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M L Johnson

Publications and source records attributed to M L Johnson.

At least 19 recordsLinked to original sources
PubMed2006

Surflan and oryzalin impair reproduction in the teleost medaka (Oryzias latipes).

We conducted studies to determine if the xenoestrogens Surflan and its active ingredient oryzalin, affect indices of reproductive fitness in medaka (Oryzias latipes). Oryzalin (0.5, 0.25mg/l) or Surflan (2.0 microl/l) and oryzalin (0.5mg/l) significantly increased the mean number of non-fertilized eggs produced by treated females paired with untreated males, or by untreated females paired with treated males. Oryzalin (1.0, 0.5, 0.25mg/l) and Surflan (3.8, 2.0, 1.0 microl/l) significantly affected the time to hatch of eggs from treated females paired with untreated males, and from untreated females paired with treated males. Surflan (3.8, 2.0, 1.0 microl/l) induced intersex lesions in 80-100% of males. Oryzalin-exposed males exhibited a significant increase in the incidence of necrotic spermatids and necrotic spermatogonia, while oryzalin-exposed females had significantly fewer immature oocytes and an increase in the occurrence of hyperplastic ovaries. Our results indicate that Surflan and oryzalin affect both reproduction and gonadal histology in male and female medaka.

Animals↗
PubMed2006

Polymorphisms in the bone morphogenetic protein 2 (BMP2) gene do not affect bone mineral density in white men or women.

INTRODUCTION: Peak bone mineral density (BMD) achieved during adulthood is a major determinant of osteoporotic fracture in later life. Although environmental factors affect peak BMD, it is a highly heritable trait. Recently, bone morphogenetic protein 2 (BMP2) was reported as a susceptibility gene for osteoporotic fractures and low BMD in Icelandic and Danish populations. METHODS: To determine whether polymorphisms in the BMP2 gene contribute to BMD variation in our population of healthy American whites, we tested seven single nucleotide polymorphisms (SNPs), four of which were associated with osteoporotic phenotypes in the previous study. BMD at the femoral neck and lumbar spine (L2-L4) were measured by dual energy X-ray absorptiometry (DXA) in 411 men (age 18-61) and 1,291 pre-menopausal women (age 20-50). SNP genotypes/haplotypes were tested for population-based association with BMD using analysis of variance. RESULTS: None of the polymorphisms tested reached statistical significance (all p values >0.05) for BMD at the femoral neck or lumbar spine in either gender. Two of the SNP haplotypes spanning the entire BMP2 gene were marginally associated with BMD in men (p values=0.019-0.043). However, these haplotypes would account for only a small, if any, portion of BMD variation and would not be significant after adjustment for multiple comparisons. CONCLUSIONS: These results demonstrate that genetic variations in BMP2 do not substantially contribute to BMD variation in our population of healthy American whites.

Absorptiometry, Photon↗
PubMed2006

MHC gene configuration variation in geographically disparate populations of California sea lions (Zalophus californianus).

Major histocompatibility complex (MHC) class II DRB genotypes were examined in two geographically isolated populations of California sea lions (Zalophus californianus) (Gulf of California and California coastal Pacific Ocean). Genomic DNA from 227 California sea lions was examined using eight sequence-specific primer (SSP) pairs flanking the putative peptide-binding site. A total of 40 different Zaca-DRB genotype configurations were identified among the 227 individuals. Using SSP-PCR, significant differences were found between coastal California and Gulf of California Zalophus populations in numbers of DRB sequences per individual and configuration of sequences within individuals. Additionally, unique local patterns of MHC diversity were identified among the Midriff Island animals. These population differences are consistent with either ecologically distinct patterns of selection pressures and/or geographical isolation. The consequences of these partitioned MHC configurations at the population level are as yet unknown; however, the worldwide increase in emerging marine diseases lends urgency to their examination.

California↗
PubMed2005

Identification of the herbicide Surflan and its active ingredient oryzalin, a dinitrosulfonamide, as xenoestrogens.

Numerous environmental contaminants have been identified as endocrine disruptors (EDs)--substances that alter endocrine homeostasis by interfering with the biological action, production, or pharmacokinetics of endogenous hormones. Xenoestrogens are those EDs whose biological activity is similar to endogenous estrogen. This report presents data that identified Surflan, a proprietary herbicide emulsion, and its active ingredient oryzalin as xenoestrogens. In vitro, Surflan and oryzalin activated an estrogen-inducible reporter gene, and oryzalin competitively displaced 17beta-estradiol from the estrogen receptor. In vivo, Surflan and oryzalin induced expression of estrogen-regulated high-molecular-weight choriogenin genes in medaka (Oryzias latipes). These results are consistent with the characteristics of previously identified xenoestrogens and indicate that Surflan and oryzalin have the potential to adversely affect numerous estrogen-regulated biological processes.

Animals↗
PubMed2005

Animal models of placental angiogenesis.

The study of the development of the fetal membranes is an ancient one, and the importance of placental vascular development to placental function has long been recognized. Animal models have been important in these studies, as they allow for controlled experiments and analysis of multiple time-points during pregnancy. Since the demonstration nearly 20 years ago that the placenta produces angiogenic factors, the major factors regulating placental angiogenesis have been identified. These major factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), the angiopoietins (ANG), and their receptors. Recently, sophisticated computerized image analysis methods have been developed to establish the pattern of placental vascular development in sheep. The maternal placental capillary bed develops primarily by increased size of capillaries, with only small increases in capillary number or surface densities. In contrast, the microvasculature of the fetal placenta develops primarily by increased branching, resulting in a large increase in capillary number and surface densities. These observations help to explain the relatively large increase in umbilical blood flow and nutrient delivery to the fetus that occurs during the last half of gestation. In addition, expression of mRNAs for VEGF, bFGF, ANG, and their receptors have recently been correlated with normal placental vascular development in sheep, and further refinement of these mathematical models is warranted. Lastly, the recent development of animal models of compromised pregnancies, including those resulting from maternal nutrition (both restriction and excess), multiple fetuses, environmental stress (heat stress and high altitude), and fetal and maternal breed effects, has already indicated that reductions in placental vascular development and expression of angiogenic factors are probably a root cause of fetal growth restriction. With these methods and models now in place, we should soon be able to establish the mechanisms involved in both normal and abnormal placental angiogenesis.

Angiopoietins↗
PubMed2004

Bone biomechanical properties in LRP5 mutant mice.

The mutation responsible for the high bone mass (HBM) phenotype has been postulated to act through the adaptive response of bone to mechanical load resulting in denser and stronger skeletons in humans and animals. The bone phenotype of members of a HBM family is characterized by normally shaped bones that are exceptionally dense, particularly at load bearing sites [Cancer Res. 59 (1999) 1572]. The high bone mass (HBM) mutation was identified as a glycine to valine substitution at amino acid residue 171 in the gene coding for low-density lipoprotein receptor-related protein 5 (LRP5) [Bone Miner. Res. 16(4) (2001) 758]. Thus, efforts have focused on the examination of the role of LRP5 and the G171V mutation in bone mechanotransduction responses [J. Bone Miner. Res 18 (2002) 960]. Transgenic mice expressing the human G171V mutation have been shown to have skeletal phenotypes remarkably similar to those seen in affected individuals. In this study, we have identified differences in biomechanical (structural and apparent material) properties, bone mass/ash, and bone stiffness of cortical and cancellous bone driven by the G171V mutation in LRP5. As in humans, the LRP5 G171V plays an important role in regulating bone structural phenotypes in mice. These bone phenotypes include greater structural and apparent material properties in HBM HET as compared to non-transgenic littermates (NTG) mice. Body size and weight in HBM HET were similar to that in NTG control mice. However, the LRP5 G171V mutation in HET mice results in a skeleton that has greater structural (femoral shaft, femoral neck, tibiae, vertebral body) and apparent material (vertebral body) strength, percent bone ash weight (ulnae), and tibial stiffness. Despite similar body weight to NTG mice, the denser and stiffer bones in G171V mice may represent greater bone formation sensitivity to normal mechanical stimuli resulting in an overadaptation of skeleton to weight-related forces.

Amino Acid Substitution↗
PubMed2004

The high bone mass family--the role of Wnt/Lrp5 signaling in the regulation of bone mass.

A G171V mutation in the low-density lipoprotein receptor-related protein 5 (LRP5) was identified as causal for an autosomal dominant high bone mass trait in a single human family. A transgenic mouse line was produced that carries this mutation and develops a high bone mass phenotype that recapitulates the human phenotype. LRP5 is a co-receptor for Wnt and we have investigated the potential role of this gene/protein and the Wnt signaling pathway in mediating the bone formation response to mechanical loading. The G171V mutation results in an increased responsiveness of bone to mechanical load and reduces the threshold of load required to elicit a response. Our studies have shown that the Wnt signaling pathway is activated in response to mechanical loading and this response is greatly enhanced in the presence of the G171V mutation. Additionally, this mutation results in increased transcription of osteoprotegerin (OPG) in response to loading. Thus, the mutation appears to have direct effects at the level of the osteoblast and may also result in a reduction in osteoclastogenesis. The identification of LRP5/Wnt signaling in bone mechanosensation has resulted in a new paradigm for understanding bone formation. Hopefully, knowledge gained from these studies will result in new therapies for treating osteoporosis.

Animals↗
PubMed2002

Effects of basic fibroblast growth factor (FGF-2) on proliferation of human skin fibroblasts in type II diabetes mellitus.

Skin fibroblasts from patients with diabetes mellitus display abnormalities in cell proliferation. The use of exogenous growth factors on diabetic wounds has been found to stimulate fibroblast proliferation and facilitate wound healing. However, the results of application of FGF-2 alone to diabetic wounds in clinical trials have been disappointing. The objective of this experiment was to study the effects of FGF-2 and media supplements on in vitro proliferation of skin fibroblasts from patients with type II diabetes and nondiabetic controls, and to evaluate the association between fibroblast proliferation and cAMP production. Fibroblast cell lines (n = 5 from diabetic and n = 5 from control individuals) were cultured in DMEM + 20% FBS for 7 days. Cells were then counted, plated into 24-well plates at a concentration of 2 x 10(4) cells/well and incubated for 24 h in DMEM with serum. The next day, medium was changed to serum-free DMEM alone or DMEM with supplements (albumin, transferrin, insulin and hydrocortisone). Cells were cultured in the presence or absence of varying doses of FGF-2 (0, 0.3, 1, 3, 10 and 30 ng/ml) for 72 hrs then counted and medium was collected for cAMP radioimmunoassay. The doubling time for cell number tended to be greater (p < 0.2) for diabetic fibroblasts than for control fibroblasts. The addition of supplements to the medium reduced (p < 0.05) the doubling time for both fibroblast types. FGF-2 stimulated (p < 0.05) proliferation of diabetic fibroblasts only in medium containing supplements. In contrast, FGF-2 stimulated proliferation of control fibroblasts in medium with or without supplements. The maximal effects of FGF-2 on fibroblast proliferation were greater (p < 0.02) in medium with supplements than in medium without supplements. The K(D) of FGF-2 for fibroblast proliferation was greater (p < 0.06) for diabetic than for control fibroblasts, and lower (p < 0.02) for medium with supplements than for medium without supplements. Fibroblasts from patients with diabetes mellitus produced more (p < 0.05) cAMP than control fibroblasts. These results demonstrate that FGF-2 requires the presence of supplements to enhance proliferation of fibroblasts from patients with type II diabetes mellitus. In addition, fibroblasts from diabetic patients showed a greater K(D) for FGF-2 in terms of cell proliferation. These data suggest a defective FGF receptor or down-regulation of the FGF receptor-mediated cascade that leads to cell proliferation. Identifying methods of reducing the K(D) of FGF-2 in stimulating the proliferation of diabetic fibroblasts may improve the clinical response of diabetic wounds to FGF-2.

Cell Division↗
PubMed2001

A macroscopic description of lipid bilayer phase transitions of mixed-chain phosphatidylcholines: chain-length and chain-asymmetry dependence.

A macroscopic model is presented to quantitatively describe lipid bilayer gel to fluid phase transitions. In this model, the Gibbs potential of the lipid bilayer is expressed in terms of a single order parameter q, the average chain orientational order parameter. The Gibbs potential is based on molecular mean-field and statistical mechanical calculations of inter and intrachain interactions. Chain-length and chain-asymmetry are incorporated into the Gibbs potential so that one equation provides an accurate description of mixed-chain phosphatidylcholines of a single class. Two general classes of lipids are studied in this work: lipid bilayers of partially or noninterdigitated gel phases, and bilayers of mixed interdigitated gel phases. The model parameters are obtained by fitting the transition temperature and enthalpy data of phosphatidylcholines to the model. The proposed model provides estimates for the transition temperature and enthalpy, van der Waals energy, number of gauche bonds, chain orientational order parameter, and bond rotational and excluded volume entropies, achieving excellent agreement with existing data obtained with various techniques.

Biophysical Phenomena↗
PubMed2001

Neurophysiological regulation and target-tissue impact of the pulsatile mode of growth hormone secretion in the human.

Neuroendocrine axes function as an ensemble of regulatory loci which communicate and maintain homeostasis via time-delayed blood-borne signals. The growth hormone (GH)-insulin-like growth factor I (IGF-I) feedback axis sustains a vividly pulsatile mode of interglandular signalling. Pulsatility is driven jointly by hypothalamic GH-releasing hormone (GHRH) and GH-releasing peptide (GHRP), and modulated by somatostatinergic restraint. Paradoxically, intermittent somatostatin inputs also facilitate somatotrope-cell responses to recurrent secretagogue stimuli, thereby amplifying pulsatile GH secretion. A concurrent low basal (8-12% of normal total) rate of GH release is controlled positively by GHRH and GHRP and negatively by somatostatin. Sex-steroid hormones (such as oestradiol and aromatizable androgen) and normal female and male puberty augment GH secretory-burst mass 1.8- to 3.5-fold, whereas ageing, relative obesity, physical inactivity, hypogonadism, and hypopituitarism mute the amplitude/mass of pulsatile GH output. An abrupt rise in circulating GH concentration stimulates rapid internalization of the GH receptor in peripheral target tissues, and evokes second-messenger nuclear signalling via the STAT 5b pathway. Discrete GH peaks stimulate linear (skeletal) growth and drive muscle IGF-I gene expression more effectually than basal (time-invariant) GH exposure. A brief pulse of GH can saturate the plasma GH-binding protein system and achieve prolonged plasma GH concentrations by convolution with peripheral distribution and clearance mechanisms. A single burst of GH secretion also feeds back after a short latency on central nervous system (CNS) regulatory centres via specific brain GH receptors to activate somatostatinergic and reciprocally subdue GHRH outflow. This autoregulatory loop probably contributes to the time-dependent physiologically pulsatile dynamics of the GH axis. More slowly varying systemic IGF-I concentrations may also damp GH secretory pulse amplitude by delayed negative-feedback actions. According to this simplified construct, GH pulsatility emerges due to time-ordered multivalent interfaces among GHRH/GHRP feedforward and somatostatin, GH and IGF-I feedback signals. Resultant GH pulses trigger tissue-specific gene expression, thereby promoting skeletal and muscular growth, metabolic and body compositional adaptations, and CNS reactions that jointly maintain health and homeostasis.

Aging↗
PubMed2001

Thermostable (SULT1A1) and thermolabile (SULT1A3) phenol sulfotransferases in human osteosarcoma and osteoblast cells.

Sulfate conjugation is an important pathway in the metabolism of many drugs, xenobiotic compounds, and hormones. Sulfotransferases (SULTs) catalyze these reactions and have been detected and characterized in various human tissues including the liver and small intestine. Substrates for SULTs that include estrogen and thyroid hormones have well-established roles affecting skeletal integrity and disease processes. We performed the following studies to determine the presence of SULTs in human osteoblast-like cells, and to compare their characteristics to SULTs expressed in other human tissues. Four osteosarcoma cell lines (SaOS-2, U2-OS, PR, and HOS-TE85) were screened for the presence of four different SULT activities. Predominant activities were found for SULT1A1 in SaOS-2 cells, and SULT-1A3 in HOS-TE85 cells. Several biochemical properties of each enzyme that included apparent K(m) values, thermal stabilities, and responses to the inhibitors 2,6-dichloro-4-nitrophenol and NaCl were used to further characterize the SULT activities. High-performance liquid chromatography (HPLC) of the reaction products confirmed the known products of SULT1A1 and SULT1A3. When the mature human osteoblast HOB-03-CE6 cell line was tested for activity alone, the predominant activity was SULT1A3, with minimal SULT1A1. The results indicate that SULT1A1 and SULT1A3 are present in human osteosarcoma and mature osteoblast cell lines, and that the characteristics of the osteosarcoma cell SULTs are similar to those expressed in other human tissues. SULTs may have regulatory roles in the deactivation of thyroid hormones or estrogenic compounds in bone, and thus may affect hormone action and bone responses in the human skeleton.

Arylsulfotransferase↗
PubMed2001

The roles of iNOS in liver ischemia-reperfusion injury.

To determine the contribution of the inducible nitric oxide synthase (iNOS) to hepatic injury following warm ischemia-reperfusion, we developed a model of partial hepatic ischemia-reperfusion in mice and studied the injury response in iNOS knockout (KO) mice. Compared with wild types, iNOS KO animals exhibited lower plasma transaminase levels after 1 and 6 h of reperfusion following 1 h of ischemia. At the 3-h time point, enzyme levels were not different between the two groups. iNOS mRNA was not detectable in the ischemic hepatic lobes of wild-type mice until 3 h of reperfusion; however, perfusion studies identified a significant delay in reperfusion of the ischemic lobe in the iNOS KO mice at the 1-h time point with similar perfusion rates at 3 and 6 h compared with wild type. By way of comparison, mice deficient in the endothelial NOS (eNOS) were also assessed for the degree of hepatic damage 3 h post-reperfusion. Plasma transaminase levels were significantly increased in eNOS KO animals compared with wild-type controls. These data suggest that systemic as well as local sources of iNOS regulate reperfusion, and local iNOS contributes to hepatic injury, while eNOS is protective in warm hepatic ischemia-reperfusion.

Alanine Transaminase↗
PubMed2001

Secretory process regularity monitors neuroendocrine feedback and feedforward signaling strength in humans.

The present experiments examine the neuroregulatory hypothesis that the degree of sample-by-sample regularity of hormone output by an interlinked hypothalamopituitary target-organ system monitors the strength of feedback and/or feedforward signaling. To test this postulate and assess its generality, we implemented a total of nine thematically complementary perturbation experiments. In particular, we altered feedback or feedforward signaling selectively in two distinct neuroendocrine systems; namely, the growth hormone (GH) insulin-like growth factor type I (IGF-I) and the luteinizing hormone-testosterone axes. Four experimental paradigms comprised preferential reduction vs. enhancement of IGF-I or testosterone feedback signal strength; and, conversely, five others entailed selective attenuation vs. augmentation of GH-releasing hormone and gonadotropin-releasing hormone feedforward signal intensity. In these independent interventions, quantitation of subordinate (nonpulsatile) secretory pattern reproducibility via the approximate entropy statistic unmasked salient changes (P values typically <10(-3)) in the conditional regularity of serial hormone output with high consistency (96-100%). In particular, approximate entropy quantified degradation of secretory subpattern orderliness under either muted feedback restraint or heightened feedforward drive. Assuming valid interpretation of the biological constraints imposed, these experimental observations coincide with earlier reductionist mathematical predictions, wherein increased irregularity of coupled parameter output mirrors attenuated feedback and/or augmented feedforward coupling within an integrative system.

Fasting↗
PubMed2001

A construct of interactive feedback control of the GH axis in the male.

Growth hormone (GH) secretion is controlled by GH-releasing hormone (GHRH), the GH release-inhibiting hormone somatostatin (SRIF), and autofeedback connections. The ensemble network produces sexually dimorphic patterns of GH secretion. In an effort to formalize this system, we implemented a deterministically based autonomous feedback-driven construct of five principal dose-responsive regulatory interactions: GHRH drive of GH pituitary release, competitive inhibition of GH release by SRIF, GH autofeedback via SRIF with a time delay, delayed GH autonegative feedback on GHRH, and SRIF inhibition of GHRH secretion. This formulation engenders a malelike pattern of successive GH volleys due jointly to positive time-delayed feedback of GH on SRIF and negative feedback of SRIF on GH and GHRH. The multipeak volley is explicated as arising from a reciprocal interaction between GH and GHRH during periods of low SRIF secretion. The applicability of this formalism to neuroendocrine control is explored by initial parameter sensitivity analysis and is illustrated for selected feedback-dependent experimental paradigms. The present construct is not overparameterized and does not require an ad hoc pulse generator to achieve pulsatile GH output. Further evolution of interactive constructs could aid in exploring more complex feedback postulates that confer the vivid sexual dimorphism of female GH profiles.

Animals↗
PubMed2001

Impact of pulsatility on the ensemble orderliness (approximate entropy) of neurohormone secretion.

Regular patterns of neurohormone secretion are driven by underlying pulsatile and subordinate (feedback sensitive) dynamics. Measures of time-series orderliness, e.g., the approximate entropy (ApEn) statistic (Pincus SM. Proc Natl Acad Sci 88: 2297-2301, 1991), vividly discriminate pathological and physiological patterns of hormone release. To investigate how specific pulsatility features impact regularity estimates, we have examined the sensitivity of the ApEn metric to systematic variations in the frequency, amplitude, and half-life of simulated neurohormone pulse trains (Veldhuis JD, Carlson ML, and Johnson ML. Proc Natl Acad Sci 84: 7686-7690, 1987) and compared the impact of a high vs. low baseline luteinizing hormone (LH) pattern regularity state mimicking the normal female luteal phase and the young male, respectively. Shortening the interpulse interval length elevated ApEn in both pulsatility models, thereby signifying greater ensemble series irregularity. The frequency sensitivity of ApEn was robust to several complementary renditions of ApEn and to variations in experimental uncertainty, basal (nonpulsatile) LH secretion, and secretory burst amplitude. ApEn rose with increasing hormone half-life, especially in the face of low baseline variability emulated by midluteal LH secretion profiles. High variability of secretory burst amplitude, pulse duration, or interpeak intervals increased ApEn in the more orderly femalelike construct; in the highly irregular malelike LH pulse model, these variability changes had little effect on ApEn. In summary, the ensemble regularity statistic, ApEn, quantifies unequal pattern orderliness in neurohormone pulse trains with minimal dependence on mean pulse amplitude, interpulse baseline, or (subthreshold) sample uncertainty. Thus ApEn monitors changing secretory event frequency and interpulse variability with sensitivity to starting pattern regularity, providing a mechanistic linkage between model evolution and statistical change.

Female↗
PubMed2001

Bioaccumulation of metals in plants, arthropods, and mice at a seasonal wetland.

Concentrations of arsenic, cadmium, copper, lead, and nickel were measured in soils, house mice (Mus musculus), and the main food items of this omnivorous mouse to examine the occurrence of these metals in selected components of a seasonal wetland. Soil concentrations of copper, lead, and (in some areas) nickel were elevated, but extractable soil concentrations indicated low bioavailability of metals. Levels of most metals in mice and composited arthropods were consistent with reference site concentrations from other studies. However, copper was found to be particularly mobile within the local ecosystem and accumulated in house mouse carcasses and composited arthropods at substantial levels. Metal residues in Scirpus robustus (alkali bulrush) roots exceeded those in seeds, consistent with patterns of bioaccumulation commonly observed in plants. Uptake and bioaccumulation factors for S. robustus seeds and roots, arthropods, and mouse carcasses and livers are reported. Concentrations of lead and nickel in S. robustus roots exhibited significant linear relationships with levels in soils. Copper levels in S. robustus seeds varied significantly with those in house mouse livers, suggesting that trophic transfer of copper from this food source to mice occurred. However, other spatial patterns of bioaccumulation in S. robustus and house mice relative to soil/seed concentrations were absent. Metal levels in house mice bore no relation to body weight or estimated age.

Animals↗
PubMed2001

Testing of metal bioaccumulation models with measured body burdens in mice.

Estimates of chemical accumulation in prey organisms can contribute considerable uncertainty to predictive ecological risk assessments. Comparing body burdens calculated in food web models with measured tissue concentrations provides essential information about the expected accuracy of risk indices. Estimates of arsenic, cadmium, copper, lead, and nickel body burdens in house mice (Mus musculus) inhabiting a seasonal wetland were generated with two small mammal bioaccumulation models. Published soil-to-small mammal bioaccumulation regression models produced accurate estimates of arsenic and lead body burdens but failed to adequately predict copper and nickel levels in mice. Incorporating conservative prediction intervals in the regression models shows potential for successful applications in screening-level risk assessments. A simple mechanistic cumulative ingestion bioaccumulation model overpredicted lead levels in mice generally by less than one order of magnitude but greatly overpredicted concentrations of arsenic, copper, and nickel. Better estimates of absorption and elimination of ingested metals and knowledge of specific arthropod taxa in house mouse diets are likely to improve the accuracy of the cumulative ingestion model. Applying Monte Carlo simulations to the soil-small mammal regression models generated probabilistic estimates of body burdens that were consistent with deterministic results. However, deterministic minimum and maximum predictions of the ingestion model were excessively conservative (widely spaced) relative to lower and upper probabilistic percentiles. Metal levels predicted in individual mice on the basis of mouse-specific parameter values and exposures were not significantly more accurate than bioaccumulation predictions for the sitewide population.

Animals↗