Kolaviron suppresses dysfunctional reproductive axis associated with multi-walled carbon nanotubes exposure in male rats

Reproductive toxicity associated with excessive exposure to multi-walled carbon nanotubes (MWCNTs), which are commonly used in medicine as valuable drug delivery systems, is well documented. Kolaviron, a bioflavonoid isolated from Garcinia kola seeds, elicits numerous health beneficial effects related to its anti-inflammatory, anti-genotoxic activities, anti-apoptotic, and antioxidant properties. However, information on the role of kolaviron in MWCNTs-induced reproductive toxicity is not available in the literature. Herein, we assessed the protective effects of kolaviron on MWCNTs-induced dysfunctional reproductive axis in rats following exposure to MWCNTs (1 mg/kg) and concurrent treatment with kolaviron (50 or 100 mg/kg body weight) for 15 successive days. Results showed that MWCNTs-induced dysfunctional reproductive axis as evidenced by deficits in pituitary and testicular hormones, marker enzymes of testicular function, and sperm functional characteristics were abrogated in rats co-administered with kolaviron. Moreover, co-administration of kolaviron-abated MWCNTs-induced inhibition of antioxidant enzyme activities increases in oxidative stress and inflammatory indices. This is evidenced by diminished levels of tumor necrosis factor-alpha, nitric oxide, lipid peroxidation, reactive oxygen, and nitrogen species as well as reduced activity of myeloperoxidase in testes, epididymis, and hypothalamus of the rats. Biochemical data on the chemoprotection of MWCNTs-induced reproductive toxicity were corroborated by histological findings. Taken together, kolaviron suppressed dysfunctional reproductive axis associated with MWCNTs exposure via abrogation of oxidative stress and inflammation in male rats.

     

Ambient air pollution and term birth weight in Texas from 1998 to 2004

Previous studies have explored the association between air pollution levels and adverse birth outcomes such as lower birth weight. Existing literature suggests an association, although results across studies are not consistent. Additional research is needed to confirm the effect, investigate the exposure window of importance, and distinguish which pollutants cause harm.

We assessed the association between ambient pollutant concentrations and term birth weight for 1,548,904 births in TX from 1998 to 2004. Assignment of prenatal exposure to air pollutants was based on maternal county of residence at the time of delivery. Pollutants examined included particulate matter with aerodynamic diameter ≤10 and ≤2.5 µm (PM₁₀ and PM_2.5), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), carbon monoxide (CO), and ozone (O₃). We applied a linear model with birth weight as a continuous variable. The model was adjusted for known risk factors and region. We assessed pollutant effects by trimester to identify biological exposure window of concern, and explored interaction due to race/ethnicity.

An interquartile increase in ambient pollutant concentrations of SO₂ and O₃ was associated with a 4.99-g (95% confidence interval [CI], 1.87–8.11) and 2.72-g (95% CI, 1.11–4.33) decrease in birth weight, respectively. Lower birth weight was associated with exposure to O₃ in the first and second trimester, whereas results were not significant for other pollutants by trimester. A positive association was exhibited for PM_2.5 in the first trimester. Effects estimates for PM₁₀ and PM_2.5 were inconsistent across race/ethnic groups.

Current ambient air pollution levels may be increasing the risk of lower birth weight for some pollutants. These risks may be increased for certain racial/ethnic groups. Additional research including consideration of improved methodology is needed to investigate these findings. Future studies should examine the influence of residual confounding.

Implications: This is one of the most comprehensive studies examining criteria air pollutants and lower birth weight in Texas. Our findings confirm results found previously for adverse effects of the air pollutant SO₂ on lower birth weight. Results from our study suggest that adverse pregnancy outcomes such as lower birth weight can occur even while maintaining air pollution levels below regulatory standards. Future studies should incorporate the assessment of differential pollutant exposure as well as effect estimates by race/ethnicity with individual and community-level social factors in order to enhance our understanding of how physical, social, and host factors influence birth outcomes.

Supplemental Materials: Supplementary information relating to characteristics of excluded births, distribution of air pollutant monitors by pollutant, and correlation coefficients of the air pollutants is available in the publisher's online edition of the Journal of the Air & Waste Management Association.     

An occupational exposure assessment of polychlorinated dibenzo-p-dioxin and dibenzofurans in firefighters

Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) are unintentional byproducts of combustion and industrial processes. Firefighters face the risk of occupational exposure to PCDD/Fs. Congener-specific analyses of 17 PCDD/Fs were performed on 20 serum samples collected from firefighters and fire scene investigators, and four soot samples that had deposited on the surfaces of the fire helmets and were collected after the firefighters had fought fires. The PCDD/F concentrations on the helmets that were contaminated by being worn at the fire scenes were 63-285 times higher than those on a clean helmet. The median serum PCDD/F concentration of the 16 firefighters (12 pg WHO₂₀₀₅-TEQ g⁻¹ lipid) was not different from those of the males from the general Taiwanese population (9.4 pg WHO₂₀₀₅-TEQ g⁻¹ lipid). However, the median PCDD/F level in the four fire scene investigators (15 pg WHO₂₀₀₅-TEQ g⁻¹ lipid) was higher than those in the male from the general Taiwanese population (Mann-Whitney U test, p < 0.01). Furthermore, the serum samples from the firefighters and fire scene investigators, and the soot samples from the fire scenes presented similarly distinctive PCDD/F profiles that had elevated proportions for 10 PCDF congeners. Limited data indicated that the fire scene investigators were occupationally exposed to PCDD/Fs at the fire scenes. We suggested that the firefighters were not occupationally exposed to PCDD/Fs at the fire scenes due to appropriate protection. However, the fire scene investigators may have had more occupational exposure to PCDD/Fs due to poor protection, and further research must be performed to confirm this.     

Inhalation of two putative Gulf War toxins by mice

We employed our inhalation methodology to examine whether biomarkers of inflammation and oxidative stress would be produced in mice following inhalation of aerosols containing carbonaceous particles or the vapor of pesticides prevalent during the first Gulf War. Exposure to two putative Gulf War Illness toxins, fine airborne particles and the pesticide malathion, increased biomarkers of inflammation and oxidative stress in Friend virus B (FVB) female mice. Mice inhaling particles 24 h before had increased lung lavage and plasma Leukotriene B4 (LTB₄) (a biomarker of inflammation) and PGF_2α (a biomarker of oxidative stress) levels, lung lavage protein and lung lavage lactic dehydrogenase (LDH) levels. These changes were a function of particle density and exposure time. Compared to particle inhalation, mice inhaling malathion 24 h before had small increase in plasma LTB₄ and PGF_2α levels but no increase in lung lavage LTB₄, lung lavage protein, lung lavage LDH, and lung lavage alveolar macrophage (AM) levels compared to unexposed control mice. AM from particle-exposed mice contained phagocytosed particles, while AM from malathion-exposed mice showed no abnormalities. Our results indicate that inhaling particles or malathion can alter inflammatory and oxidative biomarkers in mice and raise the possibility that these toxins may have altered inflammation and oxidative stress biomarkers in Gulf War-exposed individuals.     

Epidemiological Bases for Possible Air Quality Criteria for Carbon Monoxide

Exposures to adequate environmental levels of CO will increase COHb concentrations in human subjects. The amount of this increase is reasonably predictable, and must be considered in relation to exposure to CO in inhaled cigarette smoke as well as to occupational and domestic exposures. The increase in body COHb will result in some degree of impairment of tissue oxygenation.

Methods for estimating COHb levels in large populations are relatively simple. The assumption that an exposure to 30 ppm CO for eight hours will produce on the average, an increase in COHb of 5%, has been substantiated by available data.

Exposure for five hours to between 10 and 12 ppm of CO has been shown to increase the COHb levels in nonsmokers by at least 0.5%. Such an increase adds appreciably to the body burden of COHb in those who do not already have such a body burden from cigarette smoking. Longer exposures could have produced a somewhat greater increase.

Apart from increases in COHb, three possible effects have been a source of major consideration in epidemiologic studies. The first is the production of some persistent toxic reaction. This possibility has been examined with respect to occupational exposure, and the evidence for the occurrence of such a condition is insufficient.

The possible contribution of ambient community CO exposure to the mortality of persons hospitalized with myocardial infarction has been investigated. The evidence suggests that daily average CO values in excess of about 10 ppm may be associated with an increase in mortality in hospitalized patients with myocardial infarction. Substantiation of this impression will require a study of the prognosis of myocardial infarction patients in relationship to COHb levels measured at admission to the hospital.

Finally, in two studies, persons driving motor vehicles which were involved in accidents had higher COHb levels than "control" populations. Controls were not ideal, however. Possible mechanisms by which CO might affect the ability to drive a motor vehicle is suggested in the available data on CO effects upon visual sensitivity, psychological test performance and accurate estimation of time intervals. As little as 2 percent COHb can produce these effects in laboratory studies, and the available epidemiologic information confirms that such an increase in COHb levels among drivers might influence the frequency of accidents.

Specific areas where research is indicated to clarify uncertainties relating to health effects of CO are: 1. The increment in COHb which can be produced by exposures to an average of 20 ppm CO for an eight hour period and the increment which can be produced by 15 ppm for such a period and by 10 ppm for up to twenty-four hours.

2. The relationship of ambient CO levels and of COHb levels to the survival of hospitalized patients with myocardial infarction.

3. The prognostic significance with respect to cardiovascular conditions of elevated levels of COHb.

4. The relationship, if any, between ambient CO and COHb levels and the occurrence of motor vehicle accidents when weather and driving conditions, cigarette smoking, alcohol and drug use, and other factors are adjusted and controlled.

     

PCB exposure and potential future cancer incidence in Slovak children: an assessment from molecular finger printing by Ingenuity Pathway Analysis (IPA®) derived from experimental and epidemiological investigations

The risk of cancer due to PCB exposure in humans is highly debated. In eastern Slovakia, high exposure of the population to organochlorines (especially PCBs) was associated with various disease and disorder pathways, viz., endocrine disruption, metabolic disorder & diabetes, and cancer, thereby disturbing several cellular processes, including protein synthesis, stress response, and apoptosis. We have evaluated a Slovak cohort (45-month children, at lower and higher levels of PCB exposure from the environment) for disease and disorder development to develop early disease cancer biomarkers that could shed new light on possible mechanisms for the genesis of cancers under such chemical exposures, and identify potential avenues for prevention.

Microarray studies of global gene expression were conducted from the 45-month-old children on the Affymetrix platform followed by Ingenuity Pathway Analysis (IPA®) to associate the affected genes with their mechanistic pathways. High-throughput qRT-PCR TaqMan low-density array (TLDA) was performed to further validate the selected genes on the whole blood cells of the most highly exposed children from the study cohort (n = 71).

TP53, MYC, BCL2, and LRP12 differential gene expressions suggested strong relationships between potential future tumor promotion and PCB exposure in Slovak children. The IPA analysis further detected the most important signaling pathways, including molecular mechanism of cancers, prostate cancer signaling, ovarian cancer signaling, P53 signaling, oncostatin M signaling, and their respective functions (viz., prostate cancer, breast cancer, progression of tumor, growth of tumor, and non-Hodgkin’s disease). The results suggest that PCB exposures, even at the early age of these children, may have lifelong consequences for the future development of chronic diseases.

     

Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO₂ inhalation exposure

Epidemiological studies suggest that NO₂ inhalation is associated with adverse effects on heart-related health, however, existing experimental data lack relevant evidences. In this study, a role for oxidative stress, endothelial dysfunction and inflammatory responses in the heart of rats treated with different concentrations of NO₂ (0, 5, 10 and 20 mg m⁻³) was investigated. Mild heart pathology occurred after 7-d exposure (6 h d⁻¹). Marked oxidative stress were induced as evaluated by reduction/induction of antioxidants (Cu/Zn-SOD, Mn-SOD and GPx) activity and increasing formation of MDA and PCO. Also, mRNA and protein biomarkers of vasoconstriction (ET-1, eNOS) and inflammation (TNF-α, IL-1β and ICAM-1) were up-regulated, and p53 mRNA expression, bax/bcl-2 ratio and the mean number of TUNEL-positive myocytes were increased as well. All the results implicate that NO₂ exerted injuries to mammals’ heart, and the damage mechanisms were possibly associated with oxidative stress, endothelial dysfunction and inflammation.     

Sublethal Effects of Monocrotophos on Locomotor Behavior and Gill Architecture of the Mosquito Fish,Gambusia affinis

Subacute studies of monocrotophos [Dimethyl (E)-1-methyl-2-(methyl-carbamoyl) vinyl phosphate] on mosquito fish, Gambusia affinis, were carried out in vivo for 24 days to assess the locomotor behavior, structural integrity of gill, and targeted enzyme acetylcholinesterase (AChE, EC: 3.1.1.7) interactions. Monocrotophos (MCP) can be rated as moderately toxic to G. affinis, with a median lethal concentration (LC₅₀) of 20.49 ± 2.45 mgL^?1. The fish exposed to sublethal concentration of LC₁₀ (7.74 mgL^?1) were under stress and altered their locomotor behavior, such as distance traveled per unit time (m min^?1) and swimming speed (cm sec^?1) with respect to the length of exposure. Inhibition in the activity of brain AChE and deformities in the primary and secondary lamellae of gill may have resulted in failure of exchange of gases. The maximum inhibition of 95% of AChE activity was observed on days 20 and 24.

Morphological aberrations in the gills were also studied during exposure to the sublethal concentration of monocrotophos for a period ranging from 8 to 24 days. The extent of damage in gill was dependent on the duration of exposure. The findings revealed that inhibition in brain AChE activity and structural alteration in gill were responsible for altering the locomotor behavior of exposed fish.     

Metabolic effects of diazinon on the European eel

Abstract

Eels were exposed to a sublethal diazinon concentration of 0.042 mg/L for exposure times of 6, 24, 48, 72 and 96 hours. Biochemical analyses of blood composition, such as plasma glucose, total plasma cholesterol and triglycerides, plasma lactate, plasma urea and uric acid, showed significant differences between treated and control animals. Plasma glucose and lactate increased after 6 hours exposure to the insecticide. Plasma cholesterol and triglycerides content decreased during 96 hours treatment. Urea levels increased at 72 hours while uric acid content decreased significantly at 24, 72 and 96 hours exposure to the pesticide.

The observed effects of diazinon on eel metabolism suggested that the treated fish was faced with a serious metabolic crisis, and the fish looked for alternative methods of metabolism to overcome the toxic stress.     

The interaction effects of FEN1 rs174538 polymorphism and polycyclic aromatic hydrocarbon exposure on damage in exon 19 and 21 of EGFR gene in coke oven workers

Polycyclic aromatic hydrocarbon (PAH) exposure and genetic susceptibility were conductive to genotoxic effects including gene damage, which can increase mutational probability. We aimed to explore the dose-effect associations of PAH exposure with damage of exons of epidermal growth factor receptor (EGFR) and breast cancer susceptibility gene 1 (BRCA1), as well as their associations whether modified by Flap endonuclease 1 (FEN1) genotype. Two hundred eighty-eight coke oven male workers were recruited, and we detected the concentration of 1-hydroxypyrene (1-OH-pyr) as PAH exposure biomarker in urine and examined base modification in exons of EGFR and BRCA1 respectively, and genotyped FEN1 rs174538 polymorphism in plasma. We found that the damage indexes of exon 19 and 21 of EGFR (EGFR-19 and EGFR-21) were both significantly associated with increased urinary 1-OH-pyr (both P_trend < 0.001). The levels of urinary 1-OH-pyr were both significantly associated with increased EGFR-19 and EGFR-21 in both smokers and nonsmokers (both P < 0.001). Additionally, we observed that the urinary 1-OH-pyr concentrations were linearly associated with both EGFR-19 and EGFR-21 only in rs174538 GA+AA genotype carriers (both P < 0.001). Moreover, FEN1rs rs174538 showed modifying effects on the associations of urinary 1-OH-pyr with EGFR-19 and EGFR-21 (both P_interaction < 0.05). Our findings revealed the linear dose-effect association between exon damage of EGFR and PAH exposure and highlight differences in genetic contributions to exon damage and have the potential to identify at-risk subpopulations who are susceptible to adverse health effects induced by PAH exposure.

     

Exposure to pyriproxyfen (juvenile hormone agonist) does not alter maternal care and reproduction in the European earwig

Sublethal exposure to pesticides can alter the survival and reproduction of a wide range of non-target organisms. However, it remains unclear whether this exposure can alter behaviours that are often essential for long-term population dynamics and maintenance, such as parental care. In this study, we tested the effect of pyriproxyfen exposure (an insect growth regulator) on maternal care in the European earwig, an insect that is both used in pest control in pip-fruit orchards and considered a pest in stone fruit orchards. We exposed 424 females at doses either 10 times lower, equivalent or 10 times higher than normal application rates in French orchards. As maternal care can change over the weeks of family life, we exposed the earwig mothers at five different days before and after egg hatching. We then measured the expression of ten forms of maternal care towards eggs and juveniles, six non-caring behaviours, eggs and juvenile development, metabolic reserves in mothers at egg hatching and females’ production of a terminal clutch. First, our results revealed that the three tested doses of pyriproxyfen were non-lethal and confirmed that maternal care decreased throughout both pre- and post-hatching family life. However, we did not detect any effect of pyriproxyfen on maternal care and non-care behaviours, eggs and juvenile development, quantities of lipids, proteins and glycogen in mothers at egg hatching, and on the production of a future clutch. Overall, these findings suggest that the maximal doses of pyriproxyfen authorized in French orchards is likely to have limited effects on the short- and long-term maintenance of populations of the European earwig and raises fundamental questions about the nature of the link between juvenile hormone and parental care in insects.

     

Influence of nutrition in PCB-induced vascular inflammation

The nutritional profile of an individual can influence the toxicity of persistent environmental toxicants. Polychlorinated biphenyls (PCBs), prevalent environmental pollutants, are highly lipid-soluble toxic compounds that biomagnify through trophic levels and pose cancer, neurocognitive, and atherosclerotic risk to human populations. There is a growing body of knowledge that PCBs can initiate inflammatory responses in vivo, and this inflammation can be either exacerbated or ameliorated by nutrition. Data indicate that diets high in certain dietary lipids such as omega-6 fatty acids can worsen PCB-induced vascular toxicity while diets enriched with bioactive food components such as polyphenols and omega-3 polyunsaturated fatty acids can improve the toxicant-induced inflammation. There is evidence that bioactive nutrients protect through multiple cell signaling pathways, but we have shown that lipid raft caveolae and the antioxidant defense controller nuclear factor (erythroid-derived 2)-like 2 (Nrf2) both play a predominant role in nutritional modulation of PCB-induced vascular toxicity. Interestingly, there appears to be an intimate cross-talk between caveolae-related proteins and cellular Nrf2, and focusing on the use of specific bioactive food components that simultaneously alter both pathways may produce a more effective and efficient cytoprotective response to toxicant exposure. The use of nutrition as a protective tool is an economically beneficial means to address the toxicity of persistent environmental toxicants and may become a sensible means to protect human populations from PCB-induced vascular inflammation and associated chronic diseases.     

Genotype-specific responses of fluctuating asymmetry and of preadult survival to the effects of lead and temperature stress in Drosophila melanogaster

Although fluctuating asymmetry (FA) increases with exposure to certain types of environmental stressors such as temperature extremes, relatively little is known about the effects of interaction (e.g., synergism) between known sources of environmental stress on FA. Knowledge of such interaction effects, and of the magnitude of genotype-by-environment interaction, are of fundamental importance toward predicting the usefulness of FA as a bioindicator of environmental pollution. We tested for synergistic effects on FA between elevated temperature and exposure to lead, and examined FA responses simultaneously in four genetic strains of Drosophila melanogaster known to differ in their degree of developmental instability, and presumably in their buffering capacity. In the absence of heavy metal, bristle FA increased with temperature, but in the presence of lead, FA at high temperature (30 (degrees)C) was reduced to levels similar, or below, that at lower temperature (25 (degrees)C). This temperature by lead interaction was statistically significant, but paradoxical in that the disruptive effects of temperature appeared to be attenuated in the presence of the heavy metal. In no case was there a significant effect of lead on bristle FAs, despite documented assimilation of heavy metal by flies, and in no case was the genotype by environment interaction significant. Whereas lead treatment did not influence survival, survival was reduced at the high temperature, but significantly so only in one genetic strain (Oregon-R). There was no relationship between survival and FA across stress treatments within lines. Thus, any disproportionate stress-induced mortality in developmentally unstable classes (developmental selection) was unlikely to bias the FA results. Our results underscore the need for independent replication of significant findings before FA-based biomonitoring can be responsibly and effectively implemented. The results call for caution in using FA as a biomarker of stress, because stress factors may interact in complex and unpredictable ways, which could result in erroneous conclusions about real levels of stress present in field populations, under the unduly simplistic assumption that stress factors will act additively to increase FA.     

Investigation of chloramine-T impact on crayfish Astacus leptodactylus (Esch., 1823) cardiac activity

The crayfish play an essential role in the biomonitoring and may reflect ambient water quality through the biochemical, behavioural and physiological reactions. To assess whether narrow-clawed crayfish Astacus leptodactylus can respond by heart rate changes to presence in water of such biocide as chloramine-T, adult males were exposed to its low (2 and 5 mg L^?1), moderate (10 mg L^?1, commonly used in industry and aquaculture) and exceeded (20 and 50 mg L^?1) concentrations. In addition, a physical stress test evaluated energy expenditure following the chemical trials. Three key reactions (cardiac initial, first-hour and daily prolonged exposure) were discussed with particular focus on crayfish initial reaction as the most meaningful in on-line water quality biomonitoring. After short-term exposure to both chloramine-T concentrations, crayfish were found to respond rapidly, within 2–5 min. According to heart rate changes, the 1-h exposure did not adversely affect crayfish at either concentration, as well as during daily exposure to 10 mg L^?1. As assessed by the heart rate, the 24-h exposure to 50 mg L^?1 of chloramine-T was toxic for crayfish and led to substantial loss of energy that became apparent during subsequently conducted physical stress. The results supported a hypothesis that crayfish vital functions are connected with environment they inhabit closely enough to serve as biological monitors. Crayfish were tolerant to short-term chloramine-T exposure, while rapid crayfish reaction to an increased chemical level indicated their high sensitivity, an essential attribute of real-time environmental assessment.     

Bioconcentration,behavioral, and biochemical effects of the non-steroidal anti-inflammatory drug diclofenac in Daphnia magna

The non-steroidal anti-inflammatory drug (NSAID) diclofenac is one of the most frequently studied as well as controversially discussed pharmaceutically active drug on the subject of its relevance to the environment. This study was conducted to assess the bioconcentration potential of diclofenac and its behavioral and biochemical effects in Daphnia magna. The bioconcentration factors of diclofenac determined after 48 h of aqueous exposure in Daphnia magna were 70.94 and 8.02 for the nominal exposure concentrations of 5 and 100 μg/L, respectively. Diclofenac exposure obviously decreased the filtration and ingestion rates of the daphnids. A significant increase of the acetylcholinesterase activity that was observed in this study indicates that diclofenac might not have neurobehavioral toxicity in Daphnia magna. Significant induction of malondialdehyde content is an indication of overproduction of reactive oxygen species leading to oxidative damage in daphnids after diclofenac exposure. Moreover, significant inhibition of the superoxide dismutase, catalase, and glutathione reductase activities implies that the antioxidant defense system of Daphnia magna was overwhelmed. Also, significant inhibition of glutathione s-transferase activity might point to the fact that the enzyme was not capable to detoxify diclofenac in Daphnia magna. These findings indicate that diclofenac can accumulate and consequently stimulate behavioral and biochemical disturbances in Daphnia magna.

     

Ecotoxicological impact assessment of the brine discharges from a desalination plant in the marine waters of the Algerian west coast,using a multibiomarker approach in a limpet,Patella rustica

The aim of our study is to evaluate the impact of Bousfer desalination plant brine discharges on the Algerian west coast, on a natural population of the marine gastropod mollusc Patella rustica. The effects of a chronic exposure to such discharges are complex to understand due to the combined effects of environmental physico-chemical parameters (e.g., high salinity) and different pollutants that can modulate the physiological responses of this species to stress. In this context, we assessed the biological effects in a marine species P. rustica, by a multibiomarker approach that provided information on the health status of organisms in response to such an environmental stress. We measured biomarkers in the whole soft tissues of limpets as indicators of neurotoxicity (AChE activity), oxidative stress (CAT, SOD, GR, and GPx activities), biotransformation (GST), oxidative damage (LPO through TBARS levels), and genotoxicity (CSP 3-like activity). In parallel, hydrological parameters were measured in the Bay of Oran, at four selected sites: site H considered as a “hotspot,” located at Bousfer desalination plant; two other sites E and W, at the east and the west of H respectively; finally, site R “reference” located in Madragh, which is considered as a remote clean site. Our analyses revealed that the activities of antioxidant defense enzymes reached the highest levels in P. rustica collected from site H. The activation of antioxidant defense system in these organisms translated the alteration of their status health, reflecting a level of environmental disruption generated by the desalination plant brine discharges and the high salinity in this area. We also observed that the tissues of limpets collected from site H as well as the two other sites, E and W, had undergone molecular damage, confirmed by the high levels of CSP 3-like activity. This damage resulted from chronic exposure to environmental conditions, potentially genotoxic, due to the desalination plant discharges. The present results indicate the adverse impact of brine effluents from desalination plants on marine fauna and suggest the need for a more consistent approach to environmental management of brine discharges.

     

Inhalation of Concentrated Ambient Particulate Matter near a Heavily Trafficked Road Stimulates Antigen-Induced Airway Responses in Mice

Abstract

The goal of this study was to test the following hypotheses:(1) exposure to mobile emissions from mobile sources close to a heavily trafficked roadway will exacerbate airway inflammation and allergic airway responses in a sensitized mouse model, and (2) the magnitude of allergic airway disease responses will decrease with increasing distance from the roadway. A particle concentrator and a mobile exposure facility were used to expose ovalbumin (OVA)-sensitized BALB/c mice to purified air and concentrated fine and concentrated ultrafine ambient particles at 50 m and 150 m downwind from a roadway that was heavily impacted by emissions from heavy duty diesel-powered vehicles. After exposure, we assessed interleukin (IL)-5, IL-13, OVA-specific immunoglobulin E, OVA-specific immunoglobulin G1, and eosinophil influx as biomarkers of allergic responses and numbers of polymorphonuclear leukocytes as a marker of inflammation. The study was performed over a two-year period, and there were differences in the concentrations and compositions of ambient particulate matter across those years that could have influenced our results. However, averaged over the two-year period, exposure to concentrated ambient particles (CAPs) increased the biomarkers associated with airway allergies (IL-5, immunoglobulin E, immunoglobulin G1 and eosinophils). In addition, mice exposed to CAPs 50 m downwind of the roadway had, on the average, greater allergic responses and showed greater indications of inflammation than did mice exposed to CAPs 150 m downwind. This study is consistent with the hypothesis that exposure to CAPs close to a heavily trafficked roadway influenced allergic airway responses.     

Effects of the lichen Peltigera canina on Cucurbita pepo spp. pepo grown in soil contaminated by DDTs

Lichens consisting of a symbiotic association of green algae or cyanobacteria and fungi are found in a variety of environmental conditions worldwide. Terricolous lichens, located in soils, affect the living and lifeless environment of the soil due to their effective secondary metabolite and enzymatic content. Terricolous lichens can increase the biological, chemical, and physical usefulness of soil. However, their effects in ensuring the bioavailability of contaminated soil are not known, especially on soil pollution caused by DDTs (p,p′-DDE, p,p′-DDD, p,p′-DDT). This research focuses on the effect of terricolous lichens on zucchini (Cucurbita pepo spp. pepo) grown in soil contaminated by DDTs, utilizing their secondary metabolite and enzymatic contents. Firstly, Peltigera canina, a terricolous lichen species, was added to soil contaminated by DDTs as powdered and intact thallus. After lichen addition to soil, zucchini was planted in. The oxidative stress and antioxidative enzyme activities of zucchini were measured. According to the results, P. canina treatments have a positive effect on the growth and development of zucchini, although oxidative stress was observed. Also, it was determined that powdered application had more effective results than intact thallus application.