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Copyright of Kocatepe Veterinary Journal / Kocatepe Veteriner Dergisi is the property of Afyon Kocatepe University, Faculty of Veterinary Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Faculty of Pharmacy of Ankara University / Ankara Üniversitesi Eczacilik Fakültesi Dergisi is the property of Ankara University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The polychlorinated biphenyls (PCBs) in aquatic environment adversely affect non-target organisms, including fish. Especially, the male reproduction and next generation can be damaged through high exposure to these pollutants. Hence, the sperm cells were exposed to sublethal concentrations of Aroclor 1254 (0, 1, 5, 10, or 25 mg/l) for 4 h. The sperm quality parameters were analyzed by SCA (Sperm Class Analyzer). The fertility, eyeing, and hatching rates were determined as gamete markers. Lipid peroxidation (malondialdehyde-MDA), glutathione (GSH), and antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT)] were measured for determination of oxidative stress. Our results showed that Aroclor 1254 negatively affected the motility rate and duration, fertilization rate, embryogenesis, and hatching and also triggered antioxidant defense mechanisms at the highest concentration (25 mg L−1). Furthermore, linear speed (VSL), linearity index (LIN), and amplitude lateral head (ALH) were significantly changed after exposure to 25 mg L−1, and the lowest concentrations (1 and 10 mg L−1) did not significantly affect the motility and fertilizing capacity. The embryogenesis and hatching were significantly affected by sperm exposure to 1, 10, and 25 mg L−1 of Aroclor 1254. Consequently, Aroclor 1254 causes potential hazards in male germ cells, and the exposure of sperm cells to pollutants can adversely affect next generation of wild populations. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the osteotoxicity of polychlorinated biphenyls in murine osteoblastic MC3T3-E1 cells, and to explore the underlying mechanism focused on oxidative stress. The cells were exposed to Aroclor 1254 at concentrations of 2.5-20 µmol/L, and then cell viability, oxidative stress, intracellular calcium concentration, osteocalcin content, and calcium nodules formation were measured. Aroclor 1254 reduced cell viability and induced overproduction of intracellular reactive oxygen species in a dosedependent manner. Activity of superoxide dismutase was decreased, and malondialdehyde content was promoted after exposure. Moreover, inhibitory effects of Aroclor 1254 on calcium metabolism and mineralization of osteoblasts were observed, as indicated by reduction of the intracellular calcium concentration, osteocalcin content, and modules formation rate. The decreased expression of osteocalcin, alkaline phosphatase, bone sialoprotein, and transient receptor potential vanilloid 6 further confirmed the impairment of Aroclor 1254 on calcium homeostasis and osteoblast differentiation. Addition of the antioxidant N-acetyl-L-cysteine partially restored the inhibitory effects on calcium metabolism and mineralization. In general, Aroclor 1254 exposure reduces calcium homeostasis, osteoblast differentiation and bone formation, and oxidative stress plays a vital role in the underlying molecular mechanism of osteotoxicity. [ABSTRACT FROM AUTHOR]

The present study was designed to establish the epigenetic mechanisms by which lactational exposure to PCBs affects the Leydig cell function in progeny rats. The lactating dams were oral gavaged with different doses of PCBs [1, 2 and 5 mg/kg or corn oil ] and Leydig cells were isolated from the testes of progeny rats at postnatal day (PND) 60. We assessed the expression of transcription factors regulating steroidogenic machinery and the promoter methylation of LHR and AR in the Leydig cells. Our results confirmed hypermethylation of SF‐1, Sp1/3, LHR and AR genes. There was a significant reduction in the gene expression of SF‐1 and Sp1. The mRNA expression of Sp3 was decreased. Interestingly, there was an increased gene expression levels of DNA methyltransferases (Dnmts) (Dnmt1, Dnmt3a/b and Dnmt3l) and unaltered histone deacetylase‐1 (Hdac‐1). Furthermore, increased percentage of 5‐methylcytosine was observed in PCBs exposed Leydig cells. Taken together, our findings suggest that promoter hypermethylation of SF‐1, Sp1/3, LHR and AR could have led to transcriptional repression of these genes in Leydig cells. In conclusion, our study demonstrates that lactational exposure to PCBs caused epigenetic changes in the Leydig cells which could have impaired the Leydig cell function in progeny (PND60) rats. [ABSTRACT FROM AUTHOR]

Introduction: the bioassay with the bioindicator species Daphnia magna Strauss, 1820 makes it possible to obtain the individual acute ecotoxicological effect and in a mixture of various chemical toxics by means of the mean lethal concentration (LC50). Objective: to determine the ecotoxicological effect of the mixture of aroclor 1254 and lead (Pb2+) on D. magna. Materials and Methods: LC50 was measured with arochlor 1254> Pb2+, and subsequently the concentration without ecological effect (PNEC) for the individual effect and as a mixture. PNEC values were contrasted with category 4-E1 (lagoons and lakes) and E2 (rivers) of the Peruvian Environmental Quality Standard (Supreme Decree No. 004 2017-MINAM-Peru). Results: LC50 values gradually decreased after 48 h of exposure for both compounds individually and as a mixture. The proportion-synergy (PS) was calculated in ratios of 1:1, 3:2 and 4:1 (arochlor 1254: Pb2+), obtaining higher PS values in 3:2 and 4:1 in contrast to 1:1. Conclusions: the PNEC estimated arochlor 1254 concentration is similar to the conservation value of the aquatic environment category 4-E1 and E2, and the maximum concentration for Pb2+ is not adequate and should be reduced to strengthen the conservation of aquatic biota. Finally, the bioindicator D. magna ideally determined the mixture of aroclor 1254 and Pb2+. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the protective effect of quercetin on polychlorinated biphenyls (PCB)-induced liver and embryo damage in pregnant Sprague–Dawley rats. Pregnant rats were divided into five groups, and then were orally gavaged daily with peanut oil (vehicle) or a commercial PCB mixture (Aroclor 1254) — with or without co-treatment with 75, 150, or 300 mg/kg quercetin — on gestation days (GD) 4–7. At GD 9, all rats were euthanized, and their blood, liver, and uterus were collected. Expressions of CYP450 mRNA and protein in liver, cytokines (IFNγ, IL-2, IL-4, and IL-6) and IFNγ/IL-4 ratios in liver and sera, liver morphology, and the status of implanted embryos were analyzed. The results showed Aroclor 1254 treatment alone caused hepatic cord damage (i.e. cell disorganization, swelling, decreased cytoplasm, vacuolization), and that quercetin co-treatment appeared to mitigate this damage. Similarly, levels of CYP1A1 and CYP2B1 mRNA in livers of Aroclor 1254-only-treated rats were significantly higher than those in rats co-treated with quercetin. Hepatic and sera levels of IFNγ, IL-2, IL-6, and IFNγ/IL-4 ratios, and the ratio of delayed-development embryos, all increased in Aroclor 1254-treated rats, but were relatively decreased as a result of quercetin co-treatments. IL-4 levels were decreased by Aroclor 1254 and tended to increase back to normal when quercetin was used. The results indicated that quercetin imparted a protective effect against Aroclor 1254-induced toxicity in pregnant rats, in part, by modulating levels of important pro-inflammatory cytokines and reducing induced CYP1A1 and CYP2B1 expression.

Polychlorinated biphenyls (PCBs) are well-known persistent organic pollutants; they have toxic effects on the immune system, reproductive system, and endocrine system by changing the metabolism of the body. To elucidate the underlying molecular mechanism, the clam Meretrix meretrix was exposed to 10 and 1000 ng/L Aroclor 1254 and natural seawater (control). Samples from clams exposed to natural seawater and those exposed to Aroclor 1254 for 1 and 3 days were individually collected for transcriptome analysis. After assembly, more than 535,157 transcripts with a mean length of 949 bp and an N50 length of 1279 bp were obtained; a final set of 177,142 unigenes was generated. In the present study, 5101 differentially expressed genes were identified. The differentially expressed genes were related to detoxification metabolism, oxidative stress, immune response, and endocrine system disruption. Of these genes, under the Aroclor 1254 exposure, cytochrome P450 20A1 (2.06–4.46 folds), glutathione S-transferase (2.25–3.80 folds), multidrug resistance-associated protein 1-like (1.49–2.92 folds), peroxidase-like protein (1.33–4.26 folds), lysozyme (1.61–2.05 folds), bcl-2 like 1 protein (1.14–2.29 folds) and vitellogenin (1.09–1.19 folds) showed been significantly induced expressed. At the same time, some genes were down regulated, including cytochrome P450 2J5 (−1.20 ~ −2.86 folds), cytochrome P450 3A24 (−1.40 ~ −4.08 folds), C1q (−1.27 ~ −1.66 folds), Sulfotransferase (−1.51 ~ −1.84 folds), monocarboxylate transporter 10 (−1.30 ~ −4.70 folds), 3-beta hydroxysteroid dehydrogenase (−1.43 ~ −2.81 folds) and beta-galactosidase (−1.23 ~ −2.23 folds). Furthermore, it showed that the expression levels of CYP2J5, glutathione S-transferase, 3-beta hydroxysteroid dehydrogenase and beta-galactosidase had time responses and dose responses. The present study provided insights into the toxic effects of Aroclor 1254 exposure in M. meretrix.

PCBs are persistent organic pollutants which, due to high environmental hazards, must be traced, determined, and decomposed to reduce their risks. . To detect this material in the soil, the method of extraction and appropriate measuring conditions should be investigated. Two soil samples with two kg weight were selected with two different soil textures and the solutions of soil were made with the 1000 µg/ml aroclor 1254 mixture in a GC device. . Agilent GC-MS with stationary phase (CP 7477) was used to measure aroclor 1254. The analysis of variance and the test of the extraction mean of aroclor 1254 were compared in two soil textures. The results suggested that coarse texture soil (sandy loam) had a higher extract than the fine one (silty loam). The difference was statistically significant (P< 0.01). These findings suggested that the soil texture affected the extraction of aroclor from soil. In addition, four different levels of moisture (5%, 10%, 15% and 20%) produced in two soil textures and aroclor were measured. The highest level of extraction was obtained at 20% moisture, which was significantly higher than that in other levels (P< 0.01). The difference between the mean of extractions in the soil samples with 10% and 15% levels of moisture was non-significant (P> 0.05).

The present study aimed to investigate the protective effect of quercetin on polychlorinated biphenyls (PCB)-induced liver and embryo damage in pregnant Sprague–Dawley rats. Pregnant rats were divided into five groups, and then were orally gavaged daily with peanut oil (vehicle) or a commercial PCB mixture (Aroclor 1254) — with or without co-treatment with 75, 150, or 300 mg/kg quercetin — on gestation days (GD) 4–7. At GD 9, all rats were euthanized, and their blood, liver, and uterus were collected. Expressions of CYP450 mRNA and protein in liver, cytokines (IFNγ, IL-2, IL-4, and IL-6) and IFNγ/IL-4 ratios in liver and sera, liver morphology, and the status of implanted embryos were analyzed. The results showed Aroclor 1254 treatment alone caused hepatic cord damage (i.e. cell disorganization, swelling, decreased cytoplasm, vacuolization), and that quercetin co-treatment appeared to mitigate this damage. Similarly, levels of CYP1A1 and CYP2B1 mRNA in livers of Aroclor 1254-only-treated rats were significantly higher than those in rats co-treated with quercetin. Hepatic and sera levels of IFNγ, IL-2, IL-6, and IFNγ/IL-4 ratios, and the ratio of delayed-development embryos, all increased in Aroclor 1254-treated rats, but were relatively decreased as a result of quercetin co-treatments. IL-4 levels were decreased by Aroclor 1254 and tended to increase back to normal when quercetin was used. The results indicated that quercetin imparted a protective effect against Aroclor 1254-induced toxicity in pregnant rats, in part, by modulating levels of important pro-inflammatory cytokines and reducing induced CYP1A1 and CYP2B1 expression. [ABSTRACT FROM AUTHOR]

BackgroundThe "developmental origins of adult disease" hypothesis was originally derived from evidence linking low birth weight to cardiovascular diseases including stroke. Subsequently, it has been expanded to include developmental exposures to environmental contaminants as risk factors for adult onset disease.ObjectiveOur goal in this study was to test the hypothesis that developmental exposure to poly-chlorinated biphenyls (PCBs) alters stroke outcome in adults.MethodsWe exposed rats to the PCB mixture Aroclor 1254 (A1254) at 0.1 or 1 mg/kg/day in the maternal diet throughout gestation and lactation. Focal cerebral ischemia was induced at 6-8 weeks of age via middle cerebral artery occlusion, and infarct size was measured in the cerebral cortex and striatum at 22 hr of reperfusion. PCB congeners were quantified in brain tissue by gas chromatography with microelectron capture detection, and cortical and striatal expression of Bcl2 and Cyp2C11 were quantified by quantitative reverse transcriptase-polymerase chain reaction.ResultsDevelopmental exposure to A1254 significantly decreased striatal infarct in females and males at 0.1 and 1 mg/kg/day, respectively. Predominantly ortho-substituted PCB congeners were detected above background levels in brains of adult females and males exposed to A1254 at 1 but not 0.1 mg/kg/day. Effects of developmental A1254 exposure on Bcl2 and Cyp2C11 expression did not correlate with effects on infarct volume.ConclusionOur data provide proof of principle that developmental exposures to environmental contaminants influence the response of the adult brain to ischemic injury and thus represent potentially important determinants of stroke susceptibility.

Objective: To evaluate the dose and duration dependent cytotoxicity of aroclor 1254 on mice testis.Methods: The study tests the hypothesis that in vivo exposure of very low dose aroclor 1254, comparable to that of possible human exposure from different environmental sources, will provoke dose and duration dependent histological damage in the mice testis. Male mice were orally administered with the two doses 0.1 and 1.0 mg/kg b.w /d. of aroclor 1254 for 7, 14, 21 and 28 d.Results: Results showed the degenerative changes in the testis of mice, namely, atrophied seminiferous tubules, expanded space in interstitial and necrosis in the germinal epithelial cells of seminiferous tubules, of the seminiferous tubules and deceleration of spermatogenesis.Conclusions: Therefore, the results of the present study suggested that the sub-acute exposure of very low doses of aroclor 1254, can subsequently mediate the cytoskeleton dysfunction in the testis of mice.

Polychlorinated biphenyls (PCBs) are common environmental contaminants that represent a considerable risk to reproductive toxicity in exposed human populations. Although some experimental studies have suggested an association between the levels of PCBs and semen quality, the direct effects of PCBs on human sperm parameters remain largely unexplored. To this aim, a short-term in vitro incubation experiment that better imitated the putative exposure of sperm to Aroclor 1254 (a commercial PCB mixture) in male reproduction tissue was conducted. Human sperm were incubated with various concentrations (0, 1, 5, or 25 mg l−1) of Aroclor 1254 for different amounts of time (3 and 6 h) in vitro. Sperm motility parameters were analyzed with computer-assisted sperm analysis (CASA). The proportion of sperm with high mitochondrial membrane potential (ΔΨm) and the levels of intracellular reactive oxygen species (ROS) were detected to explore the probable cause of sperm impairment. Human sperm exposed to continuous Aroclor 1254 exhibited: (i) reduced sperm motility and kinematic parameters, (ii) a proportion of sperm with high ΔΨm that decreased in a dose-dependent manner (P < 0.05), and (iii) increased levels of ROS compared with controls (P < 0.05). In conclusion, Aroclor 1254 can decrease sperm motility, which may culminate in increased ROS and general mitochondrial dysfunction, thus affecting the fertilization potential of sperm. Our findings suggest a broader understanding of the effect of Aroclor 1254 on human sperm.

• Aroclor 1254 exposure influences endocrine and osmoregulatory systems in fish acclimated to SW. • The energetic reorganization due to the stress situation induced in HSW-transferred fish is exacerbated by Aroclor 1254. • A clear blockage of vasotocinergic system is produced by Aroclor 1254 at central, plasma and peripheral levels. • Aroclor 1254 compromises the hypoosmoregulatory function of vasotocinergic system. The present study assesses the response of vasotocinergic system in the gilthead sea bream (Sparus aurata) after administering two doses of the polychlorinated biphenyl Aroclor 1254 (15 or 50 μg g−1 fresh body mass). Seven days post-administration, eight fish of each experimental group were sampled, and the remaining animals were challenged with a hyperosmotic stress by being transferred from seawater (36 ppt) to high salinity water (55 ppt) and being sampled 3 days post-transfer. Aroclor 1254 affected gene expression of avt , together with Avt concentrations in pituitary and plasma, inhibiting the stimulation observed in vasotocinergic system after hyperosmotic challenge. This was noted by the accumulation of Avt at hypophyseal level as well as by its undetectable values in plasma. Hyperosmotic transfer significantly changed branchial avtrv1a , avtrv2, atp1a and cftr mRNA expression levels in control fish, while in Aroclor 1254-treated fish they remained mostly unchanged. This desensitization also occurred for avtr s in hypothalamus, caudal kidney and liver. In addition, an enhancement in plasma cortisol concentration, together with the orchestration of several players of the Hypothalamic-Pituitary-Interrenal axis (crh , crhbp , trh , star), was also observed mostly at the highest dose used (50 μg g−1 body mass), affecting plasma and hepatic metabolites. Our results demonstrated that Aroclor 1254 compromises the hypoosmoregulatory function of vasotocinergic system in S. aurata , also inducing a concomitant stress response. In summary, this study demonstrates that Aroclor 1254 can be considered an important endocrine disruptor in relation with the correct arrangement of vasotocinergic, metabolic and stress pathways after their stimulation by transfer to hyperosmotic environments. [ABSTRACT FROM AUTHOR]

Abstract Polychlorinated biphenyls (PCBs) cause serious impacts on the environment and organisms, due to their hypertoxicity, thermal stability and persistence. This study investigated the effects of temperature, reaction time and total flow rate on the low-temperature catalytic decomposition of Aroclor 1254. A modified iron-exchange method was adopted because it allows higher metal loading rates than the traditional impregnation method. We used this method to prepare three active carbon supported Fe/Ni bimetallic catalysts with different Fe/Ni molar ratios. The results indicated that the Fe/Ni bimetallic catalysts showed great potential in Aroclor 1254 decomposition. Among Fe/Ni molar ratios, Fe/Ni-1/3-C demonstrated the strongest performance with a decomposition efficiency greater than 90% even at the relatively low temperature of 200 °C. Thermodynamic analysis confirmed that the dechlorination of Aroclor 1254 over Fe/Ni-1/3-C obtained the minimum activation energy of 8.0 kJ/mol. Aroclor 1254 was decomposed rapidly over Fe/Ni-1/3-C, with a total decomposition efficiency of 83.4% at 10 min and 93.8% at 30 min. The kinetics analysis indicated a stepwise dechlorination of Aroclor 1254 over Fe/Ni-1/3-C. In addition, the total flow rate indicated a negative effect on the decomposition of Aroclor 1254 due to the decreased retention time. Graphical abstract Unlabelled Image Highlights • Aroclor 1254 can be decomposed efficiently over AC-based Ni-Fe bimetallic catalyst. • Decomposition efficiency of Aroclor 1254 was over 93% at low temperature of 250 °C. • Fe/Ni-1/3-C was the most potential for Aroclor 1254 degradation at 200–250 °C. • The flow rate of carrier gas showed less effect on Aroclor 1254 degradation. • Aroclor 1254 was dechlorinated stepwise over Fe/Ni-1/1-C by kinetics analysis. [ABSTRACT FROM AUTHOR]

Aroclor 1254 is a commercial mixture of polychlorinated biphenyls (PCBs), which are widespread environmental pollutants. It is used as non-flammable heat transfer agent and plasticizer. Animal studies have reported that Aroclor 1254 exerted toxic effects in different organs and systems. Although the evidences are limited, it seems reasonable that Aroclor 1254 may have a potential for similar adverse effects in humans. Selenium (Se) is a trace element and an important component of cellular antioxidant defense. This study was designed to investigate the effects of different Se status on the genotoxicity of Aroclor 1254 in sperm and different organs of Sprague-Dawley rats using Comet assay. Se deficiency (SeD) was generated by feeding 3-week old Sprague-Dawley rats with <0.05 Se mg/kg diet for 5 weeks. Se supplementation groups (SeS) were fed with 1 mg Se/kg diet. Aroclor 1254-treated rats received 10 mg/kg dose by gavage during the last 15 d of feeding period. SeD increased DNA damage in all of the organs as well as in lymphocytes and sperm. Aroclor 1254 treatment caused pronounced changes in liver, kidney and brain cells along with marked increases in lymphocytes and sperm. Se supplementation provided full or partial protection decreases in Aroclor 1254-induced DNA damage in sperm and all of tissues. Se deficiency aggravated the toxicity by increasing DNA damage caused by Aroclor 1254. Further studies should be performed to clarify the mechanism(s) underlying the protective role of Se status against Aroclor 1254 genotoxicity. [ABSTRACT FROM AUTHOR]

PCBs are persistent organic pollutants which, due to high environmental hazards, must be traced, determined, and decomposed to reduce their risks. . To detect this material in the soil, the method of extraction and appropriate measuring conditions should be investigated. Two soil samples with two kg weight were selected with two different soil textures and the solutions of soil were made with the 1000 μg/ml aroclor 1254 mixture in a GC device. . Agilent GCMS with stationary phase (CP 7477) was used to measure aroclor 1254. The analysis of variance and the test of the extraction mean of aroclor 1254 were compared in two soil textures. The results suggested that coarse texture soil (sandy loam) had a higher extract than the fine one (silty loam). The difference was statistically significant (P< 0.01). These findings suggested that the soil texture affected the extraction of aroclor from soil. In addition, four different levels of moisture (5%, 10%, 15% and 20%) produced in two soil textures and aroclor were measured. The highest level of extraction was obtained at 20% moisture, which was significantly higher than that in other levels (P< 0.01). The difference between the mean of extractions in the soil samples with 10% and 15% levels of moisture was nonsignificant (P> 0.05). [ABSTRACT FROM AUTHOR]

Abstract: Although marine and coastal environments which are contaminated with xenobiotic organic compounds often become hypoxic during the summer, the interactive effects of hypoxia and xenobiotic exposure on marine species such as teleost fishes remain poorly understood. The expression and activity of monooxygenase enzyme cytochrome P450‐1A (CYP1A) in fishes are upregulated by exposure to polychlorinated biphenyls (PCBs), whereas they are down‐regulated during hypoxia exposure. We investigated the interactive effects of hypoxia and PCB co‐exposure on hepatic CYP1A expression in Atlantic croaker and on potential regulators of CYP1A. Croaker were exposed to hypoxia (1.7 mg/L dissolved oxygen), 3,3′,4,4′‐tetrachlorobiphenyl (PCB 77, dose: 2 and 8 µg/g body weight), and Aroclor 1254 (a common PCB mixture, dose: 0.5 and 1 µg/g body weight), alone and in combination for 4 weeks. PCB 77 exposure markedly increased hepatic CYP1A mRNA and protein expression, and ethoxyresorufin‐O‐deethylase (EROD, an indicator of CYP1A enzyme) activity and increased endothelial nitric oxide synthase (eNOS) protein expression. PCB 77 treatment also increased interleukin‐1β (IL‐1β, a cytokine) mRNA levels and protein carbonyl (PC, an indicator of reactive oxygen species, ROS) contents. These marked PCB 77‐ and Aroclor 1254‐induced increases in CYP1A mRNA levels and EROD activity were significantly attenuated by co‐exposure to hypoxia, whereas the increases in hepatic eNOS protein and IL‐1β mRNA expression, and PC contents were augmented by hypoxia co‐exposure. The results suggest that biotransformation of organic xenobiotics by CYP1A is reduced in fish during co‐exposure to hypoxia and is accompanied by alterations in eNOS, ROS, and IL‐1β levels. [ABSTRACT FROM AUTHOR]

In ecotoxicology, transcriptomics is an effective way to detect gene expression changes in response to environmental pollutants. Such changes can be used to identify contaminants or contaminant classes and can be applied as early warning signals for pollution. To do so, it is important to distinguish contaminant-specific transcriptomic changes from genetic alterations due to general stress. Here we present a first step in the identification of contaminant class-specific transcriptome signatures. Embryos of zebrafish (Danio rerio) were exposed to three substances (methylmercury, chlorpyrifos and Aroclor 1254, each from 24 to 48 hpf exposed) representing sediment typical contaminant classes. We analyzed the altered transcriptome to detect discriminative genes significantly regulated in reaction to the three applied contaminants. By comparison of the results of the three contaminants, we identified transcriptome signatures and biologically important pathways (using Cytoscape/ClueGO software) that react significantly to the contaminant classes. This approach increases the chance of finding genes that play an important role in contaminant class-specific pathways rather than more general processes. [ABSTRACT FROM AUTHOR]

Aroclor 1254 (A1254) is the most toxic commercial PCB mixture produced, primarily due to its relatively high concentrations of dioxin-like congeners. This study demonstrates a comparative evaluation of dechlorination of A1254 and PCB-118 by indigenous organohalide respiring bacteria enriched from three PCB impacted sites: Grasse River (GR), NY; Fox River (FR), WI; and Baltimore Harbor (BH), MD. PCB-118 dechlorination rates in GR, BH, and FR was 0.0308, 0.015, and 0.0006 Cl − /biphenyl/day, respectively. A1254 dechlorination rates in GR, FR, and BH were 0.0153, 0.0144, and 0.0048 Cl − /biphenyl/day, respectively. A1254 dechlorination was achieved through the removal of doubly-/singly-flanked chlorines in meta and para positions of mostly penta- followed by hexa- and hepta-chlorinated congeners by 88%, 69%, and 51% in GR, and 88%, 87%, and 83% in FR, respectively, while in BH mostly hepta- (70%) followed by hexa-chlorinated congeners (66%) were dechlorinated. A previously developed Anaerobic Dechlorination Model (ADM) quantified a total of 17 toxicity-related dechlorination pathways in all three sediment microcosms. The toxic equivalency of A1254 based on seven dioxin-like congeners decreased by about 53%, 45% and 21%, in GR, FR and BH microcosms, respectively. The dechlorination products were generally tetra- and tri-chlorinated congeners with unflanked chlorines, all of which is susceptible to further degradation by aerobic bacteria. Concerning the toxic congeners, ADM can be useful to initiate further research focusing on the stimulation of the toxicity reducing pathways for risk assessment and effective remediation strategies. [ABSTRACT FROM AUTHOR]

The present study was aimed to determine the effects of lactational exposure of PCBs (Aroclor 1254) on Leydig cellular steroidogenesis in F 1 progeny rats. Lactating dams were orally treated by gavage with different doses of PCBs (1, 2 and 5 mg/kg b.wt./day). Male progenies were sacrificed on PND60. Our results demonstrated that exposure to PCBs decreased the body weight, testis weight and anogenital distance (AGD) index in the F 1 progeny rats. Importantly, PCBs exposure reduced the serum levels of LH, testosterone and estradiol. Interestingly, PCBs caused a decrease in the Leydig cell population along with decreased activities of steroidogenic enzymes 3β- and 17β-HSD. Additionally, we observed a significant decrease in LHR, SR-B1, StAR protein, Cyp11a1, 3β-HSD, Cyp17a1, 17β-HSD, 5α-reductase, Cyp19a1 and AR gene expression in the Leydig cells of progeny rats. In conclusion, our study demonstrates that lactational exposure of PCBs alters Leydig cellular steroidogenesis in the F 1 progeny rats. [ABSTRACT FROM AUTHOR]

Polychlorinated biphenyls ( PCBs) are environmental contaminants. The present study was aimed to test the effect of lactational exposure of PCBs on Leydig cellular mRNA and protein expressions of 5α-reductase, aromatase and androgen receptor (AR) in F1 male offspring. Lactating dams were orally gavaged with different doses of PCBs (Aroclor 1254) 0, 1, 2 and 5 mg kg b.wt−1 day−1, respectively, from PND1 to PND21. Male offsprings were sacrificed at PND21. Testes were used to isolate Leydig cells. Blood was collected. Serum testosterone (T) and oestradiol (E2) were measured. Anogenital distance was measured. Dams' milk lipid and serum lipids of male pups were estimated. PCB (Aroclor 1254) concentration of dams' milk and serum of male pups were analysed by GC- ECD. Leydig cellular mRNA and protein expressions of 5α-reductase, aromatase and AR were significantly decreased. Our data suggest that lactational exposure of PCBs downregulates selected genes in Leydig cells of F1 generation on post-natal day 21. [ABSTRACT FROM AUTHOR]

This study examined the effect of Aroclor 1254 on arginase activity and protective role of vitamin E among adult rats, pregnant rats and their offsprings. Totally 90 Sprague-Dawley rats were divided into three main groups as 30 pregnant, 30 adult and 30 offsprings (pups of the pregnant rats) based on the treatments administered during the pregnancy period (20 days) with subcutaneous daily injections of Aroclor 1254 (2 mg/kg/day) alone or associated with vitamin E (50 mg/kg/day) or normal saline in controls. Female rats and their offsprings (10 offsprings per groups) were analyzed in terms of the arginase activity in liver. A statistically significant increase was determined in liver arginase activity of adult rats exposed to Aroclor 1254 (p<0.05). Vitamin E administered simultaneously with Aroclor enabled liver arginase activity of adult rats to approach statistically normal values. A statistically insignificant increase was found in the arginase activity among pregnant rats and offsprings. While vitamin E administered simultaneously with Aroclor was ineffective in pregnant rats, it caused a statistically significant increase in offsprings (p<0.05). We recommend that addition of vitamin E can prevent the increase in the liver arginase activity caused by Aroclor 1254. [ABSTRACT FROM AUTHOR]

Introduction: Aroclor 1254, a commercial polychlorinated biphenyls (PCBs) mixture, was found to elicit various adverse effects on human health.Objectives: This study aimed to investigate the structural alterations in the epididymis induced by aroclor 1254, and to assess the possible protective role of L-NAME (NG-Nitro-L arginine methyl ester).Materials and methods: Thirty-five adult male albino rats were divided into three groups: control group (15 rats), equally subdivided into subgroup a; negative control group, subgroup b: received intraperitoneal corn oil (5 ml/kg/day), and subgroup c: received intraperitoneal L-NAME (10 mg/kg/day). Aroclor-treated group (10 rats): received aroclor 1254 (2 mg/kg/day, intraperitoneal), and aroclor + L-NAME-treated group (10 rats): received aroclor 1254 combined with L-NAME in the same previous regimen. After 30 days, blood samples were collected for hormonal assay. Specimens from the epididymis were prepared for histological study and assessment of sperm count.Results: Rats in aroclor-treated group revealed a significant reduction in serum testosterone level and sperm count, in comparison with the control group. The epididymal caput showed stratification and detachment of the epithelium with vacuoles, mitotic figures, and electron-dense bodies together with increased collagen fibers in the interstitium. In addition, a strong reaction of androgen receptors (ARs) was seen in the cytoplasm of epithelial and stromal cells. These effects were attenuated by L-NAME administration.Conclusion: Aroclor 1254 provoked morphological and functional changes in the epididymis of adult rats, which were attenuated by L-NAME administration. [ABSTRACT FROM AUTHOR]

Aroclor 1254 was the second most produced commercial PCB mixture and is found in soils, sediments and sewage throughout the globe. This commercial PCB mixture is considered particularly toxic because of the relatively high concentrations of congeners with dioxin-like properties. The potential for risk reduction by microbial reductive dechlorination of Aroclor 1254 (A1254) was investigated in sediment microcosms from Grasse River (GR), Massena, NY. The specificity of A1254 dechlorination was doubly- and singly-flanked chlorines in meta positions and to a less extent doubly-flanked para chlorines of 2345-substituted chlorobiphenyl rings. The average dechlorination rate of A1254 was 0.0153 Cl − /biphenyl/day, and dechlorination rates of single congeners ranged between 0.001 and 0.0074 Cl − /biphenyl/day. Potential risk associated with A1254 based on the toxic equivalency factors of the dioxin-like congeners was reduced by 83%. Additional potential risk associated with bioaccumulation in fish was reduced by 35% based on biota-sediment accumulation factor estimates for all detected congeners. Finally, the dechlorination end-products were tri- and tetra-chlorobiphenyls with unflanked chlorines, all of which are susceptible to further degradation by aerobic microorganisms. The combined results indicate that microbial reductive dechlorination has the potential for reducing risk associated with toxicity and bioaccumulation in fish in sites contaminated with A1254. [ABSTRACT FROM AUTHOR]

Objectives The present subacute study was designed to evaluate the effect of coenzyme Q 10 (CoQ10) in the 28 days aroclor 1254 exposure induced oxidative stress in mice brain. Methods Biochemical estimations of brain lipid peroxidation (LPO), reduced glutathione (GSH), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and acetyl cholinesterase (AChE), and histopathological investigations of brain tissue were carried out. Results Oral exposure of aroclor 1254 (5 mg/kg) led to significant decrease in levels of GSH, and activities of SOD, CAT, GPx, and AChE, and increase in LPO. These aberrations were restored by CoQ10 (10 mg/kg, intraperitoneal injection [IP]). This protection offered was comparable to that of L-deprenyl (1 mg/kg, IP) which served as a reference standard. Conclusions Aroclor 1254 exposure hampers the activities of various antioxidant enzymes and induces oxidative stress in the brains of Swiss albino mice. Supplementation of CoQ10 abrogates these deleterious effects of aroclor 1254. CoQ10 also apparently enhanced acetyl cholinesterase activity which reflects its influence on the cholinergic system.

Fish is the main single source of polychlorinated biphenyls (PCBs) exposure in men. Anecdotal reports suggest high wild fish consumption rates among sport fishermen in Sanski Most area, Bosnia and Herzegovina (BiH). Presence of PCBs in the environment in BiH was previously documented. The main objective of this work was to estimate the magnitude of PCBs exposure and assess the potential health risk in sport fishermen in Sanski Most. The fishing pattern and magnitude of fish consumption were estimated in the questionnaire survey conducted during April 2012 among members (n= 60) of the local sport fishermen association in Sanski Most. Calculated median and high-end (90th percentile) fish consumption rates were 31 g d−1and 126 g d−1, respectively. The PCB concentrations (as Aroclor 1254 equivalents), determined by ELISA immunoassay in 28 fish fillets ranged from undetectable to 208 μg kg−1. Two different exposure scenarios were used: (a) median exposure, calculated from the median fish consumption rate and median PCB concentrations, and (b) “worst case” scenario, calculated from the high-end fish consumption rate and mean PCB concentrations. The results suggest negligible lifelong cancer and non-cancer risks in case of low to moderate fish consumption rate, but possibly unacceptable risk levels in high-end consumers. [ABSTRACT FROM PUBLISHER]

The polychlorinated biphenyl (PCB) mixture Aroclor 1254 alters bone tissue properties. However, the mechanisms responsible for the observed effects have not yet been clarified. This study compared the effect of Aroclor 1254 on the expression of osteoblast differentiation markers in MC3T3-E1 cells with the corresponding effect of the dioxin reference compound 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), and two PCB congeners belonging to the category of non-dioxin-like PCBs. The aim of the study was to quantify the relative influence of dioxin-like and non-dioxin-like PCB-components on osteoblast differentiation. Expression of marker genes for AhR activity and osteoblast differentiation were analyzed, and relative potency (REP) values were derived from Benchmark concentration-effect curves. Expression of alkaline phosphatase and osteocalcin were decreased by both Aroclor 1254 and TCDD exposure, while the PCB-congeners PCB19 and PCB52 slightly induced the expression. The relative potency of Aroclor 1254 for inhibitory effects on osteoblast differentiation marker genes was within the expected range as estimated from the chemical composition of Aroclor 1254. These results are consistent with previously observed bone modulations following in vivo exposure to Aroclor 1254 and TCDD, and demonstrate that the inhibitory effects of Aroclor 1254 on osteoblast differentiation by the dioxin-like constituents are over-riding the contribution of non-dioxin-like PCBs. [ABSTRACT FROM AUTHOR]

To study the acute toxic effects of PCBs on airway exposure, the cell viability, apoptosis and mitochondrial functions of human lung cancer cell line A549 were measured and compared after Aroclor 1254 exposure for different time. The results showed that Aroclor 1254 could inhibit cell viability and increase cell apoptosis in a concentration- and time-dependent manner. The mitochondrial apoptosis pathway was confirmed playing an important role. ROS elevation was an early response within 1h treatment of Aroclor 1254. Then after 4 h of Aroclor 1254 exposure, the intracellular calcium level increased and mitochondrial transmembrane potential (ΔΨm) collapsed, accompanying with Cytochromec(Cyt-c) leakage, boosting expression of Bax, Apaf-1 and miRNA155, which were involved in the mitochondrial apoptosis pathway. After 24 h of Aroclor 1254 exposure, ROS returned to normal level, but cell apoptosis rate was higher than that at 4 h with ΔΨmcontinued collapsing and intracellular calcium increased. In conclusion, Aroclor 1254 could suppress cell viability and induce apoptosis in A549 cells, which was associated with ROS over-production and elevated cellular Ca2+level, which may result in mitochondrial dysfunction, inducing expression of Bax/Cyt-c/Apaf-1 and miRNA155. [ABSTRACT FROM AUTHOR]

ABSTRACT Di(2-ethylhexyl) phthalate (DEHP) and polychlorinated biphenyls (PCBs) are two widely distributed pollutants that are of great concern due to their adverse health effects. However, few studies have investigated the combined effects of DEHP and PCBs. In this study, adult mice were continuously exposed to mixtures of DEHP (15 mg/kg bodyweight/day) and Aroclor 1254 (7.5 mg/kg bodyweight/day) for 12 days to investigate the combined effects of these compounds. The results showed that the ratio of the liver weight to the body weight was higher in the treated group than that in the control group. The effects of combined exposure on three important receptors, the proliferator-activated receptor (PPAR), estrogen receptor (ER), and aryl hydrocarbon receptor (AHR), were investigated. The mRNA level of PPARγ was significantly up-regulated after exposure. The expression level of ERα was decreased in the male treated group. In contrast, the expression levels of AHR and related genes (cyp1a1 and cyp1b1) were not markedly affected. The expression level of phospholipase A (PLA) was significantly down-regulated at both the mRNA and protein levels in male mice after combined treatment. In all, our study demonstrated the combined effects of DEHP and PCBs on the expression levels of key receptors in mice. The combined exposure led to a decrease in phospholipase in male mice. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 197-204, 2015. [ABSTRACT FROM AUTHOR]

Polychlorinated biphenyls (PCBs) induce a broad spectrum of biochemical and toxic effects in mammals including alterations of the vital retinoid (vitamin A) system. The aim of this study was to characterize alterations of tissue retinoid levels in rat offspring and their dams following gestational and lactational exposure to the PCB mixture Aroclor 1254 (A1254) and to assess the interrelationship of these changes with other established sensitive biochemical and toxicological endpoints. Sprague-Dawley rat dams were exposed orally to 0 or 15 mg/kg body weight/day of A1254 from gestational day 1 to postnatal day (PND) 23. Livers, kidneys and serum were collected from the offspring on PNDs 35, 77 and 350. Tissue and serum retinoid levels, hepatic cytochrome P450 (CYP) enzymes and serum thyroid hormones were analyzed. A multivariate regression between A1254 treatment, hepatic retinoid levels, hepatic CYP enzymes activities, thyroid hormone levels and body/liver weights was performed using an orthogonal partial least-squares (PLS) analysis. The contribution of dioxin-like (DL) components of A1254 to the observed effects was also estimated using the toxic equivalency (TEQ) concept. In both male and female offspring short-term alterations in tissue retinoid levels occurred at PND35, i.e. decreased levels of hepatic retinol and retinoic acid (RA) metabolite 9-cis-4-oxo-13,14-dihydro-RA with concurrent increases in hepatic and renal all-trans-RA levels. Long-term changes consisted of decreased hepatic retinyl palmitate and increased renal retinol levels that were apparent until PND350. Retinoid system alterations were associated with altered CYP enzyme activities and serum thyroid hormone levels as well as body and liver weights in both offspring and dams. The estimated DL activity was within an order of magnitude of the theoretical TEQ for different endpoints, indicating significant involvement of DL congeners in the observed effects. This study shows that tissue retinoid levels are affected both short- and long-term by developmental A1254 exposure and are associated with alterations of other established endpoints of toxicological concern. [ABSTRACT FROM AUTHOR]

Chronic exposure to polychlorinated biphenyls (PCBs) affect the immune system of fish and could lead to a decreased disease resistance. The effects of Aroclor 1254, PCB mixtures, on the Diplodus puntazzo innate immunity were examined by assaying the zymosan stimulated chemiluminescence response (CL) of peritoneal cavity cells (PCCs) at various times (1, 24, 48 h and 1-4 weeks) from intraperitoneal injection of the xenobiotic (1 mg kg-1 body weight). Controls were performed by assaying cells from medium-treated fish. Since the kinetic of the chemiluminescence response showed the highest peak at 25 min after the zymosan stimulation of the cells, the values found at that time were considered. The CL enhancement observed at 1 h after the treatment with xenobiotic was followed by a decreased response at 24 h and appeared to be lower at 1-4 weeks when compared to the CL response of the control, suggesting a protracted effect of PCBs on the peritoneal cavity. Since PCCs incubated in vitro for 1 h with 0.05 and 0.1 µg ml-1 Aroclor showed an enhanced CL, the effect of the xenobiotic could be exerted on the cell responsiveness to zymosan. It is known that fish CL response of PCCs can be imputed to phagocyte (macrophages and neutrophils) activation, these cells and their responsiveness to zymosan can be used in immunotoxicology assay to monitor the fish health in polluted environment. [ABSTRACT FROM AUTHOR]

The Arctic sea urchin Strongylocentrotus droebachiensis is considered to be a potential indicator species for assessing aquatic environmental conditions in the polar region. To develop a gene resource for the Arctic sea urchin, we sequenced S. droebachiensis cDNAs using a GS-20 sequencer and obtained expressed sequence tags information. In the assembly stage, 31,526 transcripts were obtained and showed a 32 % hit rate in the GenBank non-redundant database with 9,995 unigenes. Of the transcripts obtained in this species, we found several stress- and cellular defense-related genes (antioxidant-related genes and genes from the heat shock protein family) that are useful for the monitoring of pollutant-triggered stress responses at the molecular level. To validate the usefulness of these potential biomarker genes, we analyzed the transcript profiles of selected genes in response to polychlorinated biphenyls (PCB) mixtures (Aroclor 1254) for 48 h. PCB contamination is a present-day threat to the health of individual organisms and ecosystems in the polar region. We showed that 11 of 14 genes responded to PCB treatment at transcriptional levels, with the most dramatic upregulation observed in the hsp70.5 gene. In this paper, we summarize the expressed cDNA information and discuss its potential use in ecotoxicological genomic studies on PCB exposure. [ABSTRACT FROM AUTHOR]

Highlights: [•] 2,3,4,7,8-PnCDF and PCB77 induce EROD and reduce prey capture in Fundulus larvae. [•] The ReP of 2,3,4,7,8-PnCDF to TCDD for inducing EROD activity was 2.40. [•] No embryotoxic effects were observed on larvae exposed to PCB52 or PCB110. [•] Aroclor 1254 caused embryotoxic effects similar to that of dioxin-like compounds. [•] The TCDD-TEQ approach overestimated the toxic potency of Aroclor 1254. [ABSTRACT FROM AUTHOR]

Highlights: [•] Aroclor 1254 inhibited cell proliferation and induced apoptosis in mouse spermatocyte GC-2 cells. [•] Aroclor 1254 caused the arrest of cells in G0/G1 phase in GC-2 cells. [•] The protein expression levels of Bcl-2 and cyclin D1 decreased while cleaved caspase-3 increased. [•] ERα and ERβ were involved in all these effects above induced by Aroclor 1254. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the osteotoxicity of polychlorinated biphenyls in murine osteoblastic MC3T3-E1 cells, and to explore the underlying mechanism focused on oxidative stress. The cells were exposed to Aroclor 1254 at concentrations of 2.5-20 µmol/L, and then cell viability, oxidative stress, intracellular calcium concentration, osteocalcin content, and calcium nodules formation were measured. Aroclor 1254 reduced cell viability and induced overproduction of intracellular reactive oxygen species in a dose-dependent manner. Activity of superoxide dismutase was decreased, and malondialdehyde content was promoted after exposure. Moreover, inhibitory effects of Aroclor 1254 on calcium metabolism and mineralization of osteoblasts were observed, as indicated by reduction of the intracellular calcium concentration, osteocalcin content, and modules formation rate. The decreased expression of osteocalcin, alkaline phosphatase, bone sialoprotein, and transient receptor potential vanilloid 6 further confirmed the impairment of Aroclor 1254 on calcium homeostasis and osteoblast differentiation. Addition of the antioxidant N-acetyl-L-cysteine partially restored the inhibitory effects on calcium metabolism and mineralization. In general, Aroclor 1254 exposure reduces calcium homeostasis, osteoblast differentiation and bone formation, and oxidative stress plays a vital role in the underlying molecular mechanism of osteotoxicity., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Chen, Cai, Chen, Li, Lu, Yu, Wang, Fang and Xu.)

Methylmercury (MeHg) and polychlorinated biphenyls (PCBs) are environmentally persistent neurodevelopmental toxicants. In Japan, the most common source of human exposure is the consumption of contaminated fish and seafood. We investigated the accumulation of MeHg and PCBs in the brains of dams and offspring mice maternally exposed to MeHg and/or PCBs. Pregnant mice (C57BL/6Cr) were assigned to one of four exposure groups: control, MeHg alone (MeHg in diet at 5 mg/kg as Hg), PCB alone (Aroclor1254 by gavage at the dose of 18 mg/kg body weight/3 days) and MeHg+PCB. Levels of MeHg and PCBs were measured in the whole brains of dams and offspring mice on postnatal day 21 (PND21) and at 9 weeks of age. Total mercury, MeHg and PCB congener concentrations were determined by CVAAS, GC-ECD and HRGC/HRMS, respectively. For the mercury concentrations, there were no significant differences between MeHg alone and MeHg+PCB except for pups at 9 weeks. The maternal PCB levels were not significantly different between MeHg+PCB and PCB alone. In pup brain on PND21, MeHg+PCB resulted in a significantly higher PCB level than PCB alone. Although the levels of lightly chlorinated (= 4CBs) homologues were lower for MeHg+PCB than for PCB alone, those of highly chlorinated (>= 5CBs) homologues were significantly higher on PND21 for MeHg+PCB. The PCB composition in dams and pups shifted to higher chlorinated homologues compared with the composition of administered Aroclor1254. For these reasons, further detailed studies are necessary to clarify the interactional effects of PCB metabolism after coexposure to MeHg and PCBs. [ABSTRACT FROM AUTHOR]

Highlights: [•] The nature and mechanism of action of Aroclor 1254 on rat sperm in vitro were elucidated. [•] Aroclor 1254 decreased sperm motility, viability, acrosome reaction and Δψm. [•] Aroclor 1254 decreased DNA integrity and ATP content. [•] Mitochondria cytochrome c content was decreased, while caspase-3 activity was increased. [•] Aroclor 1254 induced oxidative stress in rat sperm. [ABSTRACT FROM AUTHOR]