Abortion in two foals associated with Nocardia infection.
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Abortion, Veterinary↗
Biomedical subjects
B Bolon
Publications and source records attributed to B Bolon.
Microscopic features of Sarcocystis falcatula in skeletal muscle from a Patagonian conure.
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Animals↗
Brain monoamine levels in suckling mice following postnatal exposure to secalonic acid D via the dam's milk.
Mice were gavage-fed on day 13 of pregnancy with 0 (groups N, 15, 25) or 25 (group P) mg/kg of secalonic acid D (SAD) and again while nursing their offspring on postgestational days 1-10 with 0 (N,P), 15(15) or 25(25) mg/kg/day. SAD residues were present in the stomach of pups nursed by SAD-treated dams. Postnatal exposure to SAD decreased (P less than 0.05) body weight gains of offspring. Treatment decreased the developmental levels of norepinephrine and dopamine in the prosencephalon (forebrain) and cerebellum-pons of the offspring on postnatal days (PND) 7 and 7-16, respectively. On PND 7-16 serotonin and 5-hydroxyindoleacetic acid levels decreased in the prosencephalon and cerebellum-pons of offspring exposed prenatally (P) or postnatally (15,25) to SAD.
Animals↗
Conjugated avidin-peroxidase as a stain for mast cell tumors.
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Animals↗
Secalonic acid D mycotoxin affects ontogeny of brain catecholamines and swimming in mice.
Suckling mice exposed to secalonic acid D (SAD) mycotoxin postnatally (by gavaging dams with 0, 15 or 25 mg/kg on postgestational days 1 to 10) or prenatally (by gavaging with 25 mg/kg on gestational day 13 to produce a positive behavioral teratogenic control group) manifested subtle preweaning neurobehavioral, neurochemical and growth deficits. Gestational length, maternal weight gain, neonatal sex ratio and physical appearance of pups at birth were unaffected by treatment. Prenatal SAD (25 mg/kg) delayed (p less than 0.05) ontogeny of swimming on postnatal days (PND) 11 and 13 and reduced norepinephrine (NE) and dopamine (DA) levels in prosencephalon on PND 7 and in cerebellum-pons on PND 7-16. In the postnatal treatment groups, pup body weight gains were decreased from PND 9-22. Swimming was delayed in the 15 mg/kg postnatal exposure group on PND 11 and 13, while 25 mg/kg delayed swimming on PND 11-15. Postnatal exposure to 25 mg/kg also reduced NE and DA levels in prosencephalon and cerebellum-pons on PND 7-16. SAD thus caused concomitant ontogenetic delays in growth, swimming behavior and brain catecholamine levels following either prenatal (transplacental) or early postnatal (transmammary) exposure. These data indicate that both in utero and lactational exposures must be considered when assessing potential risks posed to developing mammals by environmental neurotoxicants.
Animals↗
Influence of sampling on the reproducibility of ovarian follicle counts in mouse toxicity studies.
Different ovarian follicle counting procedures were investigated to reduce labor while retaining statistical power. Intact ovaries of untreated CD-1 mice (20/group) from National Toxicology Program Reproductive Assessment by Continuous Breeding (RACB) studies were serially sectioned at 6 microm. Mean numbers of small and growing follicles were used to assess sampling efficiency. In 10 mice per group, comparisons were made between 10% nonrandom samples from every 10th section starting at either the first or sixth section having follicles (approximately 40 sections per ovary). These 10% counts were compared with 5% (20 sections) and 20% (80 sections) nonrandom samples and with 1% (4 sections), 5%, or 10% random samples from the same 10 animals. For two studies, a 10% nonrandom sample was analyzed from 20 mice per group. Follicle counts for each group were comparable regardless of the sampling paradigm. Four to 10 animals provided 90% confidence that a 20% difference in mean counts would be detected. The 1% sample had a larger error term and, thus, slightly reduced statistical power. These data suggest that follicle counts from 1% or 5% random samples may provide a suitable screen for ovarian toxicity.
Animals↗
Comparative and correlative neuroanatomy for the toxicologic pathologist.
Xenobiotic-induced neuroanatomic alterations are always regarded as adverse and are commonly used to define reference doses to manage neurotoxic risk. Thus, the neuropathologist plays an essential role in evaluating potential neurotoxicants. The pathologist must be able to recognize the morphologic differences that exist among species, strains, and ages or between genders (comparative neuroanatomy) and to grasp the impact of structural damage on neural function (correlative neuroanatomy). Brain anatomy and function may be used to group the mammals used in neurotoxicity bioassays into 3 classes: rodent, carnivore, and primate. Neural function may or may not be affected by the structural divergence. Rodents are preferred for neurotoxicity assays because their reduced body size allows optimal perfusion at little cost and their smaller brain size permits screening of multiple regions using few sections. However, care must be exercised when interpreting rodent neuropathology data because the rodent paleocortex does not recapitulate the sophisticated neocortical circuitry and functions of carnivores and primates. Knowledge of the neuroanatomic variations that exist among test species assists the neuropathologist in defining the relevance of structural alterations, the potential clinical sequelae of such findings, and the possible significance of similar changes in humans.
Animals↗
Evolution of alachlor-induced nasal neoplasms in the Long-Evans rat.
The chloracetanilide herbicide alachlor (2-chloro-2',6-diethyl-N-(methoxymethyl)-acetanilide) induces nasal neoplasms in rats following chronic dietary exposure. The present study sought to identify the cellular origin and mechanisms of tumor induction and progression. Male Long-Evans rats were fed alachlor (0 or 126 mg/kg/day) beginning at 6 weeks of age. Following 1 month of alachlor ingestion, neither histological abnormalities nor enhanced cell division (assessed by BrdU incorporation) occurred in any region of the nasal cavity. Six months of alachlor exposure resulted in proliferation of basal and nonbasal cells in the olfactory mucosa while inducing nasal masses in 7 of 15 animals. Tumors ranged from dysplastic plaques to polypoid adenomas and originated in the olfactory regions of the nasal cavity. Neoplasms were associated with regions of respiratory metaplasia and were often covered with a low cuboidal, poorly ciliated epithelium. Tumor cells did not express characteristics of the olfactory mucosa, including olfactory marker protein (OMP, for neurons) and NMa (antibody recognizing cytochrome P450 [CYP] 2A3, found in Bowman's glands). Sites of plaque and tumor development coincided with regions of NMa immunoreactivity. These data suggest that local metabolism is important in alachlor-induced olfactory tumors and support the concept that metaplastic respiratory epithelial cells give rise to the observed neoplasms.
Acetamides↗
Histopathologic approaches to chemical toxicity using primary cultures of dissociated neural cells grown in chamber slides.
Morphologic lesions have received only limited attention as in vitro endpoints of toxicity. In the present work, "tissue" and cell morphology of control and toxicant-treated primary dissociated cerebrocortical cell cultures from fetal mice were examined using phase-contrast and bright-field microscopy. In untreated control cultures, a reproducible sequence of developmental events included cellular reaggregation, intercolony bridging with cell migration, and neuronal apoptosis, with maturation yielding confluent monolayers containing both neurons and glia. Because even mature cultures had regions of varying differentiation, an understanding of the normal developmental sequence was essential when assessing toxicant-treated cultures for damage. Chemicals induced neuronotoxic, gliotoxic, and cytotoxic (i.e., nonspecific) patterns of morphologic damage in growing (< 6 day old) or mature (6-15 day old) cultures in both a concentration-dependent and cell type-specific manner. In addition, exposure to some toxicants consistently reduced the staining intensity for glial fibrillary acidic protein in the astrocyte carpet prior to the appearance of structural damage. These data indicate that histopathologic endpoints, including methods for neural-specific markers, represent potentially valuable criteria for in vitro assessments of neurotoxicity.
Animals↗