Comparative sensitivity of harbour and grey seals to several environmental contaminants using in vitro exposure (original) (raw)
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Aquatic Mammals, 2010
This study investigated in vitro the effects of methylmercury chloride (CH3HgCl), zinc chloride (ZnCl2), cadmium chloride (CdCl2), lead acetate (Pb(C2H3O2)2), and PCBs (Aroclor mixtures) on the proliferation of T lymphocytes from the thymus, lymph node, and blood from one female grey seal (Halichoerus grypus) juvenile. After exposure to heavy metals, a dose-response curve was observed with a decrease in proliferation of both T lymphocytes from blood and the lymph node. Exposure to Aroclor mixtures led to a mostly reduced proliferation of thymocytes and T lymphocytes from the lymph node and blood. Lymph node cells seem less sensitive to heavy metals than peripheral blood lymphocytes. Lymph node lymphocytes are more sensitive to PCBs than peripheral blood lymphocytes but less than thymocytes. These results suggest that the sensitivity of T lymphocytes from one grey seal to contaminants may be due to inherent tissue/matrix differences in the sensitivity of these cells to contaminants; however, an individual response cannot be excluded in the present case. That is, samples from a single individual are not extrapolated to the species as a whole in this paper but discussed relative to exposure response by tissues.
Mercury immune toxicity in harbour seals: links to in vitro toxicity
Environmental health : a global access science source, 2008
Background: Mercury is known to bioaccumulate and to magnify in marine mammals, which is a cause of great concern in terms of their general health. In particular, the immune system is known to be susceptible to long-term mercury exposure. The aims of the present study were (1) to determine the mercury level in the blood of free-ranging harbour seals from the North Sea and (2) to examine the link between methylmercury in vitro exposure and immune functions using seal and human mitogen-stimulated peripheral blood mononuclear cells (T-lymphocytes).
Aquatic Toxicology, 2013
In vitro culture of peripheral blood leucocytes (PBLs) is currently used in toxicological studies of marine mammals. However, blood cells of wild individuals are exposed in vivo to environmental contaminants before being isolated and exposed to contaminants in vitro. The aim of this study was to highlight potential relationships between blood contaminant levels and in vitro peripheral blood lymphocyte proliferation in free-ranging adult harbour seals (Phoca vitulina) from the North Sea. Blood samples of 18 individuals were analyzed for trace elements (Fe, Zn, Se, Cu, Hg, Pb, Cd) and persistent organic contaminants and metabolites ( PCBs, HO-PCBs, PBDEs, 2-MeO-BDE68 and 6-MeO-BDE47, DDXs, hexachlorobenzene, oxychlordane, trans-nonachlor, pentachlorophenol and tribromoanisole). The same samples were used to determine the haematology profiles, cell numbers and viability, as well as the in vitro ConA-induced lymphocyte proliferation expressed as a stimulation index (SI). Correlation tests (Bravais-Pearson) and Principal Component Analysis with multiple regression revealed no statistically significant relationship between the lymphocyte SI and the contaminants studied. However, the number of lymphocytes per millilitre of whole blood appeared to be negatively correlated to pentachlorophenol (r = −0.63, p = 0.005). In adult harbour seals, the interindividual variations of in vitro lymphocyte proliferation did not appear to be directly linked to pollutant levels present in the blood, and it is likely that other factors such as age, life history, or physiological parameters have an influence. In a general manner, experiments with in vitro immune cell cultures of wild marine mammals should be designed so as to minimize confounding factors in which case they remain a valuable tool to study pollutant effects in vitro.
Developmental & Comparative Immunology, 2003
Mercury is the principal metal contaminant in the St Lawrence Estuary. It impairs humoral, cellular and non-specific immune responses in many species. Since the immune system of juvenile seals is immature, it should react differently to the effects of contamination compared to that of mature animals. Phagocytosis and lymphoblastic transformation responses have been evaluated in the peripheral blood leukocytes of eight juvenile grey seals at different intervals of time over 11 weeks. Doseresponse curves of 10 29-10 23 M of methylmercury chloride have also been performed in vitro for evaluation of these two immune functions. The immune response of grey seals differs during their development. The phagocytosis response increased from the 2nd to 5th week post-weaning and then reached a plateau. As for the lymphoblastic transformation response, it was stable from the 2nd to the 3rd week post-weaning, increased significantly at week 4 post-weaning and then reached a plateau. These data suggest that these animals should be particularly vulnerable to infections, diseases and parasites before the 5th week post-weaning. Furthermore, mercury decreased the immune response, and age of seals had an effect on cell sensitivity to mercury. Concentrations of 10 25 M of methylmercury chloride decreased phagocytosis and lymphoblastic transformation responses. Phagocytosis is more affected by MeHgCl contamination before this immune function reaches complete development which occurs at week 5 post-weaning. On the other hand, lymphoblastic transformation is more affected by this contaminant after its complete development which occurs at week 4 post-weaning.
Metal-Induced Impairment of the Cellular Immunity of Newborn Harbor Seals (Phoca Vitulina)
Archives of Environmental Contamination and Toxicology, 2008
The cellular immunity of newborn harbor seals and the influence of pollutants are rarely investigated. This study evaluated the lymphocyte proliferation using a lymphocyte proliferation test (LTT) to understand the dynamics of immune response in seal pups of varying ages from the moment they arrived in a seal center after active beaching until their release into wildlife 3 months later after rehabilitation. Moreover, the effect of various metals (Ag, Al, Au, Be, Cd, Co, Cr, Cu, different Hg compounds, Mo, Ni, Pb, Pd, Pt, Sn, Ti) on lymphocyte proliferation in terms of immunosuppression and hypersensitivity was investigated. First, a strong lymphocyte proliferation in newborns as a reflection of relative immunocompetence was found. Second, different metal-induced influences on lymphocyte proliferation such as specific inhibition by Be, Cd, Hg, and Sn as well as stimulation induced by Mo and Ni were determined. For seals tested repeatedly, the suppressive effect was detected in newborns but not found in the same animals when they were older and had become immunologically competent. Summarizing, the lymphocyte proliferation used as a marker in this investigation provided useful immunological information on these developing animals, and its application for toxicological studies on pollutants can be recommended.
Immunotoxic effects of environmental pollutants in marine mammals
Due to their marine ecology and life-history, marine mammals accumulate some of the highest levels of environmental contaminants of all wildlife. Given the increasing prevalence and severity of diseases in marine wildlife, it is imperative to understand how pollutants affect the immune system and consequently disease susceptibility. Advancements and adaptations of analytical techniques have facilitated marine mammal immunotoxicology research. Field studies, captive-feeding experiments and in vitro laboratory studies with marine mammals have associated exposure to environmental pollutants, most notable polychlorinated biphenyls (PCBs), organo-chlorine pesticides and heavy metals, to alterations of both the innate and adaptive arms of immune systems, which include aspects of cellular and humoral immunity. For marine mammals, reported immunotoxicology endpoints fell into several major categories: immune tissue histopathology, haematology/circulating immune cell populations, functional immune assays (lymphocyte proliferation, phagocytosis, respiratory burst, and natural killer cell activity), immunoglobulin production, and cytokine gene expression. Lymphocyte proliferation is by far the most commonly used immune assay, with studies using different organic pollutants and metals predominantly reporting immunosuppressive effects despite the many differences in study design and animal life history. Using combined field and laboratory data, we determined effect threshold levels for suppression of lymphocyte proliferation to be between b0.001–10 ppm for PCBs, 0.002–1.3 ppm for Hg, 0.009–0.06 for MeHg, and 0.1–2.4 for cadmium in polar bears and several pinniped and cetacean species. Similarly, thresholds for suppression of phagocytosis were 0.6–1.4 and 0.08–1.9 ppm for PCBs and mercury, respectively. Although data are lacking for many important immune endpoints and mechanisms of specific immune alterations are not well understood, this review revealed a systemic suppression of immune function in marine mammals exposed to environmental contaminants. Exposure to immunotoxic contaminants may have significant population level consequences as a contributing factor to increasing anthropogenic stress in wildlife and infectious disease outbreaks.
Immunological Impact of Metals in Harbor Seals ( Phoca vitulina ) of the North Sea
Environmental Science & Technology, 2005
Environmental pollutants may affect the immune system of marine mammals in many areas of the industrialized world. This study provides the first evidence for metal-induced hypersensitivity in harbor seals and demonstrates a relationship between this immunopathy and the level of metals in blood. The concentrations of 20 essential and nonessential elements were analyzed in the blood of 13 harbor seals from the North Sea. In addition, their T-lymphocyte response to metals in terms of hypersensitivity was investigated using a lymphocyte transformation test (LTT) according to the MELISA (memory lymphocyte immunostimulation assay) modification. The results showed metal hypersensitivities in 7 of 11 seals investigated in MELISA (data from two seals could not be assessed), reflecting a positive or possible positive reaction in 13 of 154 total single tests. Four animals responded to one metal and three animals to multiple metals. The sensitizing metals were molybdenum (Mo), titanium (Ti), nickel (Ni), chromium (Cr), aluminum (Al), lead (Pb), and tin (Sn). Furthermore, the seals with a Ni-, Al-, and Cr-sensibilization showed the highest concentrations of these metals in blood. In 8 of the 13 positive cases, elevated blood metal concentrations correlated with the hypersensitivity reaction. Summarizing, we demonstrate in this first pilot study the potential immunological impact of metals in seals, a topic rarely investigated previously. Our results show the value of a combined biological and effect-monitoring tool to investigate pollution-induced immunopathies in live animals.
Study of Methylmercury and Selenium Effects on Harbor Seal (Phoca Vitulina) T Lymphocytes in Vitro
Belgium, 27 November 2009: VLIZ Special Publication, 43. Vlaams Instituut voor de Zee (VLIZ): Oostende, Belgium. xiii+ 221 pp., 2009
Mercury (Hg) is a widespread pollutant which organic form, methylmercury (MeHg), gains particular attention because of its numerous toxic properties, notably towards the immune system. The MeHg is formed by methylation of inorganic mercury through microbial activity, and undergoes the process of biomagnification leading to increasing concentrations at higher trophic levels (Palmisano et al., 1995). It is mainly absorbed by the digestive tract of marine mammals and constitutes the predominant form of mercury present in their blood ( ...
Proliferative Responses of Harbor Seal (Phoca vitulina) T Lymphocytes to Model Marine Pollutants
Developmental Immunology, 2002
In recent years, population declines related to viral outbreaks in marine mammals have been associated with polluted coastal waters and high tissue concentrations of certain persistent, lipophilic contaminants. Such observations suggest a contributing role of contaminant-induced suppression of cell-mediated immunity leading to decreased host resistance. Here, we assessed the effects of the prototypic polycyclic aromatic hydrocarbon (PAH), benzo[a]pyrene (B[a]P), and two polychlorinated biphenyls (PCBs), CB-156 and CB-80, on the T-cell proliferative response to mitogen in harbor seal peripheral lymphocytes. Despite the variability associated with our samples from free-ranging harbor seals, we observed a clear suppressive effect of B[a]P (10 uM) exposure on T cell mitogenesis. Exposures to 10 uM CB-156 and CB-80, and 1.0 and 0.1 uM B[a]P, did not produce significant depression in lymphoproliferation. Exposure to the model PAH at 10 uM resulted in a 61% (range 34 -97%) average reduction in lymphoproliferation. We were able to rule out a direct cytotoxic effect of B[a]P, indicating that observed effects were due to altered T cell function. Based on our in vitro results, we hypothesize that extensive accumulation of PAH by top-trophic-level marine mammals could alter T cell activation in vivo and impaired cell-mediated immunity against viral pathogens.
Aquatic Toxicology, 2005
Polychlorinated biphenyls (PCBs) are known to have detrimental effects on the innate immune system of several mammalian species. Top predators such as marine mammals may be badly affected as PCBs can bioaccumulate in their blubber to high concentrations and previous studies have suggested that harbour seals may be particularly vulnerable to the immunotoxic effects of such contaminants. To investigate the effects of PCBs on innate immune functions in phocid seals, blood samples were collected from harbour and grey seals and exposed in vitro to a mixture of Aroclors. Separated mononuclear (PBMCs) and polymorphonuclear (PMNCs) leukocytes from each species were incubated with Aroclors (at 3 and 30 ng ml −1 ) for 3 and 24 h incubation periods, after which phagocytosis, respiratory burst and cytotoxic activity were measured. The phagocytic activity of harbour seal PMNCs was decreased at both incubation times and at both Aroclor concentrations tested, but there was no effect on the grey seals. Similarly, the respiratory burst activity of harbour seals was decreased at both incubation times, but only at the higher concentration used. There were no differences in the cytotoxic activity of the PBMCs with respect to incubation times or concentrations in either species. However, differences were observed in the level of cytotoxic activity against YAC-1 target cells, with the grey seal PBMCs showing higher levels of activity. The observed differences in phagocytosis, respiratory burst and cytotoxic activity of the leukocytes following incubation with PCBs may have implications for the previously recorded differences in disease susceptibility between grey and harbour seals.