Multiomics Analysis of PCB126's Effect on a Mouse Chronic-Binge Alcohol Feeding Model.

BACKGROUND: Environmental pollutants, including polychlorinated biphenyls (PCBs) have been implicated in the pathogenesis of liver disease. Our group recently demonstrated that PCB126 promoted steatosis, hepatomegaly, and modulated intermediary metabolism in a rodent model of alcohol-associated liver disease (ALD). OBJECTIVE: To better understand how PCB126 promoted ALD in our previous model, the current study adopts multiple omics approaches to elucidate potential mechanistic hypotheses. METHODS: Briefly, male C57BL/6J mice were exposed to 0.2mg/kg polychlorinated biphenyl (PCB) 126 or corn oil vehicle prior to ethanol (EtOH) or control diet feeding in the chronic-binge alcohol feeding model. Liver tissues were collected and prepared for mRNA sequencing, phosphoproteomics, and inductively coupled plasma mass spectrometry for metals quantification. RESULTS: Principal component analysis showed that PCB126 uniquely modified the transcriptome in EtOH-fed mice. EtOH feeding alone resulted in >4,000 differentially expressed genes (DEGs), and PCB126 exposure resulted in more DEGs in the EtOH-fed group (907 DEGs) in comparison with the pair-fed group (503 DEGs). Top 20 significant gene ontology (GO) biological processes included "peptidyl tyrosine modifications," whereas top 25 significantly decreasing GO molecular functions included "metal/ion/zinc binding." Quantitative, label-free phosphoproteomics and western blot analysis revealed no major significant PCB126 effects on total phosphorylated tyrosine residues in EtOH-fed mice. Quantified hepatic essential metal levels were primarily significantly lower in EtOH-fed mice. PCB126-exposed mice had significantly lower magnesium, cobalt, and zinc levels in EtOH-fed mice. DISCUSSION: Previous work has demonstrated that PCB126 is a modifying factor in metabolic dysfunction-associated steatotic liver disease (MASLD), and our current work suggests that pollutants also modify ALD. PCB126 may, in part, be contributing to the malnutrition aspect of ALD, where metal deficiency is known to contribute and worsen prognosis. https://doi.org/10.1289/EHP14132.

Modeled Pathways and Fluxes of PCB Dechlorination by Redox Potentials.

Dechlorination is one of the main processes for the natural degradation of polychlorinated biphenyls (PCBs) in an anaerobic environment. However, PCB dechlorination pathways and products vary with PCB congeners, types of functional dechlorinating bacteria, and environmental conditions. The present study develops a novel model for determining dechlorination pathways and fluxes by tracking redox potential variability, transforming the complex dechlorination process into a stepwise sequence. The redox potential is calculated via the Gibbs free energy of formation, PCB concentrations in reactants and products, and environmental conditions. Thus, the continuous change in the PCB congener composition can be tracked during dechlorination processes. The new model is assessed against four measurements from several published studies on PCB dechlorination. The simulation errors in all four measurements are calculated between 2.67 and 35.1% under minimum (n = 0) and maximum (n = 34) numbers of co-eluters, respectively. The dechlorination fluxes for para-dechlorination pathways dominate PCB dechlorination in all measurements. Furthermore, the model also considers multiple-step dechlorination pathways containing intermediate PCB congeners absent in both the reactants and the products. The present study indicates that redox potential might be an appropriate indicator for predicting PCB dechlorination pathways and fluxes even without prior knowledge of the functional dechlorinating bacteria.

Distribution of 2,2',5,5'-Tetrachlorobiphenyl (PCB52) Metabolites in Adolescent Rats after Acute Nose-Only Inhalation Exposure.

Inhalation of PCB-contaminated air is increasingly recognized as a route for PCB exposure. Because limited information about the disposition of PCBs following inhalation exposure is available, this study investigated the disposition of 2,2',5,5'-tetrachlorobiphenyl (PCB52) and its metabolites in rats following acute, nose-only inhalation of PCB52. Male and female Sprague-Dawley rats (50-58 days of age, 210 ± 27 g; n = 6) were exposed for 4 h by inhalation to approximately 14 or 23 µg/kg body weight of PCB52 using a nose-only exposure system. Sham animals (n = 6) were exposed to filtered lab air. Based on gas chromatography-tandem mass spectrometry (GC-MS/MS), PCB52 was present in adipose, brain, intestinal content, lung, liver, and serum. 2,2',5,5'-Tetrachlorobiphenyl-4-ol (4-OH-PCB52) and one unknown monohydroxylated metabolite were detected in these compartments except for the brain. Liquid chromatography-high resolution mass spectrometry (LC-HRMS) analysis identified several metabolites, including sulfated, methoxylated, and dechlorinated PCB52 metabolites. These metabolites were primarily found in the liver (7 metabolites), lung (9 metabolites), and serum (9 metabolites) due to the short exposure time. These results demonstrate for the first time that complex mixtures of sulfated, methoxylated, and dechlorinated PCB52 metabolites are formed in adolescent rats following PCB52 inhalation, laying the groundwork for future animal studies of the adverse effects of inhaled PCB52.

Black Carbon Impacts on Paraburkholderia xenovorans Strain LB400 Cell Enrichment and Activity: Implications toward Lower-Chlorinated Polychlorinated Biphenyls Biodegradation Potential.

Volatilization of lower-chlorinated polychlorinated biphenyls (LC-PCBs) from sediment poses health threats to nearby communities and ecosystems. Biodegradation combined with black carbon (BC) materials is an emerging bioaugmentation approach to remove PCBs from sediment, but development of aerobic biofilms on BC for long-term, sustained LC-PCBs remediation is poorly understood. This work aimed to characterize the cell enrichment and activity of biphenyl- and benzoate-grown Paraburkholderia xenovorans strain LB400 on various BCs. Biphenyl dioxygenase gene (bphA) abundance on four BC types demonstrated corn kernel biochar hosted at least 4 orders of magnitude more attached cells per gram than other feedstocks, and microscopic imaging revealed the attached live cell fraction was >1.5× more on corn kernel biochar than GAC. BC characteristics (i.e., sorption potential, pore size, pH) appear to contribute to cell attachment differences. Reverse transcription qPCR indicated that BC feedstocks significantly influenced bphA expression in attached cells. The bphA transcript-per-gene ratio of attached cells was >10-fold more than suspended cells, confirmed by transcriptomics. RNA-seq also demonstrated significant upregulation of biphenyl and benzoate degradation pathways on attached cells, as well as revealing biofilm formation potential/cell-cell communication pathways. These novel findings demonstrate aerobic PCB-degrading cell abundance and activity could be tuned by adjusting BC feedstocks/attributes to improve LC-PCBs biodegradation potential.

Efficient biostimulation of microbial dechlorination of polychlorinated biphenyls by acetate and lactate under nitrate reducing conditions: Insights into dechlorination pathways and functional genes.

Microbial-catalyzed reductive dechlorination of polychlorinated biphenyls (PCBs) is largely affected by the indigenous sediment geochemical properties. In this study, the effects of nitrate on PCB dechlorination and microbial community structures were first investigated in Taihu Lake sediment microcosms. And biostimulation study was attempted supplementing acetate/lactate. PCB dechlorination was apparently inhibited under nitrate-reducing conditions. Lower PCB dechlorination rate and less PCB dechlorination extent were observed in nitrate amended sediment microcosms (T-N) than those in non-nitrate amended microcosms (T-1) during 66 weeks of incubation. The total PCB mass reduction in T-N was 17.6% lower than that in T-1. The flanked-para dechlorination was completely inhibited, while the ortho-flanked meta dechlorination was only partially inhibited in T-N. The 7.5 mM of acetate/lactate supplementation recovered PCB dechlorination by resuming ortho-flanked meta dechlorination. Repeated additions of lactate showed more effective biostimulation than acetate. Phylum Chloroflexi, containing most known PCB dechlorinators, was found to play a vital role on stability of the network structures. In T-N, putative dechlorinating Chloroflexi, Dehalococcoides and RDase genes rdh12, pcbA4, pcbA5 all declined. With acetate/lactate supplementation, Dehalococcoides grew by 1-2 orders of magnitude and rdh12, pcbA4, pcbA5 increased by 1-3 orders of magnitude. At Week 66, parent PCBs declined by 86.4% and 80.9% respectively in T-N-LA and T-N-AC compared to 69.9% in T-N. These findings provide insights into acetate/lactate biostimulation as a cost-effective approach for treating PCB contaminated sediments undergoing nitrate inhibition.

Comprehensive exploration of the anaerobic biotransformation of polychlorinated biphenyls in Dehalococcoides mccartyi CG1: Kinetics, enantioselectivity, and isotope fractionation.

Anaerobic microbial transformation is a key pathway in the natural attenuation of polychlorinated biphenyls (PCBs). Much less is known about the transformation behaviors induced by pure organohalide-respiring bacteria, especially kinetic isotope effects. Therefore, the kinetics, pathways, enantioselectivity, and carbon and chlorine isotope fractionation of PCBs transformation by Dehalococcoides mccartyi CG1 were comprehensively explored. The results indicated that the PCBs were mainly dechlorinated via removing their double-flanked meta-chlorine, with their first-order kinetic constants following the order of PCB132 > PCB174 > PCB85 > PCB183 > PCB138. However, PCBs occurred great loss of stoichiometric mass balance during microbial transformation, suggesting the generation of other non-dehalogenation products and/or stable intermediates. The preferential transformation of (-)-atropisomers and generation of (+)-atropisomers were observed during PCB132 and PCB174 biotransformation with the enantiomeric enrichment factors of -0.8609 ± 0.1077 and -0.4503 ± 0.1334 (first half incubation times)/-0.1888 ± 0.1354 (second half incubation times), respectively, whereas no enantioselectivity occurred during PCB183 biotransformation. More importantly, although there was no carbon and chlorine isotope fractionation occurring for studied substrates, the δ13C values of dechlorination products, including PCB47 (-28.15 ± 0.35‰ âˆ¼ -27.77 ± 0.20‰), PCB91 (-36.36 ± 0.09‰ âˆ¼ -34.71 ± 0.49‰), and PCB149 (-28.08 ± 0.26‰ âˆ¼ -26.83 ± 0.10‰), were all significantly different from those of their corresponding substrates (PCB85: -30.81 ± 0.02‰ âˆ¼ -30.22 ± 0.21‰, PCB132: -33.57 ± 0.15‰ âˆ¼ -33.13 ± 0.14‰, and PCB174: -26.30 ± 0.09‰ âˆ¼ -26.01 ± 0.07‰), which further supported the generation of other non-dehalogenation products and/or stable intermediates with enrichment or depletion of 13C. These findings provide deeper insights into the anaerobic microbial transformation behaviors of PCBs.

Complex roles for sulfation in the toxicities of polychlorinated biphenyls.

Polychlorinated biphenyls (PCBs) are persistent organic toxicants derived from legacy pollution sources and their formation as inadvertent byproducts of some current manufacturing processes. Metabolism of PCBs is often a critical component in their toxicity, and relevant metabolic pathways usually include their initial oxidation to form hydroxylated polychlorinated biphenyls (OH-PCBs). Subsequent sulfation of OH-PCBs was originally thought to be primarily a means of detoxication; however, there is strong evidence that it may also contribute to toxicities associated with PCBs and OH-PCBs. These contributions include either the direct interaction of PCB sulfates with receptors or their serving as a localized precursor for OH-PCBs. The formation of PCB sulfates is catalyzed by cytosolic sulfotransferases, and, when transported into the serum, these metabolites may be retained, taken up by other tissues, and subjected to hydrolysis catalyzed by intracellular sulfatase(s) to regenerate OH-PCBs. Dynamic cycling between PCB sulfates and OH-PCBs may lead to further metabolic activation of the resulting OH-PCBs. Ultimate toxic endpoints of such processes may include endocrine disruption, neurotoxicities, and many others that are associated with exposures to PCBs and OH-PCBs. This review highlights the current understanding of the complex roles that PCB sulfates can have in the toxicities of PCBs and OH-PCBs and research on the varied mechanisms that control these roles.

Immunotoxicity of microplastics and polychlorinated biphenyls alone or in combination to Crassostrea gigas.

Microplastics (MPs) and polychlorinated biphenyls (PCBs) are pervasive pollutants in the marine environment, exerting adverse effects on marine organisms. While it is suggested that their exposure may compromise the immune responses of marine organisms, the cumulative immunotoxic effects remain uncertain. Additionally, the intricate mechanisms underlying the immunotoxicity of PCBs and MPs in marine organisms are not yet fully comprehended. To illuminate their combined biological impacts, Crassostrea gigas were exposed to 50 µg/L MPs (30-µm porous) alone, as well as 10 or 100 ng/L PCBs individually or in combination with 50 µg/L of MPs for 28 days. Our data demonstrated that oysters treated with the pollutants examined led to decreased total haemocyte count, inhibited phagocytosis of haemocytes, enhanced the intracellular contents of reactive oxygen species, lipid peroxidation and DNA damage, reduced lysozyme concentration and activity, gave rise to superoxide dismutase. Catalaseand glutathione S-transferaseactivity. The expression of three immune-related genes (NF-κB, TNF-α, TLR-6) was drastically suppressed by the PCBs and MPs treatment, while the apoptosis pathway-related genes (BAX and Caspase-3) showed a significant increase. In addition, compared to oysters treated with a single type of pollutant, coexposure to MPs and PCBs exerted more severe adverse impacts on all the parameters investigated, indicating a significant synergistic effect. Therefore, the risk of MPs and PCBs chemicals on marine organisms should be paid more attention.

Under explored roles of microbial ligninolytic enzymes in aerobic polychlorinated biphenyl transformation.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants in the environment that are responsible for many adverse health effects. Bioremediation appears to be a healthy and cost-effective alternative for remediating PCB-contaminated environments. While some microbial species have been observed to be capable of transforming PCBs, only two different microbial pathways (rdh and bph pathways) have been described to be involved in PCB transformations. Ligninolytic enzymes have been observed or are under suspicion in some microbial PCB transformations. However, the role of these promising PCB-transforming enzymes, which are produced by fungi and some aerobic bacteria, is still unclear. The present review describes their role by identifying microbial PCB-transforming species and their reported ligninolytic enzymes whether proven or suspected to be involved in PCB transformations. There are several lines of evidence that ligninolytic enzymes are responsible for PCB transformations such as (1) the ability of purified laccases from Myceliophthora thermophila, Pycnoporus cinnabarinus, Trametes versicolor, Cladosporium sp, and Coprinus cumatus to transform hydroxy-PCBs; (2) the increased production of laccases and peroxidases by many fungi in the presence of PCBs; and (3) the enhanced PCB transformation by Pseudomonas stutzeri and Sinorhizobium meliloti NM after the addition of ligninolytic enzyme enhancers. However, if the involvement of ligninolytic enzymes in PCB transformation is clearly demonstrated in some fungal species, it does not seem to be implicated in all microbial species suggesting other still unknown metabolic pathways involved in PCB transformation and different from the bph and rdh pathways. Therefore, PCB transformation may involve several metabolic pathways, some involving ligninolytic enzymes, bph or rdh genes, and some still unknown, depending on the microbial species. In addition, current knowledge does not fully clarify the role of ligninolytic enzymes in PCB oxidation and dechlorination. Therefore, further studies focusing on purified ligninolytic enzymes are needed to clearly elucidate their role in PCB transformation.

Two novel glutathione S-transferase (GST) genes in the toxic marine dinoflagellate Alexandrium pacificum and their transcriptional responses to environmental contaminants.

The present study identified two novel glutathione S-transferase (GST) genes from the toxic dinoflagellate Alexandrium pacificum and examined their molecular characteristics and transcriptional responses to algicides and environmental contaminants. Bioinformatic analysis revealed that both ApGSTs are cytosolic, belonging to the chi-like class (ApGST1) and an undefined class (ApGST2). The overall expression of ApGSTs showed similar patterns depending on the exposed contaminants, while they were differently regulated by polychlorinated biphenyl (PCB). Copper treatments (CuCl2 and CuSO4) did not significantly induce the expression of ApGSTs. The highest up-regulations of ApGST1 and ApGST2 were under 6-h treatments of 0.10 and 0.50 mg L-1 NaOCl. Interestingly, only ApGST1 increased significantly after 0.10, 0.50, and 1.00 mg L-1 of PCB exposure (6 h). Intracellular reactive oxygen species (ROS) increased considerably under NaOCl; however, it was not significantly higher in the PCB-treated cells. GST activity was increased by NaOCl and PCB treatments, but only PCB caused apoptosis. These results suggest that GSTs are involved in the first line of phase II detoxification, protecting dinoflagellate cells against oxidative damage.

Insight into the mechanism of melatonin in attenuating PCB126-induced liver injury: Resistance to ROS-dependent NETs formation to alleviate inflammation and lipid metabolism dysfunction.

3,3',4',4',5-Polychlorinated biphenyls (PCB126) is classified as a persistent organic environmental pollutant that can cause liver damage by producing excessive reactive oxygen species (ROS). ROS also can stimulate neutrophil extracellular traps (NETs) formation, which cause damage to organism if NETs are produced in excess. Melatonin is generally considered to possess strong antioxidant and anti-inflammation prosperities, but it is unclear whether it can alleviate PCB126-induced injury. To explore whether PCB126-induced liver injury is related to the formation of NETs and whether melatonin has a potent protective effect, we established PCB126 exposure/ PCB126 and melatonin co-treatment mouse models by gavage. To further clarify the specific mechanism, we also cultured neutrophils and AML12 cells to replicate in vivo model. Here, we found PCB126 exposure resulted in an elevation in the activities of MDA, LPO, PCO, and 8-OHdG, and a reduction in the activities of CAT, GSH-PX and SOD. We found that PCB126 exposure led to an elevation in the expression levels of chemokines (CCL2, CCL3, CCL4, CXCL12, and CXCL8) and marker factors for NETs formation (MPO, NE, NOX2, PKCα, and PKCζ) in the PCB126 group. IF, SYTOX staining, and SEM results also revealed that PCB126 could stimulate NETs formation. In addition, results of a co-culture system of PBNs and AML12 cells revealed that the expression levels of inflammatory cytokines (IL-1ß, IL-6, and TNF-α) significantly decreased and the expression levels of metabolism factors (Fas, Acc, and Srebp) slightly decreased for scavenging NETs, indicating NETs formation aggravated PCB126-induced hepatic damages. Noteworthy, treatment with melatonin reversed these results. In summary, our findings revealed that melatonin alleviated hepatic damage aggravated by PCB126-induced ROS-dependent NETs formation through suppressing excessive ROS production. This finding not only enriches toxicological mechanism of PCB126, but more importantly extends biological effects of melatonin and its potential application values.

Three distinct metabolic phases of polychlorinated biphenyls/biphenyl degrader Acidovorax sp. KKS102 in nutrient broth.

Acidovorax sp. KKS102 is a beta-proteobacterium capable of degrading polychlorinated biphenyls (PCBs). In this study, we examined its growth in liquid nutrient broth supplemented with different carbon sources. KKS102 had at least 3 distinct metabolic phases designated as metabolic phases 1-3, with phase 2 having 2 sub-phases. For example, succinate, fumarate, and glutamate, known to repress the PCB/biphenyl catabolic operon in KKS102, were utilized in phase 1, while acetate, arabinose, and glycerol in phase 2, and glucose and mannose in phase 3. We also showed that the BphQ response regulator mediating catabolite control in KKS102, whose expression level increased moderately through the growth, plays important roles in carbon metabolism in phases 2 and 3. Our study elucidates the hierarchical growth of KKS102 in nutrient-rich media. This insight is crucial for studies exploiting microbial biodegradation capabilities and advancing studies for catabolite regulation mechanisms.

Metabolic Synergy of Dehalococcoides Populations Leading to Greater Reductive Dechlorination of Polychlorinated Biphenyls.

Polychlorinated biphenyls (PCBs) are dioxin-like pollutants that cause persistent harm to life. Organohalide-respiring bacteria (OHRB) can detoxify PCBs via reductive dechlorination, but individual OHRB are potent in dechlorinating only specific PCB congeners, restricting the extent of PCB dechlorination. Moreover, the low biomass of OHRB frequently leads to the slow natural attenuation of PCBs at contaminated sites. Here we constructed defined microbial consortia comprising various combinations of PCB-dechlorinating Dehalococcoides strains (CG1, CG4, and CG5) to successfully enhance PCB dechlorination. Specifically, the defined consortia consisting of strains CG1 and CG4 removed 0.28-0.44 and 0.23-0.25 more chlorine per PCB from Aroclor1260 and Aroclor1254, respectively, compared to individual strains, which was attributed to the emergence of new PCB dechlorination pathways in defined consortia. Notably, different Dehalococcoides populations exhibited similar growth when cocultivated, but temporal differences in the expression of PCB reductive dehalogenase genes indicated their metabolic synergy. Bioaugmentation with individual strains (CG1, CG4, and CG5) or defined consortia led to greater PCB dechlorination in wetland sediments, and augmentation with the consortium comprising strains CG1 and CG4 resulted in the greatest PCB dechlorination. These findings collectively suggest that simultaneous application of multiple Dehalococcoides strains, which catalyze complementary dechlorination pathways, is an effective strategy to accelerate PCB dechlorination.

Unveiling the PCB biodegradation potential and stress survival strategies of resuscitated strain Pseudomonas sp. HR1.

The exploration of resuscitated strains, facilitated by the resuscitation promoting factor (Rpf), has substantially expanded the pool of cultivated degraders, enhancing the screening of bio-inoculants for bioremediation applications. However, it remains unknown whether these resuscitated strains can re-enter the viable but non-culturable (VBNC) state and the specific stress conditions that trigger such a transition. In this work, the whole genome, and polychlorinated biphenyl (PCB)-degrading capabilities of a resuscitated strain HR1, were investigated. Notably, the focus of this exploration was on elucidating whether HR1 would undergo a transition into the VBNC state when exposed to low temperature and PCBs, with and without the presence of heavy metals (HMs). The results suggested that the resuscitated strain Pseudomonas sp. HR1 harbored various functional genes related to xenobiotic biodegradation, demonstrating remarkable efficiency in Aroclor 1242 degradation and strong resistance against stress induced by low temperature and PCBs. Nevertheless, when exposed to the combined stress of low temperature, PCBs, and HMs, HR1 underwent a transition into the VBNC state. This transition was characterized by significant decreases in enzyme activities and notable changes in both morphological and physiological traits when compared to normal cells. Gene expression analysis revealed molecular shifts underlying the VBNC state, with down-regulated genes showed differential expression across multiple pathways and functions, including oxidative phosphorylation, glycolysis, tricarboxylic acid cycle, amino acid metabolism, translation and cytoplasm, while up-regulated genes predominantly associated with transcription regulation, membrane function, quorum sensing, and transporter activity. These findings highlighted the great potential of resuscitated strains as bio-inoculants in bioaugmentation and shed light on the survival mechanisms of functional strains under stressful conditions, which should be carefully considered during bioremediation processes.

Transformation of hydroxylated polychlorinated biphenyls by bacterial 2-hydroxybiphenyl 3-monooxygenase.

Monohydroxylated PCBs (OH-PCBs) are an (eco)toxicologically significant group of compounds, as they arise from the oxidation of polychlorinated biphenyls (PCBs) and, at the same time, may exert even more severe toxic effects than their parent PCB molecules. Despite having been widely detected in environmental samples, plants, and animals, information on the fate of OH-PCBs in the environment is scarce, including on the enzymatic machinery behind their degradation. To date, only a few bacterial taxa capable of OH-PCB transformation have been reported. In this study, we aimed to obtain a deeper insight into the transformation of OH-PCBs in soil bacteria and isolated a Pseudomonas sp. strain P1B16 based on its ability to use o-phenylphenol (2-PP) which, when exposed to the Delor 103-derived OH-PCB mixture, depleted a wide spectrum of mono-, di, and trichlorinated OH-PCBs. In the P1B16 genome, a region designated as hbp was identified, which bears a set of putative genes involved in the transformation of OH-PCBs, namely hbpA encoding for a putative flavin-dependent 2-hydroxybiphenyl monooxygenase, hbpC (2,3-dihydroxybiphenyl-1,2-dioxygenase), hbpD (2-hydroxy-6-oxo-6-phenylhexa-2,4-dienoate hydrolase), and the transcriptional activator-encoding gene hbpR. The hbpA coding sequence was heterologously expressed, purified, and its substrate specificity was investigated towards the Delor 103-derived OH-PCB mixture, individual OH-PCBs, and multiple (chlorinated) phenolics. Apart from 2-PP and 2-chlorophenol, HbpA was also demonstrated to transform a range of OH-PCBs, including a 3-hydroxy-2,2',4',5,5'-pentachlorobiphenyl. Importantly, this is the first direct evidence of HbpA homologs being involved in the degradation of OH-PCBs. Moreover, using a P1B16-based biosensor strain, the specific induction of hbp genes by 2-PP, 3-phenylphenol, 4-phenylphenol, and the OH-PCB mixture was demonstrated. This study provides direct evidence on the specific enzymatic machinery responsible for the transformation of OH-PCBs in bacteria, with many implications in ecotoxicology, environmental restoration, and microbial ecology in habitats burdened with PCB contamination.

Dietary Exposure to Environmentally Relevant Levels of Chemical Contaminants Reduces Growth and Survival in Juvenile Chinook Salmon.

Chemical pollution can degrade aquatic ecosystems. Chinook salmon in contaminated habitats are vulnerable to health impacts from toxic exposures. Few studies have been conducted on adverse health outcomes associated with current levels and mixtures of contaminants. Fewer still address effects specific to the juvenile life-stage of salmonids. The present study evaluated contaminant-related effects from dietary exposure to environmentally relevant concentrations and mixture profiles in juvenile Chinook salmon from industrialized waterways in the U.S. Pacific Northwest using two end points: growth assessment and disease susceptibility. The dose and chemical proportions were reconstituted based on environmental sampling and analysis using the stomach contents of juvenile Chinook salmon recently collected from contaminated, industrialized waterways. Groups of fish were fed a mixture with fixed proportions of 10 polychlorinated biphenyls (PCBs), 3 dichlorodiphenyltrichloroethanes (DDTs), and 13 polycyclic aromatic hydrocarbons (PAHs) at five concentrations for 35 days. These contaminant compounds were selected because of elevated concentrations and the widespread presence in sediments throughout industrialized waterways. Fork length and otolith microstructural growth indicators were significantly reduced in fish fed environmentally relevant concentrations of these contaminants. In addition, contaminant-exposed Chinook salmon were more susceptible to disease during controlled challenges with the pathogen Aeromonas salmonicida. Our results indicate that dietary exposure to contaminants impairs growth and immune function in juvenile Chinook salmon, thereby highlighting that current environmental exposure to chemicals of potential management concern threatens the viability of exposed salmon.

Varying temporal trends in the levels of six groups of legacy persistent organic pollutants (POPs) in liver of three gadoid species from the North Sea.

From 2005 to 2019, three gadoid species, Atlantic cod (Gadus morhua), haddock (Melanogrammus aeglefinus) and saithe (Pollachius virens), were sampled approximately every third year in the northeastern part of the North Sea. Liver samples were analyzed to investigate levels and temporal trends of six groups of persistent organic pollutants (POPs): polychlorinated biphenyls (PCBs), dichlorodiphenyltrichloroethane (DDT) and its degradation products, hexachlorocyclohexanes (HCHs), hexachlorobenzene (HCB), trans-nonachlor (TNC), and polybrominated diphenyl ethers (PBDEs). Some of the highest average concentrations were found in cod, the levels otherwise being similar between the three species and mostly below established threshold values. The levels of all the contaminants except HCB and TNC were higher than previously reported for cod and haddock in the Barents Sea. Significantly decreasing levels were found for Σ7PCBs, ΣDDTs, ΣHCHs and Σ15PBDEs in all three species, and for TNC in haddock and saithe, while there was no significant trend for TNC in cod. HCB levels increased significantly in cod and haddock and showed only a minor decrease in saithe. The observed time trends of legacy POPs demonstrate the persistence of some of the studied pollutants despite efforts to eliminate them from the marine environment.

New insights into survival strategies and PCB bioremediation potential of resuscitated strain Achromobacter sp. HR2 under combined stress conditions.

The resuscitated strains achieved through the addition of resuscitation promoting factor (Rpf) hold significant promise as bio-inoculants for enhancing the bioremediation of polychlorinated biphenyls (PCBs). Nevertheless, the potential of these resuscitated strains to transition into a viable but non-culturable (VBNC) state, along with the specific stressors that initiate this transformation, remains to be comprehensively elucidated. In this study, a resuscitated strain HR2, obtained through Rpf amendment, was employed to investigate its survival strategies under combined stress involving low temperature (LT), and PCBs, in the absence and presence of heavy metals (HMs). Whole-genome analysis demonstrated that HR2, affiliated with Achromobacter, possessed 107 genes associated with the degradation of polycyclic aromatic compounds. Remarkably, HR2 exhibited effective degradation of Aroclor 1242 and robust resistance to stress induced by LT and PCBs, while maintaining its culturability. However, when exposed to the combined stress of LT, PCBs, and HMs, HR2 entered the VBNC state. This state was characterized by significant decreases in enzyme activities and notable morphological, physiological, and molecular alterations compared to normal cells. These findings uncovered the survival status of resuscitated strains under stressful conditions, thereby offering valuable insights for the development of effective bioremediation strategies.

Strategy for Remediation of Polychlorinated Biphenyls-Contaminated Soil Through Redox Management Based on Electronegativity of the Contaminants.

Literature review reveals that Persistent Organic Pollutants (POPs), such as polychlorinated biphenyls (PCBs), are electron deficient compounds due to the presence of highly electronegative groups. Hence, they are more amenable to anaerobic biodegradation rather than oxidative metabolism. However, the studies on PCBs bioremediation are more inclined towards aerobic treatment. Besides, the past studies are mainly centered on screening and application of PCB-degrading microorganisms. In our opinion the degradative capacity is already present in the native microflora, and choice of electron donor is of paramount importance for faster reductive metabolism of PCBs. In this study, the use of methanol as electron donor with cow dung as the general microbial inoculum resulted in high specific rate of degradation (0.0542-0.0637 /day) for high-chlorinated biphenyls. The % removal of PCBs ranged between 67.7 and 71.7%. It may be the first study on the application of methanol as a cheap electron donor for PCBs biodegradation without bioaugmentation with specifically selected microorganisms.

Identification of Species-Specific Prey Uptake and Biotransformation of Chiral Polychlorinated Biphenyls (PCBs) in Riparian and Aquatic Food Webs.

The atropisomeric enrichment of chiral polychlorinated biphenyls (PCBs) can trace the movement of PCBs through food webs, but it is a challenge to elucidate the prey uptake and stereoselective biotransformation of PCBs in different species. The present study investigated the concentrations and enantiomer fractions (EFs) of chiral PCBs in invertebrates, fishes, amphibians, and birds. Chiral PCB signature was estimated in total prey for different predators based on quantitative prey sources. The nonracemic PCBs in snakehead (Ophiocephalus argus) were mainly from prey. EFs of PCBs in amphibians and birds were mainly influenced by biotransformation, which showed enrichment of (+)-CBs 132 and 135/144 and different enantiomers of CBs 95 and 139/149. Biomagnification factors (BMFs) of chiral PCBs were higher than 1 for amphibians and passerine birds and lower than 1 for kingfisher (Alcedo atthis) and snakehead. BMFs were significantly correlated with EFs of chiral PCBs in predators and indicative of atropisomeric enrichment of PCBs across different species. Trophic magnification factors (TMFs) were higher in the riparian food web than in the aquatic food web because of the high metabolism capacity of chiral PCBs in aquatic predators. The results highlight the influences of species-specific prey sources and biotransformation on the trophic dynamics of chiral PCBs.