Telomere length (TL) is an index of cellular aging and can predict the incidences of many age-related diseases. Change of TL might be affected by environmental pollution and individual's genetic background. In this cohort study, we aimed to evaluate the associations between polycyclic aromatic hydrocarbons (PAHs) exposure and longitudinal TL shortening, and investigate whether genetic variations in TERT-CLPTM1L can modify these associations. We measured the baseline concentrations of twelve urinary PAH metabolites and genotyped six variants at TERT-CLPTM1L among 1243 coke-oven workers. The relative leukocyte TL was detected in both baseline and follow-up (4 years later) visits. The TL shortening were estimated by TL decline and TL ratio. We found that the urinary level of 1-hydroxypyrene (1-OHP) had significant dose-response relationships with increased TL decline [β(95%CI) = 0.078(0.023, 0.133), P = 0.005] and TL ratio [β(95%CI) = 0.096(0.037, 0.155), P = 0.002]. Besides, urinary 1-hydroxynaphthalene (1-OHNa) was marginally dose-related with elevated TL decline [β(95%CI) = 0.053(-0.001, 0.107), P = 0.055] and TL ratio [β(95%CI) = 0.057(-0.002, 0.116), P = 0.058]. Analyses of TERT-CLPTM1L variants showed that the rs401681 and rs465498 could modify the effect of 1-OHP on increasing TL decline (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.012 and 0.035, respectively) and TL ratio (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.014 and 0.067, respectively), which were pronounced among rs401681TT and rs465498CC carriers, but not seen among rs401681TC + CC and rs465498CT + TT carriers. In conclusion, elevated exposure to PAHs can accelerate the TL shortening and this effect can be modified by TERT-CLPTM1L variants. These results may add potential evidence for gene-environment interactions on dynamic changes of telomere length. Further studies are warranted to validate these findings and uncover the underlying mechanisms.

Productive coastal and estuarine habitats can be degraded by contaminants including persistent organic pollutants (POPs) such as PCBs, dioxins, and organochlorine insecticides to the extent of official designation as contaminated sites. Top-predatory wildlife may continue to use such sites as the habitat often appears suitable, and thus bioaccumulate POPs and other contaminants with potential consequences on their health and fitness. Victoria and Esquimalt harbours are located on southern Vancouver Island, British Columbia (BC) and are federally designated contaminated sites due mainly to past heavy industrial activities, such as from shipyards and sawmills. We collected scat samples from river otters (Lontra canadensis) throughout an annual cycle, and combined chemical analysis with DNA genotyping to examine whether the harbour areas constituted a contaminant-induced ecological trap for otters. We confirmed spatial habitat use by radio telemetry of a subsample of otters. Fifteen percent of otter scat contained PCB concentrations exceeding levels considered to have adverse effects on the reproduction of mink (Neovison vison), and there were significant positive correlations between concentrations of PCBs and of thyroid (T3) and sex (progesterone) hormones in fecal samples. Radio telemetry data revealed that otters did not show directional movement away from the harbours, indicating their inability to recognize the contaminated site as a degraded habitat. However, analysis and modeling of the DNA genotyping data provided no evidence that the harbour otters formed a sink population and therefore were in an ecological trap. Despite the highly POP-contaminated habitat, river otters did not appear to be adversely impacted at the population level. Our study demonstrates the value of combining chemical and biological technologies with ecological theory to investigate practical conservation problems.

Prenatal disinfection by-products (DBPs) exposure is linked with adverse birth outcomes. Genetic susceptibility to DBP metabolism may modify the exposure-outcome associations.To investigate whether CYP2E1 and GSTZ1 genetic polymorphisms modified the associations of prenatal DBP exposures with adverse birth outcomes.Two biomarkers of DBP exposures including trihalomethanes (THMs) in blood and trichloroacetic acid (TCAA) in urine were determined among 426 pregnant women from a Chinese cohort study. CYP2E1 (rs2031920, rs3813867, and rs915906) and GSTZ1 (rs7975) polymorphisms in cord blood were genotyped. Statistical interactions between prenatal DBP exposures and newborns CYP2E1 and GSTZ1 polymorphisms on birth outcomes (birth weight, birth length, and gestational age) were examined by multivariable linear regression with adjustment for potential confounders.We found that newborns CYP2E1 genetic polymorphisms (rs2031920 and rs3813867) modified the associations of maternal blood THMs or urinary TCAA levels with birth outcomes. However, these interactions were nonsignificant after Bonferroni correction for multiple comparisons, except for the interaction between maternal blood BrTHMs [sum of dibromochloromethane (DBCM), bromodichloromethane (BDCM), and bromoform (TBM)] and newborns CYP2E1 gene rs2031920 polymorphisms on birth weight (P for interaction = 0.003).Newborns genetic variations of CYP2E1 rs2031920 may modify the impacts of prenatal BrTHM exposure on birth weight. This finding needs to be further confirmed.

Environmental antimicrobial resistance (AMR) has drawn increasing attention due to its great risk to human health. The aim of this study was to investigate AMR and genotyping of Vibrio parahaemolyticus isolates (n = 114) recovered from shrimp mariculture environment in China. The isolates exhibited a high rate of resistance to streptomycin (78.9%), ampicillin (64.9%) and gentamicin (53.5%). Furthermore, multi-drug resistance was highly prevalent (61.4%), in which 95.9% of these ampicillin-resistant isolates were primarily mediated by blaCARB-17. Surprisingly, doxycylcine, florfenicol, and trimethoprim/sulfamethoxazole (TMP/SMZ) resistance genes occurred in susceptible isolates. Moreover, 114 isolates were grouped into unique pulsed field gel electrophoresis patterns. These findings suggest the need for the prudent use of antimicrobial agents on mariculture farms, in order to control the dissemination of antimicrobial resistant V. parahaemolyticus.

Mitochondria play an essential role to supply the cell with metabolic energy in the form of adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS). As a consequence, they are also the primary source of cellular reactive oxygen species (ROS) which can cause oxidative damage of individual respiratory chain complexes. Indeed, affected OXPHOS subunits result in decreases in ATP production and increases in ROS formation which generate oxidative phosphorylation deficiency leading to mitochondrial dysfunctions. It has been suggested that ROS play a vital role in the pathogenesis of mitochondrial diseases. To the best of our knowledge, this is the first study which aimed to investigate the genetic variant effect of the antioxidant enzymes GSTM1 and GSTT1 on mitochondrial disease among a Tunisian population. In this report, 109 patients with mitochondrial disease and 154 healthy controls were genotyped by multiplex PCR amplification, and data were analyzed by SPSS v20 software. The results showed that GSTM1 null genotype was found to be associated with mitochondrial disease with a protective effect; however, no significant association of GSTT1 polymorphism with mitochondrial disease risk was revealed. But, interestingly, our findings highlight that GSTM1 active and GSTT1 null genotype combination increased by three fold the risk of developing mitochondrial disease with p c = 0.020, notably mitochondrial myopathy with p c = 0.046 and Leigh syndrome with p c = 0.042. In conclusion, this study suggests that GSTM1 active and GSTT1 null genotype combination might be a risk factor in developing mitochondrial disease.

The aim of the study was to determine the antimicrobial resistance profile and the occurrence of extended-spectrum beta-lactamase genes and to analyze the genetic diversity of Escherichia coli strains isolated from the environment of horse riding centers. The study was conducted using E. coli strains isolated from the air, manure, and horse nostril swabs in three horse riding centers differing in the system of horse keeping—stable (OJK Pegaz and KJK Szary) and free-range (SKH Nielepice). Resistance to antibiotics was determined using the disk-diffusion method, and the PCR technique was employed to detect the extended-spectrum β-lactamase (ESBL) genes, while the genetic diversity of strains was assessed by rep-PCR. A total of 200 strains were collected during the 2-year study, with the majority isolated from KJK Szary, while the smallest number was obtained from SKH Nielepice. The strains were mostly resistant to ampicillin, aztreonam, and ticarcillin. The tested strains were most frequently resistant to one or two antibiotics, with a maximum of ten antimicrobials at the same time. Two multidrug-resistant (MDR) strains were detected in OJK Pegaz while in KJK Szary there were two MDR and one extensively drug-resistant (XDR) strain. The ESBL mechanism was most frequently observed in OJK Pegaz (20.31% of strains) followed by KJK Szary (15.53% of strains) and SKH Nielepice (15.15% of strains). Among the ESBL-determining genes, only blaTEM and blaCTXM-9 were detected—blaTEM was mostly found in KJK Szary (53.40% of strains), while the second detected gene—blaCTXM-9—was most frequent in SKH Nielepice (6.06% of strains). The rep-PCR genotyping showed high variation among the analyzed strains, whereas its degree differed between the studied facilities, indicating that the type of horse keeping (stable vs. free-range) affects the genetic diversity of the E. coli strains. Having regard to the fact that the tested strains of E. coli were derived from non-hospitalized horses that were not treated pharmacologically, we can assume that the observed antimicrobial resistance may be of both—natural origin, i.e., not the result of the selection pressure, and acquired, the source of which could be people present in the horse riding facilities, the remaining horses which were not included in the study, and air, as well as water, fodder, and litter of the animals. Therefore, it can be concluded that the studied horses are the source of resistant E. coli and it is reasonable to continue monitoring the changes in antimicrobial resistance in those bacteria.