­1 transcriptionally regulates NUPR1. Moreover, knockdown of NUPR1 significantly reduced colony formation and anchorage­independent growth in Ni­transformed BEAS­2B cells. Therefore, these results collectively demonstrate a novel mechanism of NUPR1 induction following Ni exposure, and provide a molecular basis by which NUPR1 may contribute to lung carcinogenesis.

Toxic Effects of Polychlorinated Biphenyl Congeners and Aroclors on Embryonic Growth and Development.

Polychlorinated biphenyls (PCBs) cause significant health and reproductive problems in many vertebrates. Exposure during embryogenesis likely leads to defects in organ development, compromising survival and growth through adulthood. The present study identifies the impact of PCBs on the embryonic development of key organs and resulting consequences on survival and growth. Zebrafish embryos were treated with individual PCB congeners (126 or 104) or one of 4 Aroclor mixtures (1016, 1242, 1254, or 1260) and analyzed for changes in gross embryonic morphology. Specific organs were assessed for defects during embryonic development, using a variety of transgenic zebrafish to improve organ visualization. Resulting larvae were grown to adulthood while survival and growth were assayed. Embryonic gross development on PCB treatment was abnormal, with defects presenting in a concentration-dependent manner in the liver, pancreas, heart, and blood vessel organization. Polychlorinated biphenyl 126 treatment resulted in the most consistently severe and fatal phenotypes, whereas treatments with PCB 104 and Aroclors resulted in a range of more subtle organ defects. Survival of fish was highly variable although the growth rates of surviving fish were relatively normal, suggesting that maturing PCB-treated fish that survive develop compensatory strategies needed to reach adulthood. Life span analyses of fish from embryogenesis through adulthood, as in the present study, are scarce but important for the field because they help identify foci for further studies. Environ Toxicol Chem 2021;40:187-201. © 2020 SETAC.

RUNX2/miR­31/SATB2 pathway in nickel­induced BEAS­2B cell transformation.

Nickel (Ni) compounds are classified as Group 1 carcinogens by the International Agency for Research on Cancer (IARC) and are known to be carcinogenic to the lungs. In our previous study, special AT­rich sequence­binding protein 2 (SATB2) was required for Ni­induced BEAS­2B cell transformation. In the present study, a pathway that regulates the expression of SATB2 protein was investigated in Ni­transformed BEAS­2B cells using western blotting and RT­qPCR for expression, and soft agar, migration and invasion assays for cell transformation. Runt­related transcription factor 2 (RUNX2), a master regulator of osteogenesis and an oncogene, was identified as an upstream regulator for SATB2. Ni induced RUNX2 expression and initiated BEAS­2B transformation and metastatic potential. Previously, miRNA­31 was identified as a negative regulator of SATB2 during arsenic­induced cell transformation, and in the present study it was identified as a downstream target of RUNX2 during carcinogenesis. miR­31 expression was reduced in Ni­transformed BEAS­2B cells, which was required to maintain cancer hallmarks. The expression level of miR­31 was suppressed by RUNX2 in BEAS­2B cells, and this increased the expression level of SATB2, initiating cell transformation. Ni caused the repression of miR­31 by placing repressive marks at its promoter, which in turn increased the expression level of SATB2, leading to cell transformation.

Exploring a low temperature glassy state, exchange bias effect, and high magnetic anisotropy in Co2C nanoparticles.

It is interesting to explore the connections between the exchange bias effect (EBE) and magnetic anisotropy (MA). It is often found that materials exhibiting a strong EBE also have enhanced MA. Here we explore 40 nm diameter Co2C nanoparticles (NPs) that exhibit ferromagnetism with a blocking temperature exceeding 300 K. We report the first observation of EBE in these Co2C NPs below 50 K. The effect arises from the exchange coupling of frozen ferromagnetic spins with a freely rotatable spin component. The dynamics of the freely rotatable component freezes in a temperature range between 5 K to 20 K resulting in low-temperature coexistence of a glassy behavior along with ferromagnetism. In fact, Co2C displays a unique separation of onset temperatures of spin freezing (∼20 K), vanishing of EBE (∼50 K), and magnetic blocking (⩾450 K). Our calculations show that Co2C NPs have a core-shell structure. Our study suggests that modifying chemical co-ordination in the shell is one of the effective routes to manipulating MA compared to manipulating EBE.

Arsenic Methyltransferase and Methylation of Inorganic Arsenic.

Arsenic occurs naturally in the environment, and exists predominantly as inorganic arsenite (As (III) and arsenate As (V)). Arsenic contamination of drinking water has long been recognized as a major global health concern. Arsenic exposure causes changes in skin color and lesions, and more severe health conditions such as black foot disease as well as various cancers originating in the lungs, skin, and bladder. In order to efficiently metabolize and excrete arsenic, it is methylated to monomethylarsonic and dimethylarsinic acid. One single enzyme, arsenic methyltransferase (AS3MT) is responsible for generating both metabolites. AS3MT has been purified from several mammalian and nonmammalian species, and its mRNA sequences were determined from amino acid sequences. With the advent of genome technology, mRNA sequences of AS3MT have been predicted from many species throughout the animal kingdom. Horizontal gene transfer had been postulated for this gene through phylogenetic studies, which suggests the importance of this gene in appropriately handling arsenic exposures in various organisms. An altered ability to methylate arsenic is dependent on specific single nucleotide polymorphisms (SNPs) in AS3MT. Reduced AS3MT activity resulting in poor metabolism of iAs has been shown to reduce expression of the tumor suppressor gene, p16, which is a potential pathway in arsenic carcinogenesis. Arsenic is also known to induce oxidative stress in cells. However, the presence of antioxidant response elements (AREs) in the promoter sequences of AS3MT in several species does not correlate with the ability to methylate arsenic. ARE elements are known to bind NRF2 and induce antioxidant enzymes to combat oxidative stress. NRF2 may be partly responsible for the biotransformation of iAs and the generation of methylated arsenic species via AS3MT. In this article, arsenic metabolism, excretion, and toxicity, a discussion of the AS3MT gene and its evolutionary history, and DNA methylation resulting from arsenic exposure have been reviewed.

Multimodal chemo-/magneto-/phototaxis of 3G CNT-bots to power fuel cells.

We report the development of a 3G microswimmer, namely, CNT-bot, capable of undergoing acid-, alkali-, magneto- and phototaxis inside acidic or alkaline baths of peroxide fuel and/or water. The use of carboxyl-functionalised multi-walled carbon nanotubes (MWCNTs) facilitated the propulsion of CNT-bots in an alkaline-water solution by ejecting carbon-dioxide bubbles. Furthermore, doping of magnetite nanoparticles (FeONPs), ferrous ions (Fe2+) and titanium dioxide nanoparticles (TiONPs) induces magnetic, chemical and photonic modes of propulsion. While FeONPs stimulated magnetotaxis at a rate of up to ~10 body lengths per second under the influence of a bar magnet, chemotaxis of a similar speed in a peroxide fuel was achieved by bubble-propulsion of oxygen gas originating from the Fenton reaction. In addition, the light-stimulated photo-Fenton reaction led to phototaxis of CNT-bots. A thin coating of magnesium imparted a half-faced Janus appearance to the CNT-bots, which facilitated motion in normal or acidic water media through the ejection of hydrogen gas bubbles. This chemotaxis could be transformed into pH-stimulated directional motion by establishing an acid or alkali concentration gradient across the peroxide and/or water baths. The capacity of CNT-bots to produce oxygen (hydrogen) bubbles in peroxide (acidic water) fuel was exploited to power a PEM fuel cell to generate electricity. The pure oxygen and hydrogen gases generated by CNT-bots in separate chambers were fed directly into the fuel cell in which the incessant motions of the particle facilitated the creation and release of the pure gases to achieve on-demand electricity generation. The motor could also induce dye degradation through advanced oxidation owing to the production of intermediate hydroxyl radicals during the Fenton reaction.

Growth of Carbon Dot-Decorated ZnO Nanorods on a Graphite-Coated Paper Substrate to Fabricate a Flexible and Self-Powered Schottky Diode for UV Detection.

The fabrication of flexible as well as self-powered optoelectronic devices is a growing and challenging area of research. Some scientists have reported the fabrication of either flexible or self-powered photodetectors recently. However, most of the literature studies fail to report the fabrication of self-powered as well as flexible photodetectors. This study reports the fabrication of self-powered, carbon dot (CD)-enhanced, flexible ZnO/graphite heterojunction-based UV detector where cellulose paper has been used as the substrate. A detailed study on the crystallinity and the defects of the ZnO nanorods has been done with appropriate characterizations. The CD-enhanced ZnO/graphite heterojunction showed Schottky characteristics. The Schottky parameters such as the barrier height, ideality factor, and the series resistance have also been calculated using the Cheung-Cheung method. The observed values of barrier height, ideality factor, and the series resistance are 0.74 eV, 3.74, and 503 kΩ, respectively. The transient response at self-powered condition has been demonstrated. The response time and the recovery time at self-powered condition have also been calculated with the help of the transient response, and those values are ∼2 and ∼3.2 s, respectively. The responsivity and the specific detectivity of the fabricated UV detector have been calculated as 9.57 mA/W and 4.27×108 Jones, respectively, at 330 nm wavelength, which is quite comparable with literature-reported values, considering a self-powered photodetector.

Microarray analysis of polychlorinated biphenyl mixture-induced changes in gene expression among Atlantic tomcod populations displaying differential sensitivity to halogenated aromatic hydrocarbons.

Several populations of fishes inhabiting contaminated Atlantic Coast estuaries exhibit resistance to early life-stage (ELS) toxicities induced by halogenated aromatic hydrocarbons such as coplanar polychlorinated biphenyls (PCBs). These toxicities include mortality, circulatory failure, edema, and craniofacial malformations. The mechanisms behind resistance to halogenated aromatic hydrocarbon toxicity in these populations are unknown. First and second generation Atlantic tomcod Microgadus tomcod embryos derived from the Hudson River ([HR]; New York, USA) population are highly resistant to PCB-induced cytochrome P4501A (CYP1A) expression and ELS toxicity when compared to embryos of Miramichi River ([MR]; New Brunswick, Canada) and Shinnecock Bay ([SB]; New York, USA) origin. The present study sought to identify novel genes involved in population differences in response to PCB exposure using custom microarrays. Microarray probes consisted of unsequenced inserts of randomly picked clones from a tomcod cardiac cDNA library. Tomcod embryos from three populations (HR, MR, and SB) were exposed to two doses of an environmentally relevant mixture of coplanar PCBs and screened for dose- and population-specific patterns of gene expression. Clones displaying significant differences between populations exposed to the high dose of PCBs were identified by DNA sequencing. Of the 28 identified nonribosomal protein clones, none displayed expression patterns highly similar to CYP1A (altered in MR and SB, but not in HR). However, several transcripts representing biomarkers of cardiomyopathy in mammals (cardiac troponin T2, cathepsin L, and atrial natriuretic peptide) were differentially altered among the three tomcod populations by PCBs. Although the present study did not identify any novel genes associated with PCB resistance in tomcod, several potential molecular biomarkers of PCB exposure were revealed.

Development and use of real-time reverse transcription-polymerase chain reaction assay to quantify cytochrome P4501A1 expression in American mink.

The distribution of natural populations of American mink is restricted to locales that are in proximity to aquatic ecosystems. Because of the lipophilicity and persistence of polychlorinated biphenyls (PCBs) and reliance of mink on aquatic-based diets, mink at contaminated locales often bioacccumulate high levels of PCBs. In addition, in controlled laboratory studies, mink are highly sensitive at reproductive and developmental end points to the toxic effects of environmental PCB mixtures. It is believed that most, if not all, toxic effects of PCBs occur through activation of the aryl hydrocarbon receptor (AHR) pathway. Transcription of cytochrome P4501A1 (CYP1A1) by PCBs is also mediated through activation of AHR. Thus, levels of CYP1A1 mRNA provide a quantitative assay of exposure to and early biologic effect of PCBs on mink and may be predictive of toxicity at higher levels of biologic organization. We developed polymerase chain reaction (PCR) primers to amplify CYP1A1 as well as identified a housekeeping gene from mink cDNA. We used real-time reverse transcription-PCR to quantify and compare levels of hepatic CYP1A mRNA among groups of ranched mink kits and juveniles, which were fed diets or exposed in utero to fish that were low in PCBs (Atlantic herring) or to diets that were contaminated with three different levels of PCBs (carp) from Saginaw Bay, Lake Michigan. We found significant differences in CYP1A1 mRNA expression between mink fed the control diet and those fed a PCB-contaminated carp diet at all three treatment levels and exposure times. CYP1A1 mRNA was significantly induced 5.3- to 6.6-fold and 3.7- to 4.7-fold at 6 and 27 weeks, respectively. In previous studies, dietary exposures to PCB-contaminated carp were shown to cause mild to moderate lesions in the mandible and maxilla of these animals. This study demonstrates that hepatic CYP1A1 mRNA may be a sensitive biomarker of exposure of mink to environmentally relevant levels of PCBs and may be predictive of their effects in natural populations.

Characterization of AHR2 and CYP1A expression in Atlantic sturgeon and shortnose sturgeon treated with coplanar PCBs and TCDD.

Atlantic sturgeon and shortnose sturgeon co-occur in many estuaries along the Atlantic Coast of North America. Both species are protected under the U.S. Endangered Species Act and internationally on the IUCN Red list and by CITES. Early life-stages of both sturgeons may be exposed to persistent aromatic hydrocarbon contaminants such as PCBs and PCDD/Fs which are at high levels in the sediments of impacted spawning rivers. Our objective was to compare the PCBs and TCDD sensitivities of both species with those of other fishes and to determine if environmental concentrations of these contaminants approach those that induce toxicity to their young life-stages under controlled laboratory conditions. Because our previous studies suggested that young life-stages of North American sturgeons are among the more sensitive of fishes to coplanar PCB and TCDD-induced toxicities, we were interested in identifying the molecular bases of this vulnerability. It is known that activation of the aryl hydrocarbon receptor 2 (AHR2) in fishes mediates most toxicities to these contaminants and transcriptional activation of xenobiotic metabolizing enzymes such as cytochrome P4501A (CYP1A). Previous studies demonstrated that structural and functional variations in AHRs are the bases for differing sensitivities of several vertebrate taxa to aromatic hydrocarbons. Therefore, in this study we characterized AHR2 and its expression in both sturgeons as an initial step in understanding the mechanistic bases of their sensitivities to these contaminants. We also used CYP1A expression as an endpoint to develop Toxicity Equivalency Factors (TEFs) for these sturgeons. We found that critical amino acid residues in the ligand binding domain of AHR2 in both sturgeons were identical to those of the aromatic hydrocarbon-sensitive white sturgeon, and differed from the less sensitive lake sturgeon. AHR2 expression was induced by TCDD (up to 6-fold) and by three of four tested coplanar PCB congeners (3-5-fold) in Atlantic sturgeon, but less so in shortnose sturgeon. We found that expression of AHR2 and CYP1A mRNA significantly covaried after exposure to TCDD and PCB77, PCB81, PCB126, but not PCB169 in both sturgeons. We also determined TEFs for the four coplanar PCBs in shortnose sturgeon based on comparison of CYP1A mRNA expression across all doses. Surprisingly, the TEFs for all four coplanar PCBs in shortnose sturgeon were much higher (6.4-162 times) than previously adopted for fishes by the WHO.

Characterization of AHR1 and its functional activity in Atlantic sturgeon and shortnose sturgeon.

Sturgeon species are imperiled world-wide by a variety of anthropogenic stressors including chemical contaminants. Atlantic sturgeon, Acipenser oxyrinchus, and shortnose sturgeon, Acipenser brevirostrum, are largely sympatric acipenserids whose young life-stages are often exposed to high levels of benthic-borne PCBs and PCDD/Fs in large estuaries along the Atlantic Coast of North America. In previous laboratory studies, we demonstrated that both sturgeon species are sensitive to early life-stage toxicities from exposure to environmentally relevant concentrations of coplanar PCBs and TCDD. The sensitivity of young life-stages of fishes to these contaminants varies among species by three orders of magnitude and often is due to variation in the structure and function of the aryl hydrocarbon receptor (AHR) pathway. Unlike mammals, fishes have two forms of AHR (AHR1 and AHR2) with AHR2 usually being more highly expressed across tissues and functional in mediating toxicities. Based on previous studies in white sturgeon, A. transmontanus, we hypothesized that sturgeon taxa are unusually sensitive to these contaminants because of higher levels of expression and functional activity of AHR1 than in other fish taxa. To address this possibility, we characterized AHR1 in both Atlantic Coast sturgeon species, evaluated its' in vivo expression in young life-stages and in multiple tissues of shortnose sturgeon, and tested its ability to drive reporter gene expression in AHR-deficient cells treated with graded doses of PCB126 and TCDD. Similar to white sturgeon and lake sturgeon, AHR1 amino acid sequences in Atlantic sturgeon and shortnose sturgeon were more similar to mammalian AHRs and avian AHR1s than to AHR1 in other fishes, suggesting their greater functionality in sturgeon species than in other fishes. Exposure to graded doses of coplanar PCBs and TCDD usually failed to significantly induce AHR1 expression in young life-stages or most tissues of shortnose sturgeon. However, in reporter gene assays, AHR1 drove higher levels of gene expression than AHR2 alone, but their binary combination failed to drive higher levels of expression than either AHR alone. In total, our results suggest that AHR1 may be more functional in sturgeon species than in other fishes, but probably does not explain their heightened sensitivity to these contaminants.

Evidence of natural reproduction of Atlantic sturgeon in the Connecticut River from unlikely sources.

Atlantic Sturgeon is listed under the U.S. Endangered Species Act as five Distinct Population Segments (DPS). The "endangered" New York Bight (NYB) DPS is thought to only harbor two populations; one in the Hudson River and a second smaller one in the Delaware River. Historically, the Connecticut River probably supported a spawning population of Atlantic Sturgeon that was believed extirpated many decades ago. In 2014, we successfully collected pre-migratory juvenile specimens from the lower Connecticut River which were subjected to mitochondrial DNA (mtDNA) control region sequence and microsatellite analyses to determine their genetic relatedness to other populations coastwide. Haplotype and allelic frequencies differed significantly between the Connecticut River collection and all other populations coastwide. Sibship analyses of the microsatellite data indicated that the Connecticut River collection was comprised of a small number of families that were likely the offspring of a limited number of breeders. This was supported by analysis of effective population size (Ne) and number of breeders (Nb). STRUCTURE analysis suggested that there were 11 genetic clusters among the coastwide collections and that from the Connecticut River was distinct from those in all other rivers. This was supported by UPGMA analyses of the microsatellite data. In AMOVA analyses, among region variation was maximized, and among population within regions variation minimized when the Connecticut River collection was separate from the other two populations in the NYB DPS indicating the dissimilarity between the Connecticut River collection and the other two populations in the NYB DPS. Use of mixed stock analysis indicated that the Connecticut River juvenile collection was comprised of specimens primarily of South Atlantic and Chesapeake Bay DPS origins. The most parsimonious explanation for these results is that the Connecticut River hosted successful natural reproduction in 2013 and that its offspring were descendants of a small number of colonizers from populations south of the NYB DPS, most notably the South Atlantic DPS. Our results run contrary to the belief that re-colonizers of extirpated populations primarily originate in proximal populations.

Characterization of the aryl hydrocarbon receptor repressor and a comparison of its expression in Atlantic tomcod from resistant and sensitive populations.

Atlantic tomcod from the Hudson River, USA, are resistant to cytochrome P4501A1 (CYP1A1) mRNA induction and early life stage toxicities induced by coplanar polychlorinated biphenyls (PCBs) or tetrachlorodibenzo-p-dioxins but not polycyclic aromatic hydrocarbons. We sought to determine if basal expression or inducibility of aryl hydrocarbon receptor repressor (AHRR) mRNA is higher in tomcod from the resistant Hudson River population than in those from sensitive populations. Tomcod AHRR cDNA was characterized and its expression quantified in different tissues and life stages of tomcod from the Hudson River, Miramichi River, Canada (sensitive), and among environmentally exposed tomcod from these two sources and the St. Lawrence River, Canada. Phylogenetic analysis revealed that tomcod AHRR falls within the clade of other vertebrate aryl hydrocarbon receptors (AHRs) but is most closely related to the four previously identified AHRR genes. Induction of AHRR mRNA was observed in all tissues of PCB77-treated juvenile tomcod of Miramichi River descent, and expression differed among tissues and was significantly related to levels of CYPIAI mRNA expression. Aryl hydrocarbon receptor repressor mRNA was similarly inducible in F2 embryos of Miramichi and Hudson River descent by benzo[a]pyrene but less by PCB77 in Hudson River offspring. A significant, positive correlation was observed between CYP1A1 mRNA and AHRR mRNA concentrations in environmentally exposed tomcod from the three rivers. We conclude that differences in basal expression or inducibility of AHRR mRNA are not the mechanistic basis of resistance but that levels of AHRR often mirror those of CYP1A1, suggesting that a common AHR pathway-related mechanism may modulate expression of both genes.

Biomarkers of benzene: urinary metabolites in relation to individual genotype and personal exposure.

This report is part of an extensive biomarker study conducted in a Chinese occupational population with benzene exposures ranging from 0.06 to 122 ppm (median exposure of 3.2 ppm). All urinary benzene metabolites measured in this study were significantly elevated after exposure to benzene at or above 5 ppm. Among these metabolites, however, only S-phenylmercapturic acid (S-PMA) and trans,trans-muconic acid (t,t-MA) showed a significant exposure-response trend over the exposure range from 0 to 1 ppm (for S-PMA, p<0.0001 and for t,t-MA, p=0.006). For benzene exposure monitoring, both S-PMA and t,t-MA were judged to be good and sensitive markers, which detected benzene exposure at around 0.1 and 1 ppm, respectively. Polymorphisms of the metabolic genes, including CYP2E1, quinone oxidoreductase (NQO1), GSTT1, and myeloperoxidase (MPO), were identified and did not show significant effects on the formation of metabolites, except GSTT1 on S-PMA. The production rate of S-PMA from benzene in exposed workers with GSTT1 null alleles (24.72+/-32.48 microg/g creatinine/ppm benzene) was significantly lower than that in subjects with the wild type of GSTT1 (59.84+/-47.66 microg/g creatinine/ppm benzene, p<0.0001). Further regression analysis of S-PMA production rate on GSTT1 genotype with adjustment of sex, age, benzene exposure, and cotinine levels indicated that the genotype of GSTT1 plays a critical role in determining the inter-individual variations of S-PMA formation from benzene exposure. Therefore, the individual genotype of GSTT1 needs to be identified and considered while using S-PMA as a marker to estimate the personal exposure levels of benzene in future population studies.

Genetic variants in hormone-related genes and risk of breast cancer.

Sex hormones play a key role in the development of breast cancer. Certain polymorphic variants (SNPs and repeat polymorphisms) in hormone-related genes are associated with sex hormone levels. However, the relationship observed between these genetic variants and breast cancer risk has been inconsistent. We conducted a case-control study nested within two prospective cohorts to assess the relationship between specific genetic variants in hormone-related genes and breast cancer risk. In total, 1164 cases and 2111 individually-matched controls were included in the study. We did not observe an association between potential functional genetic polymorphisms in the estrogen pathway, SHBG rs6259, ESR1 rs2234693, CYP19 rs10046 and rs4775936, and UGT1A1 rs8175347, or the progesterone pathway, PGR rs1042838, with the risk of breast cancer. Our results suggest that these genetic variants do not have a strong effect on breast cancer risk.