PubMed Health⌕ Search

Biomedical subjects

S D Holladay

Publications and source records attributed to S D Holladay.

62 records · Page 4Linked to original sources
PubMed1983

Norepinephrine, dopamine, and serotonin in brain parts of female Japanese quail (Coturnix coturnix japonica) as found by two dissimilar fluorometric procedures.

Two dissimilar fluorometric procedures were used to compare norepinephrine, dopamine, and serotonin in the telencephalon, diencephalon, cerebellum, and brain stem of female Japanese quail. Amount of norepinephrine in the telencephalon and brain stem was similar using both procedures, but more norepinephrine was found in the cerebellum and diencephalon by the Jacobowitz-Richardson method compared to the Anton-Sayre method. Serotonin could not be determined using the Anton-Sayre procedure but was detected easily by the Jacobowitz-Richardson procedure in all brain parts assayed. The most striking difference between the two procedures was in the level of dopamine detected. Dopamine was found only in the telencephalon using the Anton-Sayre procedure, but it was found in all brain parts using the Jacobowitz-Richardson procedure. This is the first report of significant dopamine in all principle parts of the Japanese quail brain.

Animals↗
PubMedDate not supplied

Immune alterations in geriatric mice dosed subacutely with diethylstilbestrol (DES).

Exposure to both physiological and pharmacological doses of estrogenic compounds has been reported to alter immunologic responses in humans as well as in developmental and adult murine models. Despite the current therapeutic use of potent estrogens, including diethylstilbestrol (DES), in geriatric human disorders, elucidation of the effects of these agents on the aged immune system is limited. The present report describes highly significant alterations in the thymus and bone marrow of aged mice (21 +/- 1 months) exposed subacutely to DES. Severe thymic hypocellularity developed in treated mice following five consecutive days of intraperitoneal injection with 1.5 or 6.0 mg kg(-1) DES. Cell maturation within the thymus was also affected, as indicated by a significant decrease in CD4+8+ cells and a concomitant increase in CD4-8- cells. Cellularity of the bone marow was unchanged by DES. However, significant changes were observed in percentages of bone marrow cells expressing surface antigens CD45 (common leukocyte lineage), Mac-1 (macrophage lineage) and CD45R (B-lineage lymphocytes). Both percentages and total numbers of cells in the spleen expressing Thy 1.2 (T-lineage lymphocytes) were also reduced. These immune changes in geriatric mice exposed to DES were similar in direction but more severe than those reported in either young adult or perinatal models. These data may suggest a need for considering the geriatric immune system separately from other age groups when determining effects of immunosuppressive or immunotoxic compound exposure.

Aging↗
PubMedDate not supplied

Cis-urocanic acid increases immunotoxicity and lethality of dermally administered permethrin in C57BL/6N mice.

Immunomodulatory effects of a single topical permethrin exposure, 5-day exposure to cis-urocanic acid (cUCA), or a combination of the two chemicals were evaluated in 4- to 5-week-old female C57BL/6N mice. Permethrin alone decreased thymic weight and cellularity. Although cUCA alone did not affect thymic end points, coexposure to topical permethrin and cUCA exacerbated the thymolytic effects of permethrin. The single topical dose of permethrin also depressed several immune responses in isolated splenic leukocytes. This included splenic T-cell proliferative response to mitogen, splenic macrophage hydrogen peroxide production, and splenic B lymphocyte-specific antibody production. Unlike the effect of coexposure to these agents on thymic end points, cUCA did not exacerbate permethrin's adverse effect on any of the splenic end points examined. These results appear to suggest divergent mechanisms by which these compounds affect precursor and functionally mature T cells. At the doses used in this study, permethrin caused neurotoxic effects, including lethality, in a portion of the mice. For undetermined reasons, cUCA significantly increased the rate of lethality caused by permethrin. Although the permethrin doses used in this study exceed that typically used in human medicine, these results raise some concerns about the possibility that sunlight, via cUCA, may increase the risk of adverse central nervous system and immune effects caused by permethrin alone.

Administration, Cutaneous↗
PubMedDate not supplied

Effects of 2,4,6-trinitrotoluene in a holistic environmental exposure regime on a terrestrial salamander, Ambystoma tigrinum.

2,4,6-Trinitrotoluene (TNT) is a defense-related environmental contaminant present at high concentrations in soil at some military installations. Tiger salamanders (Ambystoma tigrinum, family Ambystomatidae) were exposed to TNT in a soil matrix and fed earthworms that had also been exposed to TNT via contaminated soil. Such exposure was previously shown to result in significant accumulation of both TNT and TNT metabolites by salamanders. Following 14 days of combined oral and dermal exposures, salamanders were evaluated for signs of toxicity. Control and TNT-exposed salamanders gained weight (p < 0.025). In addition, organ to body weight ratios (kidney, liver, and spleen) were not affected by treatment. The function of splenic phagocytic cells was evaluated because these cells are sensitive to certain environmental chemical exposures. Neither the chemiluminescence response (H2O2 production) nor the phagocytic capacity of such cells were different between controls and treatment groups. In like manner, no changes were seen in the peripheral hematologic parameters investigated. Histopathologic evaluations were inconclusive, yet the liver revealed the presence of heavily pigmented iron-rich phagocytes (melanomacrophages). This investigation presents a realistic approach and preliminary data for investigating the effects of xenobiotic exposure in a soil matrix on a terrestrial vertebrate.

Administration, Cutaneous↗
PubMedDate not supplied

Histopathology of acetaminophen-induced liver changes: role of interleukin 1 alpha and tumor necrosis factor alpha.

Administration of 500 mg/kg acetaminophen (APAP) to female B6C3F1 mice resulted in well-documented pathophysiological changes in the liver manifested as increased serum concentration of liver enzymes (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and serum sorbitol dehydrogenase), centrilobular congestion, and hepatocellular degeneration and necrosis. The role of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha) and interleukin 1 alpha (IL-1 alpha), on the hepatotoxicity of APAP was examined at 4, 8, 12, and 24 hr following APAP administration. Neutralization of TNF-alpha or IL-1 alpha with specific antibodies partially prevented the hepatotoxic effects of APAP at the 4- and 8-hr time points. In addition, prior administration of anti-TNF-alpha antibodies shortened the recovery time following APAP treatment. While IL-1 receptor antagonist (IL-1ra) had only a modest protective effect against APAP-induced liver damage, as determined by serum enzyme release, IL-1ra had no effect on the degree of hepatic congestion or necrosis at any of the time points examined. On the other hand, administration of antibodies against IL-1ra exacerbated APAP-induced liver toxicity. These results suggest that TNF-alpha and IL-1 alpha play an important role in the degree of damage and recovery that the liver undergoes following APAP intoxication.

Acetaminophen↗
PubMedDate not supplied

The mouse as a model for developmental immunotoxicology.

The laboratory mouse has been the most extensively used model system for demonstrating postnatal immune deficits following perinatal immunotoxicant exposure. Assays utilized have historically been those developed for adult mice. Clear gaps in the available database exist, however, regarding the predictive strength of adult mouse immune screens for detecting either transient or long-lasting postnatal immune suppression. Limited information is also available regarding postnatal ages when various immune assays can be first employed to detect developmental immunotoxicity in mice. Furthermore, difficulties and expense inherent with breeding of in-bred mice, as used for adult immunotoxicity studies, raise questions regarding the feasibility of an in-bred mouse model as a standard, widely available developmental immunotoxicity testing system. These and additional concerns will need to be addressed as a model system with utility for studying developmental immunotoxicants is produced.

Age Factors↗