Search PubMed⌕ Search

Biomedical subjects

L D Koller

Publications and source records attributed to L D Koller.

At least 73 records · Page 4Linked to original sources

Immune response in aged mice exposed to lead.

Mice were exposed to 0, 13, or 1,300 ppm lead in drinking water for 18 months. The immunological assays examined were mitogen (lipopolysaccharide E. coli, concanavalin A, and phytohemagglutinin-P) stimulation of lymphocytes; erythrocyte-antibody (EA), erythrocyte-antibody-complement (EAC), and phagocytosis of macrophages; and EAC of splenic lymphocytes. As measured by the majority of these assays, the low dosage (13 ppm) of lead tended to stimulate certain immune responses (lymphocyte mitosis, EA, and EAC) while the high dosage (1,300 pm) did not provoke an appreciable alteration. The results were interpreted by comparing data on aged mice with data on young adult mice. It was apparent from this comparison that the aged mice were naturally immunosuppressed. Therefore, the results obtained from lead-exposed mice were unpredictable.

Aging↗

Enhanced polychlorinated biphenyl lesions in Moloney leukemia virus-infected mice.

The hepatic toxicity produced by polychlorinated biphenyls (PCB) was enhanced in mice that were inoculated with an oncogenic virus, Moloney leukemia virus (MLV). Whenever there was neoplastic involvement of the spleen by MLV, the hepatic lesions produced by PCB were more pronounced than in those of non-MLV inoculated mice. Mice were exposed to PCB Aroclors, 1254, 1242, and 1221 for six months. Aroclors 1254 and 1242 were hepatotoxic with Aroclor 1254 causing death. Aroclor 1221 did not affect the mice. Liver weights in mice that were fed PCBs for six months and then maintained on a PCB-free diet for an additional three months were comparable with those of non-PCB exposed mice. These results suggest that the PCB-produced hepatic lesions (noncirrhotic) regenerate after removal of PCB from the diet. Polychlorinated biphenyls did not affect (promote or induce) the oncogenesis of MLV in this study.

Animals↗

Histopathologic study of experimental Sarcocystis hemionilatrantis infection in fawns.

Mule deer fawns (Odocoileus hemionus hemionus) inoculated with sporocysts of Sarcocystis hemionilatrantis became infected, developed clinical signs of disease, and died, due to the infection itself or from intercurrent pneumonia. Clinical signs were first noticed 18 days after infection and fawns died from postinfection days 27 to 63. Histopathologic examination revealed early lesions in skeletal muscle which consisted of perivascular necrosis with mononuclear and neutrophilic cell infiltration, accompanied by edema, degeneration, and focal necrosis of muscle. Subsequently, this reaction subsided and the cellular infiltrate dissipated. An infected macrophage usually remained in the vacuolated muscle space; each macrophage was surrounded by a clear halo. Developing Sarcocystis schizonts were identified in the cytoplasm of the macrophages, and the cytoplasmic membrane eventually ruptured releasing merozoites. The merozoites then developed into typical muscle cysts. Results of the present study indicated that S hemionilatrantis is a pathogen of mule deer under experimental conditions. Pathogenicity should be investigated to determine if S hemionilatrantis causes death or debilitation in wild mule deer under natural conditions.

Animals↗

Effect of dietary selenium on tumor induction by an oncogenic virus.

Mice exposed to selenium-supplemented or -deficient rations were inoculated with an oncogenic virus, Rauscher leukemia virus (RLV), Splenic lesions were not altered by dietary selenium supplementation or depletion. It is concluded that selenium does not affect neoplasia induced by RLV in mice.

Animals↗

Humoral antibody response in mice after single dose exposure to lead or cadmium.

A single dose of lead administered orally or intraperitoneally (IP) to mice stimulated formation of IgM antibody. Cadmium caused an increase in IgM antibody formation when injected ip but resulted in a slight decrease when given orally. Lead, orally or ip, significantly reduced IgG antibody but the IgG antibody response decreased only when cadmium was given orally and increased when injected ip. Since responses vary according to route of administration, experiments should be designed so that experimental exposure will simulate natural exposure in order to develop comparable data.

Administration, Oral↗

Hexamitiasis in cadmium-exposed mice.

Mortality was observed in 4- to 5-week-old Swiss Webster mice exposed to 300 or 3 ppm cadmium as cadmium chloride in the drinking water. Mice receiving 300 ppm cadium suffered 26% mortality as compared with 7% of those on the low cadmium dose. Death did not occur in control mice. Clinical signs and histopathology established Hexamita muris as the causative agent. Cadmium lesions were not observed. It is suggested that mortality due to hexamitiasis resulted from synergism between cadmium and H muris.

Animals↗

Antibody suppression by cadmium.

Mice exposed to subclinical doses of cadmium chloride for ten weeks and inoculated with antigen six weeks after discontinuance of exposure had a remarkable decrease in antibody-forming cells, particularly IgG. These results indicate that immunosuppression produced by environmental contaminants may persist for several months after exposure to the contaminant.

Animals↗

Experimentally induced Fasciola hepatica infections in black-tailed deer.

The susceptibility of black-tailed deer (Odocoileus hemionus columbianus) to the common liver fluke (F. hepatica) was studied. Two deer and one sheep comprised each of three experimental groups. Animals in each group were inoculated individually with 250, 500, or 1000 F. hepatica metacercariae. One deer and one sheep given 1000 metacercariae died with lesions consistent with black disease 7 weeks after inoculation. At necropsy 6 or 15 weeks postinoculation, the mean percentage recovery of the inoculum was 38.9% from the deer and 51.9% from the sheep. Fluke eggs recovered from the deer were viable and metacercariae cultured from the eggs were fully infective for sheep. Pathologic changes associated with F. hepatica infection were more severe in the infected deer; consequently, the deer were less resistant to the lethal effects of the parasite than sheep. Considering the experimental results and the fact that naturally acquired common liver fluke infection has been reported infrequently from black-tailed deer, it was concluded that black-tailed deer do not constitute a significant reservoir for F. hepatica in domestic livestock.

Animals↗

Methylmercury: effect on oncogenic and nononcogenic viruses in mice.

Mice fed methylmercury chloride at dosages of 1 or 10 ppm for 84 days had significantly higher mortality rates when inoculated with encephalomyocarditis virus (nononcogenic) than did nonmethylmercury-treated mice. However, methylmercury fed to mice which were inoculated with Rauscher leukemia virus (oncogenic) did not alter the course of neoplasia. These results demonstrate that prolonged exposure to subclinical concentrations of methylmercury increased susceptibility of a host to a nononcogenic, but not to an oncogenic, virus.

Animals↗