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PubMed1988

Potential detrimental effects of rodent viral infections on long-term experiments.

Healthy animals are of paramount importance in obtaining meaningful, reliable scientific results. Viral infections of rodents often have a significant impact on various types of biomedical research. Laboratory animal specialists and researchers must be aware of the possible consequences associated with the use of infected animals. The objective of the paper is a discussion of the frequently encountered viral infections that can complicate or invalidate the interpretation of results by altering the host's response.

Animals↗
PubMed1975

Distribution along the axon and into various subcellular fractions of molecules labeled with (3H)leucine and rapidly transported in the garfish olfactory nerve.

The distribution of molecules labeled with [3H]leucine by fast axoplasmic transport in vivo has been studied in the garfish olfactory nerve after incorporation of the amino acid by the olfactory mucosa. Owing to the size of the nerve, it has been possible to follow the fate of the labeled molecules in 10 different subcellular fractions of 6 consecutive nerve segments. Each segment represents a different part of the profile developed by the transported radioactive molecules. In order to determine the influence of the perikaryon (rate of protein synthesis and rate of protein release into the axon) transport was studied under 3 different conditions: (1) intact nerves (simply labeled with [3H]leucine); (2) nerves cut from the cell bodies 6 h after application of [3H]leucine; and (3) nerves pulse-chase labeled for 1 h. Several conclusions can be drawn. (1) The bulk of the rapidly transported molecules are membranous axonal proteins, as determined by enzyme markers. Most are found in subcellular fractions representing 17% of the total axonal protein. They are synthesized very rapidly in the cell bodies (less than 1 h after isotope deposition) and exhibit the highest specific activities measured. These high specific activities were found in the same axonal membrane fractions in both plateau and crest, suggesting that the membrane precursors are transported as particles rather than as subunits. (2) The majority of these proteins are released into the axon immediately after synthesis; however, at least 30% of the labeled axonal membranous proteins are not released with the fast wave itself but progressively over a long period of time. (3) The majority of the moving material, particularly in membranous fractions, is left behind the fast wave and is deposited in the axon. When the front base of the fast wve has covered 70% of the total nerve length, only 19% of the labeled material of the main axonal membranous fraction appears still to be moving. (4) Proteins with high specific activities are found near the cell bodies and may be the result of early axonal transport of amino acids, diffusing later into the surrounding cells and being incorporated into proteins. Some free amino acids are also transported along the axon.

Acetylcholinesterase↗
PubMed1992

Effect of prostaglandin E2 on plasma lactic dehydrogenase activity in (NZB x NZW)F1 mice with a chronic infection of lactic dehydrogenase virus.

The effect of prostaglandin E2(PGE2) on blood LDH values was investigated in (NZB x NZW)F1 mice with or without an established infection with lactic dehydrogenase virus (LDV). Plasma LDH decreased in infected mice treated with PGE2, but increased in infected mice treated with indomethacin, an inhibitor of PGE2. However no significant effect on LDH occurred in uninfected mice treated with PGE2 or indomethacin. To investigate the mechanisms of decreased LDH activities resulting from treatment with PGE2, clearance tests were performed. Clearance of LDH-5, but not LDH-1, was faster in PGE2-treated mice than in non-treated mice, whether or not they were infected with LDV. The results suggest that enhanced clearance of LDH-5 in mice treated with PGE2 may account for the fall in plasma LDH in LDV-infected mice.

Animals↗
PubMed1988

Physiological relationships among stress, viruses, and cancer in experimental animals.

Anxiety-induced psychoneural stimulation, via the hypothalamic-pituitary axis, activates the adrenal cortex to release corticosteroids, which elicit various alterations of corticoid-sensitive cell-mediated immunologic processes. Stress sensitive murine tumor-host experimental models have been utilized to demonstrate various effects of stress upon aspects of tumor development. Although many of the observed anxiety-induced alterations of tumor-related parameters can be interpreted in terms of corticoid-induced modifications of immune functions, other observations are more difficult to interpret, and may be caused in part by corticosteroid-independent modulation of lymphocyte functions. In the case of tumors induced by oncogenic viruses, anxiety-induced plasma corticoid elevations may also act independently of the immune system to stimulate tumor development via hormone binding sites on proviral DNA. Rigorously controlled environmental and experimental conditions are fundamental for the demonstration and interpretation of stress-related phenomena. Technical prerequisites include protective animal facilities, special handling procedures, the use of nontraumatic stressors, and the recognition of vital psychosocial, coping and timing factors. Various biologic factors, such as sex, genetic substrain differences and common interfering viral infections, must also be controlled or taken into consideration.

Adrenal Cortex Hormones↗
PubMed1992

Enhanced clearance of lactic dehydrogenase-5 in severe combined immunodeficiency (SCID) mice: effect of lactic dehydrogenase virus on enzyme clearance.

The lactic dehydrogenase (LDH) level in plasma and the clearance of LDH in C.B-17 scid (severe combined immunodeficiency; SCID) mice were compared with those in C.B-17 or BALB/cCrSlc mice with or without lactic dehydrogenase virus (LDV) infection. The resting enzyme level in SCID mice showed little difference from that in C.B-17 or BALB/cCrSlc mice. The degree of increased plasma LDH level in SCID mice was lower than that in C.B-17 and BALB/cCrSlc mice after LDV infection. To assess the mechanisms of decrease in LDH elevation in SCID mice infected with LDV, virus replication was compared in SCID and BALB/cCrSlc mice. The infectivity titre of plasma in SCID mice was higher (more than 10 times) than that in BALB/cCrSlc mice. Moreover, the percentage of virus antigen positive Kupffer cells was higher in SCID mice than that in BALB/cCrSlc mice. The level of endogenous LDH release as a result of carbon tetrachloride treatment was similar in the SCID and BALB/cCrSlc mice. The clearance rate of endogenous LDH was greater in SCID mice than in BALB/cCrSlc mice with or without LDV infection. The rate of clearance of intravenously injected porcine LDH-5, but not porcine LDH-1, was enhanced in SCID mice as compared with that in BALB/cCrSlc mice. Furthermore, carbon clearance was higher in SCID mice than that in BALB/cCrSlc mice. These results suggest that the smaller increase of plasma LDH after infection might be due, at least in part, to the enhanced LDH-5 clearance function by macrophages in SCID mice.

Animals↗
PubMed1990

Flow cytometry to identify cell types to which enzymes bind. Effect of lactic dehydrogenase virus on enzyme binding.

Flow cytometry was used to measure the binding of enzymes (i.e. lactate dehydrogenases 1 and 5, malate dehydrogenase, and asparaginase) to cells. Of the four enzymes studied, asparaginase showed the greatest binding. Single color analysis revealed that asparaginase bound best to preparations enriched in macrophages, and dual color analysis showed that the binding was to macrophages. Studies on continuous cell lines revealed that asparaginase bound to one mouse macrophage line, but not to another or to murine fibroblasts. Inoculation of mice with lactic dehydrogenase virus, a virus that infects macrophages, decreased the in vivo clearance of asparaginase from the circulation and the in vitro binding of asparaginase to peritoneal macrophages. It is concluded that flow cytometry can be used to study the binding of enzymes to cells, to identify the cell type to which the enzyme binds, and to measure changes in the capacity of cells to bind enzymes.

Animals↗
PubMed1988

Regulation of enzyme levels in the blood. Influence of environmental and genetic factors on enzyme clearance.

Since its discovery, lactic dehydrogenase virus (LDV) has remained unique as a model of long-term enzyme elevation due to impairment of enzyme clearance. The present study shows that mice inoculated with silica develop an increase in plasma lactate dehydrogenase (LDH) lasting for at least 6 months and that the enzyme elevation is due, at least in part, to impairment of clearance. The extent of the enzyme elevation is dependent on both the dose and route of silica administration and mice that had received both silica and LDV showed a more profound impairment of LDH clearance than mice that had received silica or LDV alone. Examination of the factors that regulate circulating enzyme levels in normal mice revealed that whereas there was no difference in resting enzyme levels among several inbred strains of mice (BALB/cAnN, NZBWF1/J,B10.D2/nSnN, and A/J mice), when mice were stressed by the administration of an enzyme load, certain inbred strains (BALB/cAnN) cleared the enzyme rapidly and others (B10.D2/nSnN) cleared the enzyme slowly. Moreover, in B10.D2/nSnN mice, enzyme clearance was age-related. When different strains of mice were infected with LDV, LDH levels were substantially higher in the circulation of slow enzyme clearers as compared to rapid enzyme clearers. It is concluded that both environmental and genetic factors influence the clearance of LDH and that impairment of enzyme clearance may be a more important factor than previously suspected in regulating enzyme levels in disease states.

Animals↗
PubMed1979

Matching of chemotherapy to mouse strain and lymphoid tumor type to prevent tumor-induced suppression of specific T- and B-cell functions.

Specific immunological and hematopoietic functions were studied during treatment with antineoplastic agents in mice bearing syngeneic lymphoid tumors: 70Z/2, a B-cell lymphoma of C57BL X DBA/2 F1 (hereafter called (BD2F1) mice; EL4, a T-cell lymphoma of C57BL/6 mice; or J774, a macrophage tumor of BALB/c mice. Both B- and T-lymphocyte function (antibody-forming cells and cell-mediated lymphocyte lympholysis toward alloantigens) were suppressed in spleen cells of mice bearing these tumors. Other hematopoietic functions (granulocyte, macrophage, and megakaryocyte progenitor cells) were variably influenced by growth of these lymphoid tumors. J774 enhanced, but 70Z/2 suppressed, megakaryocyte progenitor cells. J774 and 70Z/2 increased levels of granulocyte-macrophage progenitor cells. EL4, the T-cell lymphoma, did not influence either cell type. Significant variation in strain sensitivity to drug toxicity and drug effectiveness in different tumor-host systems was observed. Increased median survival time with reversal of tumor-induced immune dysfunction, without toxicity to hematopoietic progenitor cells, was realized in two tumor-host-drug combinations. Polyinosinic-polycytidylic acid was effective against J774, while actinomycin D was active against 70Z/2. Mitomycin C effectively reduced tumor load, as evidenced by loss of splenic tumor colony-forming cells for all three tumors. This agent prolonged survival and concomitantly restored immunological responsiveness in hosts immunosuppressed by growth of 70Z/2 or J774. Paralleling tumor reduction with mitomycin C therapy, the splenic hematopoietic progenitor and colony-forming B-cells were reduced in tumor-bearing and tumor-free mice, thus compromising its therapeutic effectiveness. 1-beta-D-Arabinofuranosylcytosine reduced tumor load with marginal toxicity toward hematopoietic progenitor and colony-forming B-cells. However, immune responsiveness was only partially restored, and median survival was not increased. The results presented show the diversity of therapeutic drug effectiveness in increasing mean survival time and influencing other life-sustaining parameters (immunological and hematopoietic functions).

Animals↗
PubMed1979

Correlation of extracts obtained by high efficiency gel chromatography of lactic dehydrogenase virus infected mouse serum and cytosol from human tumors using leukocyte adherence inhibition assay.

Immunochemically active fractions were obtained using Separon Hema-300-glc(R) from serum of lactic dehydrogenase virus (LDV) infected mice and from homogenates of human tumors. The mixture of proteins of tumorous origin from the cytosol giving a positive reaction in the leukocyte adherence inhibition (LAI) test was found in the same fractions showing maximum of absorbance at 340 nm in the spectrophotometer and a corresponding peak in the refractometer. Analogous peaks were not proved in material obtained from healthy controls, but they were found in some human placentas and fetal organs. The LDV fraction obtained from mouse serum served as a "control" antigen in LAI test for human tumor testing, and results corresponded with those obtained using cytosol specific for the tumor under study.

Animals↗
PubMed1977

Immunodepression, ascites tumour and lactate dehydrogenase virus.

The delayed hypersensitivity (DH) response to picryl chloride was studied in Ehrlich ascites tumour-bearing and normal control mice. A significant depression of the DH response was found in the tumour-bearing mice, which was associated with a marked elevation of serum lactate dehydrogenase (LDH). Depression of DH was also observed in mice receiving cell-free ascitic fluid. These mice also showed an elevated serum LDH which is assumed to be associated with the lactate dehydrogenase virus. A method for assaying DH in vivo is described.

Animals↗