Risk assessment of SARS-CoV-2 replicating and evolving in animals.

The retransmissions of SARS-CoV-2 from several mammals - primarily mink and white-tailed deer - to humans have raised concerns for the emergence of a new animal-derived SARS-CoV-2 variant to worsen the pandemic. Here, we discuss animal species that are susceptible to natural or experimental infection with SARS-CoV-2 and can transmit the virus to mates or humans. We describe cutting-edge techniques to assess the impact of a mutation in the viral spike (S) protein on its receptor and on antibody binding. Our review of spike sequences of animal-derived viruses identified nine unique amino acid exchanges in the receptor-binding domain (RBD) that are not present in any variant of concern (VOC). These mutations are present in SARS-CoV-2 found in companion animals such as dogs and cats, and they exhibit a higher frequency in SARS-CoV-2 found in mink and white-tailed deer, suggesting that sustained transmissions may contribute to maintaining novel mutations. Four of these exchanges, such as Leu452Met, could undermine acquired immune protection in humans while maintaining high affinity for the human angiotensin-converting enzyme 2 (ACE2) receptor. Finally, we discuss important avenues of future research into animal-derived viruses with public health risks.

The basis of mink susceptibility to SARS-CoV-2 infection.

Of all known airborne diseases in the twenty-first century, coronavirus disease 19 (COVID-19) has the highest infection and death rate. Over the past few decades, animal origin viral diseases, notably those of bats-linked, have increased many folds in humans with cross-species transmissions noted and the ongoing COVID-19 pandemic has emphasized the importance of understanding the evolution of natural hosts in response to viral pathogens. Cross-species transmissions are possible due to the possession of the angiotensin-converting enzyme 2 (ACE2) receptor in animals. ACE2 recognition by SARS-CoV-2 is a critical determinant of the host range, interspecies transmission, and viral pathogenesis. Thus, the phenomenon of breaking the cross-species barrier is mainly associated with mutations in the receptor-binding domain (RBD) of the spike (S) protein that interacts with ACE2. In this review, we raise the issue of cross-species transmission based on sequence alignment of S protein. Based on previous reports and our observations, we can conclude that the occurrence of one of two mutations D614G or Y453F is sufficient for infection of minks by SARS-CoV-2 from humans. Unfortunately, D614G is observed in the world's most common line of virus B.1.1.7 and the latest SARS-CoV-2 variants B.1.617.1, B.1.617.2, and B.1.617.3 too.

Urinary and plasma metabolome of farm mink (Neovison vison) after an intervention with raw or cooked poultry offal: a 1H NMR investigation.

The introduction of high amounts of cooked poultry offal in mink feed has been associated with health problems in growing mink. Cooking mink feed is a convenient way of reducing microbiological activity, but it may have a negative effect on raw material quality and animal welfare. This study investigates growth and health of mink fed raw or cooked poultry offal and describes urinary and blood plasma metabolic changes related to the feeding. A total of 65 male mink were divided in three feeding groups, two fed cooked offal and one group fed raw offal, and the plasma and urine samples were collected at 3 time points during the growth. Both bio-fluids and feed samples were measured by 1H NMR spectroscopy and resulted metabolomics data were analysed using univariate and multivariate statistical methods that revealed dominating effect of the mink growth stages and to a less extent the feeding regime. Metabolome differences in relation to low body mass index (BMI) and kidney lesions were observed in plasma. Disease and decrease in BMI was associated with high creatinine and dimethylglycine content in plasma. These molecules were also particularly indicative of the cooked feeds. Moreover, low urinary taurine levels were also associated with disease and low BMI. Individual mink appeared to show negative effects of the cooked feed diet, including impaired growth and gross pathological lesions involving the kidneys. This may be related to the absorption of essential metabolites such as amino acids and fats, necessary for mink growth, that are negatively impacted by the cooking process.

Identification and primary application of hybridomas cell secreting monoclonal antibodies against mink (Neovison vison) interferon-gamma.

Due to their susceptibility to several human viruses, the mink has been proposed as potential animal models for the study of human viral infections. However, there are no specific monoclonal antibody (mAbs) currently available for the detection of mink-specific interferon-gamma (miIFN-γ). The BALB/c mice were immunized intraperitoneally with purified recombinant miIFN-γ protein. The splenocytes were obtained and fused with murine myeloma cells. Five of 24 hybridoma clones were obtained to produce mAbs steadily with the strongest affinity to recombinant miIFN-γ protein. The isotype of the 31A, 31B and 31G were lgG 2b. The isotype of 44 and 46 were lgG 2a and 1. All five mAbs were κ light chains. Western blotting and indirect ELISA method showed that 5 mAbs were positive to miIFN-γ. Immunofluorescence showed that 2 mAbs (44 and 46) had a positive reaction to miIFN-γ. The hybridoma clone 46 had the highest sensitivity for the detection of miIFN-γ. Most importantly, our primary sandwich ELISA system (mAbs 46 and polyclonal antiserum) detected endogenous IFN-γ in mink lymphocytes infected with canine distemper virus (CDV). We have thus developed a novel mAbs could recognize miIFN-γ, and have demonstrated the first ELISA-based measurement of IFN-γ in lymphocyte of the mink.

Absorption of α-tocopheryl acetate is limited in mink kits (Mustela vison) during weaning.

Bioavailability of α-tocopherol varies with source, dose and duration of supplementation. The effect of source and dose of α-tocopherol on response of α-tocopherol stereoisomers in plasma and tissues of mink kits during the weaning period was studied. Twelve mink kits were euthanised in CO2 at the beginning of the experiment, and 156 mink kits (12 replicates per treatment group) were randomly assigned to thirteen treatment groups: no added α-tocopherol in the feed (0 dose) or four different doses (50, 75, 100 and 150 mg/kg of diet) of RRR-α-tocopherol (ALC), RRR-α-tocopheryl acetate (ACT) or all-rac-α-tocopheryl acetate (SYN). Six mink kits per treatment group were euthanised 3 weeks after initiation of the experiment, and the remaining six were euthanised 6 weeks after initiation of the experiment. The RRR-α-tocopherol content in plasma, liver, heart and lungs was affected by interaction between source and dose (P < 0.01 for all). The highest RRR-α-tocopherol content in plasma (13.6 µg/ml; LS-means for source across dose and week), liver (13.6 µg/mg), heart (7.6 µg/mg) and lungs (9.8 µg/mg) was observed in mink kits fed ALC. The RRR-α-tocopherol content in plasma and tissues depended on source and dose interaction and increased linearly with supplementation. In conclusion, the interaction between source and dose reveals a limitation in hydrolysis of ester bond in α-tocopheryl acetate in mink kits around weaning as the likely causative explanation for the higher response of ALC at the highest doses. Thus, considerable attention has to be paid to the source of α-tocopherol during weaning of mink kits fed a high dose of α-tocopherol.

Fifty Years of Research on European Mink Mustela lutreola L., 1761 Genetics: Where Are We Now in Studies on One of the Most Endangered Mammals?

The purpose of this review is to present the current state of knowledge about the genetics of European mink Mustela lutreola L., 1761, which is one of the most endangered mammalian species in the world. This article provides a comprehensive description of the studies undertaken over the last 50 years in terms of cytogenetics, molecular genetics, genomics (including mitogenomics), population genetics of wild populations and captive stocks, phylogenetics, phylogeography, and applied genetics (including identification by genetic methods, molecular ecology, and conservation genetics). An extensive and up-to-date review and critical analysis of the available specialist literature on the topic is provided, with special reference to conservation genetics. Unresolved issues are also described, such as the standard karyotype, systematic position, and whole-genome sequencing, and hotly debated issues are addressed, like the origin of the Southwestern population of the European mink and management approaches of the most distinct populations of the species. Finally, the most urgent directions of future research, based on the research questions arising from completed studies and the implementation of conservation measures to save and restore M. lutreola populations, are outlined. The importance of the popularization of research topics related to European mink genetics among scientists is highlighted.

All-trans-retinoic acid inhibits mink hair follicle growth via inhibiting proliferation and inducing apoptosis of dermal papilla cells through TGF-ß2/Smad2/3 pathway.

Dermal papilla cells (DPCs), an important component of hair follicles, its proliferation and apoptosis directly regulate and maintain the growth of hair follicles. All-trans-retinoic acid (ATRA) plays a critical role in hair growth. In this study, the effects of ATRA on cultured mink hair follicle growth were studied by administration of different concentrations of ATRA for 12 days in vitro. In addition, the proliferation and apoptosis of DPCs were measured after treating with ATRA. The mRNA and protein levels of hair follicle growth associated factor transforming growth factor-ß2 (TGF-ß2) and the phosphorylation levels of Smad2/3 were determined. Moreover, TGF-ß type I and type II receptor inhibitor LY2109761 and specific inhibitor of Smad3 (SIS3) were administered to investigate the underlying molecular mechanism. The results showed that ATRA inhibited hair follicle growth, promoted TGF-ß2 expression and activated phosphorylation of Smad2/3. In addition, ATRA inhibited cell proliferation by arresting the cell cycle at G1 phase and induced apoptosis of DPCs by enhancing the ratio of Bax/Bcl-2 and promoted the cleavage of caspase-3. Furthermore, LY2109761 or SIS3 partially reversed the decreased cell viability, increased apoptosis that were induced by ATRA. In conclusion, ATRA could inhibit hair follicle growth via inhibiting proliferation and inducing apoptosis of DPCs partially through the TGF-ß2/Smad2/3 pathway.

Comparative transcriptome analysis of embryo invasion in the mink uterus.

INTRODUCTION: In mink, as many as 65% of embryos die during gestation. The causes and the mechanisms of embryonic mortality remain unclear. The purpose of our study was to examine global gene expression changes during embryo invasion in mink, and thereby to identify potential signaling pathways involved in implantation failure and early pregnancy loss. METHODS: Illumina's next-generation sequencing technology (RNA-Seq) was used to analyze the differentially expressed genes (DEGs) in implantation (IMs) and inter-implantation sites (inter-IMs) of uterine tissue. RESULTS: We identified a total of 606 DEGs, including 420 up- and 186 down-regulated genes in IMs compared to inter-IMs. Gene annotation analysis indicated multiple biological pathways to be significantly enriched for DEGs, including immune response, ECM complex, cytokine activity, chemokine activity and protein binding. The KEGG pathway including cytokine-cytokine receptor interaction, Jak-STAT, TNF and the chemokine signaling pathway were the most enriched. A gene network was constructed, and hub nodes such as CSF3, ICAM1, FOS, IL1B, IL8, CD14 and MYC were found through network analysis. DISCUSSION: This report provides a valuable resource for understanding the mechanisms of embryo implantation in mink.

Transfer of amoxicillin to suckling mink (Neovison vison) kits via the milk from dams treated orally or intra-muscularly.

Treatment of mink kits with pre-weaning diarrhea (PWD) can be time-consuming and expensive for the farmer, and the efficacy of the treatment procedure may be questioned. Evidence-based treatment protocols for application on affected animals at farms with outbreaks of PWD are lacking. In Denmark, the dams are sometimes treated with amoxicillin, however, it is unknown if it is passed on to the mink kits via the milk. The aim of the present study was to investigate if amoxicillin is transferred via the milk to the kits after oral (PO) and intramuscular (IM) treatment, respectively, of the dam. Moreover, we estimated the concentrations of amoxicillin continuously in serum from the kits up to 8 h after administration. The concentration of amoxicillin was not affected by the route of administration (P = .64) and serum reached the highest level after 8 h (34 ng/mL, CI95% = [24.3-47.7]). The serum concentrations of amoxicillin in the mink kits achieved within 8 h were judged too low to exert antimicrobial impact on relevant bacterial species.

Effects of halogenated contaminants on reproductive development in wild mink (Neovison vison) from locations in Canada.

The concept of the Anthropocene, that humans are now re-engineering global ecosystems, is in part evidenced by the pervasive pollution by persistent organic pollutants (POPs). Certain POPs are hormone mimics and can disrupt endocrine and hence reproductive processes, shown mainly by laboratory studies with model species. There are, in contrast, fewer confirmations of such disruption from eco-epidemiological studies of wild mammals. Here we used the American mink (Neovison vison) as a sentinel species for such a study. Over the period 1998-2006, 161 mink carcasses were obtained from commercial trappers in the Canadian provinces of British Columbia and Ontario. Mink were aged, sexed, measured, and body condition assessed. Livers were analyzed either individually or pooled for organochlorine (OC) pesticides, polychlorinated biphenyls (PCBs), and subsets for polybrominated diphenyl ethers (PBDEs). We primarily addressed whether contaminants affected male reproductive development by measuring baculum size and assessing the influences of age and body condition. We also considered the influence of spatial variation on relative exposure and size of baculum. Statistical models separated by age class revealed that significant relationships between baculum length or mass and juvenile mink were mostly positive, whereas for adults and first year mink they were mostly negative. A significant negative relationship for adult mink was determined between DDE and both baculum length and mass. For juvenile mink we found significant positive relationships between ∑PCBs, DDE and ∑PBDEs with baculum length. Our results provide some indication of negative effects of halogenated contaminants on male reproductive development in wild mink, and the most likely candidate chemical is the confirmed anti-androgenic compound, DDE, rather than PCBs or other compounds.

Activation of the IGF1 receptor stimulates glycogen synthesis by mink uterine epithelial cells.

Glycogen synthesis by mink uterine epithelial cells is stimulated by estradiol (E2 ) during estrus, although the mechanism/s through which the steroid promotes glycogen accumulation are unknown. Our aim was to determine if insulin is required for E2 induced glycogen synthesis by an immortalized mink uterine epithelial cell line (GMMe). We show that the cells expressed the genes for glycogen metabolizing enzymes (hexokinase 1, glucose-6-phosphatase 3, glycogen synthase 1, and glycogen phosphorylase-muscle), receptors for insulin, insulin-like growth factor 1 and E2 (Esr1). Interestingly, treatment of cells with E2 alone failed to stimulate glycogen production, whereas supraphysiological concentrations of insulin (50 µg/ml) only, significantly increased glycogen content. Moreover, insulin + E2 increased glycogen content when compared to insulin alone (p < 0.05), an affect that was blocked when cells were treated with the pure E2 receptor antagonist ICI 182,780. Glycogen synthesis in response to insulin was significantly inhibited when cells were pre-treated with picropodophyllotoxin, an IGF1R antagonist. Treatment of cells with LY294002, a phosphatidylinositol 3-kinase (PI3K) antagonist, blocked insulin's effects on glycogen production whereas treatment with U0126, an inhibitor of mitogen activated kinase-kinase (MEK1/2) was without effect. These findings suggest to us that the affects of E2 on glycogen synthesis by GMMe cells is mediated through Esr1 and increased responsiveness of the cells to insulin. Because picropodophylotoxin blocked the effects of insulin on glycogen production, and both insulin and IGF1 act through PI3K, it is possible that IGF1 plays a role in glycogen production by these cells.

In vivo fractionation of mercury isotopes in tissues of a mammalian carnivore (Neovison vison).

The use of isotope ratios to trace Hg contamination sources in environmental compartments is now generally accepted. However, for biota and especially for mammals, it is still unknown if and/or how Hg isotopes fractionate in vivo and which tissue is most representative of the source(s) of contamination. We measured fractionation of Hg in mink (Neovison vison) tissues (fur, brain, blood, liver, kidney) collected during a controlled feeding experiment where captive mink were fed differing amounts of methylmercury. There was no significant effect of dietary MeHg concentrations on Hg fractionation in most tissues. Net fractionation of Hg, i.e., fractionation corrected for diet (δ202Hgtissue-δ202Hgdiet) was observed in all tissues with the greatest net fractionation occurring in the mink liver (-1.39‰) and kidney (-0.95‰). Less net fractionation, occurred in the brain (-0.12‰), blood (0.38‰) and fur (0.30‰). In the absence of brain tissue, fur is a suitable proxy which is readily obtainable and can be non-lethally collected. In these mink, it appears that biochemical processes such as demethylation, contribute to significant fractionation of Hg in the liver and kidney, but not as much in the brain and fur, where transport of Hg via thiol-containing complexes may be more important.

Organochlorine contaminants in wild mink from the lower Great Lakes basin, Canada, 1998-2006.

Organochlorine contaminants were measured in livers of wild mink (Neovison vison) trapped in the lower Great Lakes basin from 1998 to 2006. To assess exposure and potential risk in mink feeding on Great Lakes biota, concentrations of contaminants were compared in mink trapped within 7.8 km of the shoreline as well as at inland sites (i.e., 8-40 km). Overall, significant spatial variation in mean hepatic concentrations of sum PCBs and seven other organochlorines was found in mink from 13 Great Lakes sites, many of which are within the Great Lakes Areas of Concern. Mean sum PCB concentrations, on a lipid weight basis, ranged from 2 µg/g in mink from inland Lake Ontario sites to 44 µg/g in mink from western Lake Erie. Concentrations of other organochlorines in mink were generally low. Mink from western Lake Erie had the highest mean cumulative organochlorine burdens dominated largely by PCBs. A significant age effect was found with 1-year-old mink having significantly higher PCB burdens than mink less than 1 year in age. With respect to published PCB threshold effect concentrations, some mink exceeded those associated with effects on reproduction and survival as well as the presence of jaw lesions. This was most consistently found in western Lake Erie where the health of populations of wild mink may be adversely affected and where no mink 2 years of age or older were collected.

Using energy budgets to combine ecology and toxicology in a mammalian sentinel species.

Process-driven modelling approaches can resolve many of the shortcomings of traditional descriptive and non-mechanistic toxicology. We developed a simple dynamic energy budget (DEB) model for the mink (Mustela vison), a sentinel species in mammalian toxicology, which coupled animal physiology, ecology and toxicology, in order to mechanistically investigate the accumulation and adverse effects of lifelong dietary exposure to persistent environmental toxicants, most notably polychlorinated biphenyls (PCBs). Our novel mammalian DEB model accurately predicted, based on energy allocations to the interconnected metabolic processes of growth, development, maintenance and reproduction, lifelong patterns in mink growth, reproductive performance and dietary accumulation of PCBs as reported in the literature. Our model results were consistent with empirical data from captive and free-ranging studies in mink and other wildlife and suggest that PCB exposure can have significant population-level impacts resulting from targeted effects on fetal toxicity, kit mortality and growth and development. Our approach provides a simple and cross-species framework to explore the mechanistic interactions of physiological processes and ecotoxicology, thus allowing for a deeper understanding and interpretation of stressor-induced adverse effects at all levels of biological organization.

Estradiol stimulates glycogen synthesis whereas progesterone promotes glycogen catabolism in the uterus of the American mink (Neovison vison).

Glycogen synthesis by mink uterine glandular and luminal epithelia (GE and LE) is stimulated by estradiol (E2 ) during estrus. Subsequently, the glycogen deposits are mobilized to near completion to meet the energy requirements of pre-embryonic development and implantation by as yet undetermined mechanisms. We hypothesized that progesterone (P4 ) was responsible for catabolism of uterine glycogen reserves as one of its actions to ensure reproductive success. Mink were treated with E2 , P4 or vehicle (controls) for 3 days and uteri collected 24 h (E2 , P4 and vehicle) and 96 h (E2 ) later. To evaluate E2 priming, mink were treated with E2 for 3 days, then P4 for an additional 3 days (E2 →P4 ) and uteri collected 24 h later. Percent glycogen content of uterine epithelia was greater at E2 + 96 h (GE = 5.71 ± 0.55; LE = 11.54 ± 2.32) than E2 +24 h (GE = 3.63 ± 0.71; LE = 2.82 ± 1.03), and both were higher than controls (GE = 0.27 ± 0.15; LE = 0.54 ± 0.30; P < 0.05). Treatment as E2 →P4 reduced glycogen content (GE = 0.61 ± 0.16; LE = 0.51 ± 0.13), to levels not different from controls, while concomitantly increasing catabolic enzyme (glycogen phosphorylase m and glucose-6-phosphatase) gene expression and amount of phospho-glycogen synthase protein (inactive) in uterine homogenates. Interestingly, E2 →P4 increased glycogen synthase 1 messenger RNA (mRNA) and hexokinase 1mRNA and protein. Our findings suggest to us that while E2 promotes glycogen accumulation by the mink uterus during estrus and pregnancy, it is P4 that induces uterine glycogen catabolism, releasing the glucose that is essential to support pre-embryonic survival and implantation.

Heavy metal concentrations in female wild mink (Neovison vison) in Sweden: Sources of variation and associations with internal organ weights.

The American mink is an invasive species in Sweden, and it is legally hunted all year. Therefore, the mink is well suited as a sentinel species for environmental monitoring. In the present study female mink (n = 91) from 6 different areas in Sweden were analyzed for the concentrations of silver, cadmium, mercury and lead in liver tissue using inductively coupled plasma mass spectrometry. The wet concentrations in liver tissue were 42.6 ± 52.7 ng/g for silver, 99.5 ± 100 ng/g for cadmium, 652 ± 537 ng/g for mercury, and 196 ± 401 ng/g for lead (expressed as mean ± standard deviation). There were associations between the sample area and the concentrations of silver, lead, and mercury. The concentrations of lead and cadmium varied with season of capture and lead, cadmium, and mercury were positively associated with increasing age. Relative liver weight was positively associated with concentrations of mercury and negatively associated with lead and cadmium. Relative kidney weight was negatively associated with lead concentrations. In summary, it is of importance to take age and season of capture into account when assessing levels of heavy metals in wild mink. Also, liver and kidneys seem to be potential targets for heavy metal toxicity in wild female mink in Sweden. Environ Toxicol Chem 2017;36:2030-2035. © 2016 The Authors. Environmental Toxicology and Chemistry Published by Wiley Periodicals, Inc. on behalf of SETAC.

Fetal life malnutrition was not reflected in the relative abundances of adiponectin and leptin mRNAs in adipose tissue in male mink kits at 9.5 weeks of age.

BACKGROUND: Malnutrition in fetal life and during suckling have in some animal studies resulted in adaptive changes related to the fat and glucose metabolism, which in the long term might predispose the offspring for metabolic disorders such as obesity later in life. The objective was to study the effect of fetal life malnutrition in male mink on the gene expression of leptin and adiponectin in different adipose tissue sites. RESULTS: Thirty-two male mink, strict carnivore species, exposed to low (FL) or adequate (FA) protein provision the last 16.3 ± 1.8 days of fetal life and randomly assigned to a low (LP) or adequate (AP) protein diet from 7 to 9.5 weeks of age were used. Adipose tissues (subcutaneous, perirenal and mesenteric) were analyzed using qPCR. Fetal life or post-weaning protein provision did not affect the relative abundances of leptin and adiponectin mRNAs in adipose tissue at 9.5 weeks of age. Relative abundances of leptin and adiponectin mRNAs were different between adipose tissue sites and were significantly higher in subcutaneous than in perirenal and mesenteric tissues. CONCLUSION: Fetal life protein malnutrition in male mink, did not result in adaptive changes in the gene expression of leptin and adiponectin mRNAs in adipose tissue at 9.5 weeks of age as found in rodents. However, both leptin and adiponectin mRNAs were significantly differently expressed between tissue sites.

Interplay between aggression, brain monoamines and fur color mutation in the American mink.

Domestication of wild animals alters the aggression towards humans, brain monoamines and coat pigmentation. Our aim is the interplay between aggression, brain monoamines and depigmentation. The Hedlund white mutation in the American mink is an extreme case of depigmentation observed in domesticated animals. The aggressive (-2.06 ± 0.03) and tame (+3.5 ± 0.1) populations of wild-type dark brown color (standard) minks were bred during 17 successive generations for aggressive or tame reaction towards humans, respectively. The Hedlund mutation was transferred to the aggressive and tame backgrounds to generate aggressive (-1.2 ± 0.1) and tame (+3.0 ± 0.2) Hedlund minks. Four groups of 10 males with equal expression of aggressive (-2) or tame (+5) behavior, standard or with the Hedlund mutation, were selected to study biogenic amines in the brain. Decreased levels of noradrenaline in the hypothalamus, but increased concentrations of the serotonin metabolite, 5-hydroxyindoleacetic acid and dopamine metabolite, homovanillic acid, in the striatum were measured in the tame compared with the aggressive standard minks. The Hedlund mutation increased noradrenaline level in the hypothalamus and substantia nigra, serotonin level in the substantia nigra and striatum and decreased dopamine concentration in the hypothalamus and striatum. Significant interaction effects were found between the Hedlund mutation and aggressive behavior on serotonin metabolism in the substantia nigra (P < 0.001), dopamine level in the midbrain (P < 0.01) and its metabolism in the striatum (P < 0.05). These results provide the first experimental evidence of the interplay between aggression, brain monoamines and the Hedlund mutation in the American minks.

Rate of exposure of a sentinel species, invasive American mink (Neovison vison) in Scotland, to anticoagulant rodenticides.

Anticoagulant rodenticides (ARs) are highly toxic compounds that are exclusively used for the control of rodent pests. Despite their defined use, they are nonetheless found in a large number of non-target species indicating widespread penetration of wildlife. Attempts to quantify the scale of problem are complicated by non-random sampling of individuals tested for AR contamination. The American mink (Neovison vison) is a wide ranging, non-native, generalist predator that is subject to wide scale control efforts in the UK. Exposure to eight ARs was determined in 99 mink trapped in NE Scotland, most of which were of known age. A high percentage (79%) of the animals had detectable residues of at least one AR, and more than 50% of the positive animals had two or more ARs. The most frequently detected compound was bromadiolone (75% of all animals tested), followed by difenacoum (53% of all mink), coumatetralyl (22%) and brodifacoum (9%). The probability of mink exposure to ARs increased by 4.5% per month of life, and was 1.7 times higher for mink caught in areas with a high, as opposed to a low, density of farms. The number of AR compounds acquired also increased with age and with farm density. No evidence was found for sexual differences in the concentration and number of ARs. The wide niche and dietary overlap of mink with several native carnivore species, and the fact that American mink are culled for conservation throughout Europe, suggest that this species may act as a sentinel species, and the application of these data to other native carnivores is discussed.

Partitioning and kinetics of methylmercury among organs in captive mink (Neovison vison): A stable isotope tracer study.

Despite the importance of methylmercury (MeHg) as a neurotoxin, we have relatively few good data on partitioning and kinetics of MeHg among organs, particularly across the blood-brain barrier, for mammals that consume large quantities of fish. The objective of this study was to determine the partition coefficients between blood and brain, liver and kidney and fur for MeHg under steady-state conditions and to measure the half-lives for MeHg in these organs. Captive mink (Neovison vison) were fed a diet enriched with two stable isotopes of Hg, Me(199)Hg and Me(201)Hg for a period of 60 days. After a period of 10 days the diet was changed to contain only Me(201)Hg so that, between days 10 and 60, we were able to measure both uptake and elimination rates from blood, brain, liver kidney and fur. Liver and kidney response was very rapid, closely following changes in blood concentrations but there was a small lag time between peak blood concentrations and peak brain concentrations. Half-lives for MeHg were 15.4, 10.2 and 13.4 days for brain, liver and kidney, respectively. There was no measurable conversion of the MeHg to inorganic Hg (IHg) in the brain over the 60 day period, unlike in liver and kidney.