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PubMed1988

Phorbol ester induction of 8-lipoxygenase in inbred SENCAR (SSIN) but not C57BL/6J mice correlated with hyperplasia, edema, and oxidant generation but not ornithine decarboxylase induction.

Several responses suggested to be critical components of phorbol ester tumor promotion were compared in 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion-sensitive SSIN and TPA promotion-resistant C57BL/6J mice. SSIN mice treated topically with 2 micrograms of TPA showed extensive hyperplasia accompanied by edema, measured as a 26% increase in water content of the skin. Only a very slight hyperplasia and 7% increased water content occurred after TPA treatment of C57BL/6J mice. The induction of ornithine decarboxylase was determined to be the same both in vivo and in vitro for SSIN and C57BL/6J mice, which does not correlate with the histological observations. Because hyperplasia and inflammation can be mediated by arachidonic acid metabolites, it was hypothesized that differences in this metabolic pathway would correlate with the histological responses. No significant qualitative or quantitative differences, however, were observed in the profiles of the major cyclooxygenase products between the strains of mice. Prostaglandin E2, the principal prostaglandin, was synthesized at a 3-fold greater level than prostaglandins D2 or F2 alpha in response to TPA. The most abundant lipoxygenase product was 12-hydroxyeicosatetraenoic acid followed by 8-, 15-, and 5-hydroxyeicosatetraenoic acid. 8-Lipoxygenase activity is elevated 24 h after TPA treatment in the SSIN mice by approximately 4-fold; no elevation is seen in C57BL/6J mice. A comparison of the oxidant response to TPA as well as to phospholipase C showed that SSIN epidermal cells generated a higher level, measured by chemiluminescence, than C57BL/6J cells. This suggests that oxidant generation or possibly 8-lipoxygenase activity may be the basis for the sensitivity or resistance to TPA as a hyperplasiogen and as a tumor promoter.

Animals↗
PubMed1977

[Attempts at biotechnical induction of puberty in young female pigs. 2. Effects of various time intervals between one puberty induction with PMS and HCG to the following estrus synchronization on estrus and ovulation in animals about 190 days old].

A biological engineering approach to induce puberty in 125 young female fattening pigs aged 190 days was undertaken on the basis of a mixture of 500 IU PMS (Prolosanserum, Dessau) with 250 IU HCG (Gonabion, Dresden). The injections were made subcutaneously. Pronounced oestrus symptoms were recorded from the external genital organs of 80% of the probands up to ten days after injection, associated with toleration in 52.8% of them. Toleration usually started on the fourth to sixth days after injection. Cycles began to develop in 57.1% up to the next oestrus period. Animals with -/x weight increase per die of 400 g exhibited lower responses. Results in terms of heat and ovulation were lower along with shorter intervals, when oestric synchronisation was undertaken 53, 32, and 17 days after the induction of puberty (20 days Suisynchron, Bernburg; 750 IU PMS).

Animals↗
PubMed1993

Induction of a macrophage-like nitric oxide synthase in cultured rat aortic endothelial cells. IL-1 beta-mediated induction regulated by tumor necrosis factor-alpha and IFN-gamma.

We investigated the effects of murine rTNF-alpha, human rIL-1 beta, and rat rIFN-gamma in various concentrations and/or combinations on inducible nitric oxide (NO) production in primary cultures of rat aortic endothelial cells. Northern blot analysis of total RNA from induced and control cultures using the cloned mouse macrophage gene of inducible NO synthase as probe as well as polymerase chain reaction using a specific primer sequence gave a positive signal for activated cells only. A RNA approximately 4.4 kb of length similar to the inducible form of NO synthase in macrophages was labeled. The concentration of nitrite as a stable reaction product of NO in culture supernatants was determined 24 h after incubation with the various cytokines. IL-1 beta alone (40 to 1000 U/ml) induced formation of increasing amounts of nitrite with increasing concentrations of IL-1 beta present. Neither TNF-alpha alone (10 to 2000 U/ml) nor IFN-gamma alone 25 to 500 U/ml) showed significant effects on nitrite production. Simultaneous incubation with low concentrations of TNF-alpha (< or = 100 U/ml) and IL-1 beta abrogated the induction effect of IL-1 beta. Conversely, addition of high concentrations of TNF-alpha (> or = 500 U/ml) led to near maximal levels of nitrite formation even at lowest IL-1 beta concentrations (40 U/ml). In addition, simultaneous incubation of endothelial cells with IFN-gamma plus IL-1 beta and/or TNF-alpha led to near maximal NO production of endothelial cells, even at lowest IFN-gamma concentrations (25 U/ml). We hypothesize that the regulating effect of TNF-alpha may in vivo help to prevent local inflammatory responses from spreading to intact sites.

Amino Acid Oxidoreductases↗
PubMed1976

Suppressor cell induction in vitro. I. Kinetics of induction of antigen-specific suppressor cells.

The induction of antigen-specific suppressor cells in vitro, using high concentrations (100 mug/ml) of keyhole limpet hemocyanin (KLH) in Marbrook flasks is described. Spleen and cortisone-resistant thymocytes were the richest source of suppressor cell precursors, compared to lymph node cells, peripheral blood lymphocytes or thoracic duct lymphocytes. Suppressor cells induced with KLH only suppressed KLH-reactive helper cells, and not B cells or helper cells of other specificity. The suppressor cells were T cells, as judged by their sensitivity to anti-Thy-1.2, heterologous anti-T, but not anti-B antisera.

Animals↗
PubMed1981

Variation of interferon induction at the bone marrow level. Studies on interferon induction in relation to natural cell-mediated cytotoxic mechanisms.

The effects of interferon inducers on different cytolytic mechanisms were studied in the high leukemia mouse strain AKR. A clear depression in baseline cytolytic potential and interferon-mediated stimulation of natural killer cell activities was demonstrated. This depression was most pronounced after 8 weeks of age. In contrast, antibody-dependent, cell-mediated cytotoxicity against IgG-coated chicken red blood cells was always normal. Bone marrow chimeras between CBA and AKR mice were produced to investigate the influence of bone marrow vs. host-mediated factors in these two strains with regard to interferon induction and cytolytic functions. Bone marrow genotype was found to be the dominating factor with regard to both parameters. Mice reconstituted with AKR bone marrow were deficient both in interferon production using tilorone and Newcastle disease virus as inducers, and at the level of natural killer cells responding to exogenously administered interferon. The possible relationship between these findings and the development of lymphomas in AKR mice is discussed.

Aging↗
PubMed1985

SCE induction is uncoupled from mutation induction in mammalian cells following exposure to ethylnitrosourea (ENU).

It has been suggested not only that sister chromatid exchange (SCE) induction might serve as a qualitative indicator of mutagenesis, but also that induced SCE frequencies are linearly related to induced mutation frequencies. The consistency of the relationship between SCEs and mutations was tested in the present work. Confluent Chinese hamster ovary (CHO) cells were exposed to ethylnitrosourea (ENU) and then held at confluency for various times prior to initiation of SCE and mutation assays. Cells held at confluency are typically thought to be arrested in their progression through the cell cycle, so that "S-dependent" processes such as fixation of mutations and formation of SCEs will not occur, while DNA repair processes might continue to operate. If repair processes reduce the number of SCE-inducing lesions during the holding period and, hence, reduce the subsequently determined SCE frequencies, then mutation frequencies should similarly be reduced if SCEs and mutations are related. It was observed, however, that induced SCE frequencies decreased exponentially with holding time, while mutation frequencies remained constant. Qualitatively similar results were obtained in log-phase cells. Cell cycle analysis demonstrates that confluent CHO cells can cycle, and ways are considered in which this might affect SCE and mutation frequencies. It is concluded that the decline in SCE frequency (with time) cannot be attributed solely to the presence of cycling cells in confluent cultures. It appears, therefore, that at least some forms of ENU-induced DNA damage that can lead to SCE were repaired and as such are distinct from those forms that are mutagenic. Thus SCEs are not necessarily related to mutations, because the two events may represent manifestations of different forms of DNA damage. Whether or not this represents a universal phenomenon that would hold true for agents other than ENU remains to be determined.

Animals↗
PubMed1981

Induction of Epstein-Barr virus by an new tumor promoter, teleocidin, compared to induction by TPA.

The effect of teleocidin, a new, naturally occurring tumor promoter on induction of Epstein-Barr virus (EBV), was compared with that of a known tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Early antigen (EA) and/or capsid antigen (VCA) of EBV was induced in the EBV genome-carrying cell lines C-6 and P3HR-I cells by teleocidin, its effect being maximal at a concentration of 12.5 ng/ml. The production of infectious EBV from P3-HR-I cells was enhanced by teleocidin maximally at a concentration of 0.5 to 2.5 ng/ml. The outgrowth of EBV-transformed cells from peripheral lymphocytes of seropositive healthy donors was also enhanced by teleocidin at a concentration of 0.02 to 0.5 ng/ml. TPA tested simultaneously in all experiments exhibited the same activities as teleocidin, and was effective at similar concentrations. Teleocidin enhanced both EA and VCA synthesis in P3HR-I cells additively with n-butyrate, but not with TPA. This suggests that teleocidin and TPA have a common mechanism of action, although their chemical structures are different.

Alkaloids↗
PubMed1985

T-T cell interaction in the in vitro induction of delayed-type hypersensitivity (DTH) responses: demonstration of vaccinia virus-reactive helper T cell activity involved in enhanced induction of DTH responses.

C3H/HeN mice were inoculated i.p. with viable vaccinia virus to generate virus-reactive helper T cell activity. 850R X-irradiated spleen cells from vaccinia virus-primed or unprimed mice as helper cells were stimulated in vitro with either trinitrophenyl (TNP)-modified syngeneic spleen cells (TNP-self), vaccinia virus-infected spleen cells (virus-self), or cells modified with TNP subsequent to virus infection (virus-self-TNP) in the presence of normal C3H/HeN spleen cells (responding cells). After 5 days of culture, effector cells were tested for anti-TNP delayed-type hypersensitivity (DTH) responses by adoptive transfer into footpads of syngeneic C3H/HeN recipient mice together with TNP-self. The results demonstrate that spleen cells from virus-primed mice failed to enhance anti-TNP DTH responses when in vitro stimulation was provided by either virus-self or TNP-self alone. In contrast, spleen cells from vaccinia virus-primed mice, but not from unprimed mice, could augment anti-TNP DTH responses when stimulated by virus-self-TNP. Such a helper activity provided by vaccinia virus-primed mice was shown to be antigen-specific, and mediated by Lyt-1+2-T cells. DTH effector cells enhanced by helper cells were also antigen-specific and Lyt-1+2-T cells. Furthermore, vaccinia virus-reactive helper T cell activity could be applied to augmented induction of anti-tumor DTH responses by stimulation with virus-infected syngeneic fibrosarcoma tumor cells. Thus, these results provide evidence for the role of antigen-specific helper T cells in augmenting the development of DTH responses to cell surface antigens including tumor antigens.

Animals↗
PubMed2001

Induction of stearoyl CoA desaturase is associated with high-level induction of emerin RNA.

The genes encoding enzymes involved in fatty acid metabolism are regulated by sterols. Stearoyl CoA desaturase, a key enzyme in the synthesis of unsaturated fatty acyl-CoAs is transcriptionally regulated by fat-free diet and sterols. To identify other genes that are induced in rat liver by fat-free diet we performed an in vivo gene expression profile analysis using DNA microarrays. Here we report that among the genes highly expressed is emerin, an integral protein of the inner nuclear membrane. Mutated or nonexpressed emerin occurs in patients with muscular dystrophy. Sterol regulatory element binding proteins activate the transcription of several sterol regulated genes. To investigate whether sterol regulatory element binding proteins or indirectly cholesterol activates the transcription of stearoyl CoA desaturase and emerin, we cultured Chinese hamster ovary (CHO), either in cholesterol-rich or cholesterol-depleted mediums. We also transiently transfected the cell culture with plasmid encoding sterol regulatory element binding proteins in cholesterol-rich medium. Our data show that cholesterol-supplemented media as well as the transient transfection induced the expression of stearoyl CoA desaturase RNA 3.5- and 7-fold respectively. However, the RNA level of emerin was not altered under these conditions, implying that the parallel induction of emerin is independent of the sterol regulatory element binding regulation pathway.

Animal Population Groups↗
PubMed2002

Epstein-Barr virus latent membrane protein-1 induction by histone deacetylase inhibitors mediates induction of intercellular adhesion molecule-1 expression and homotypic aggregation.

Epstein-Barr virus (EBV) latent membrane protein (LMP)-1 induces B lymphocyte immortalization and activates constitutive signal transduction, including NF-kappaB, JNK/p38, and JAK/STAT pathways. During EBV latency, LMP-1 expression induces several B lymphocyte activation markers, including intercellular adhesion molecule (ICAM)-1. We found that various structurally distinct histone deacetylase inhibitors (HDACI), as well as phorbol ester treatment, induced homotypic aggregation in EBV-positive Burkitt's lymphoma lines. Cell-surface expression of ICAM-1 was concurrently strongly up-regulated by both HDACI and phorbol ester treatments. Cell-surface expression of ICAM-1 was concurrently strongly induced by both HDACI and phorbol ester treatment. Among several ICAM family members, only ICAM-1 was up-regulated by both HDACI and phorbol ester treatments, suggesting that up-regulated ICAM-1 expression might mediate the observed increase in homotypic aggregation. HDACI-induced homotypic aggregation was blocked by exposure to a monoclonal antibody specific for the beta-chain (CD18) of an ICAM-1 ligand, LFA-1. Unexpectedly, HDAC inhibition, but not phorbol ester treatment, induced LMP-1 expression in EBV-positive cell lines, and this LMP-1 species was identified by RT-PCR and immunoblot analyses as the latent form of LMP-1. Control of EBV LMP-1 gene expression by HDACI inhibition occurs at the transcriptional level, as indicated by nuclear runoff studies and analysis of steady-state mRNA levels. Dominant-negative LMP-1 efficiently blocked HDACI-induced ICAM-1 up-regulation, and ectopic expression of LMP-1 activated expression of an ICAM-1 promoter-driven reporter gene. The HDACI-induced up-regulation of ICAM-1, and consequent homotypic aggregation, were efficiently blocked by the addition of N-acetyl-L-cysteine and by ectopic expression of a super-repressor IkappaBalpha, while LPM-1 induction was unaffected, suggesting that these effects are mediated by NF-kappaB. We demonstrate, therefore, that the latent isoform of LMP-1 is induced by HDAC inhibition, and that HDACI-induced latent LMP-1 expression, through NF-kappaB activation, is responsible for ICAM-1 expression up-regulation and homotypic adhesion.

Antibodies, Monoclonal↗
PubMed2002

Hyperthermic induction of apoptosis in malignant fibrous histiocytoma cells: possible involvement of a p53-independent pathway in the induction of bax gene.

We have previously reported the unique heat sensitivity of a cell line of malignant fibrous histiocytoma cells, the MFH-2NR cell line. In the present study, treatment of MFH-2NR cells, at 43 degrees C for 1 h evoked typical apoptosis in these cells, which showed characteristic morphological changes, such as internucleosomal DNA fragmentation (DNA ladders), cell shrinkage, and chromatin condensation. Under these conditions, we examined p53 and bax protein levels, and p53 and bax mRNA expression to assess the potential relationship between these two proteins for the induction of apoptosis. The p53 protein, which is usually detected in trace amounts in normal cells, was highly expressed in untreated MFH-2NR cells, and the level did not increase after heat treatment, whereas the bax protein level increased from 30 min after the treatment. No change in p53 mRNA was found, but a transient increase in bax mRNA, peaking at 30 min, was detected by Northern blotting. DNA sequence analysis of the p53 gene from MFH-2NR cells demonstrated a GGG right arrow GAG homozygous point mutation in codon 242 of exon 6. These results suggest that the expression of bax protein and mRNA was augmented by a p53-independent pathway in the hyperthermia-induced apoptosis of MFH-2NR cells.

Animals↗
PubMed1979

In vitro induction of cytotoxic effector cells against human neoplasms. I. Sensitization conditions and effect of cryopreservation on the induction and expression of cytotoxic responses to allogeneic leukemia cells.

Peripheral blood lymphocytes (PBL) from normal human donors were sensitized in vitro against allogeneic human acute myelocytic leukemia (AML) cells by means of an unidirectional mixed lymphocyte-tumor cell culture (MLTC) technique. The cytotoxic responsiveness of the sensitized lymphocytes, as determined in vitro by the 51Cr-release assay, varied among individual lymphocyte donors and was greatly dependent on the sensitization culture conditions. Induction of cytotoxic effector cells was augmented appreciably by adding to the cultures minute amounts of the immunopotentiating agent MER-BCG. Responding lymphocytes and stimulating leukemia cells cryopreserved for several weeks in liquid nitrogen were as effective as fresh cells in generating effector lymphocytes; the cytotoxic capacity of already sensitized lymphocytes was fully retained by cryopreservation. The implications of these findings for possible clinical employment of in vitro sensitized lymphocytes in adoptive immunotherapy of cancer are discussed.

Adult↗
PubMed1987

Opioids and hibernation. II. Effects of kappa opioid U69593 on induction of hibernation in summer-active ground squirrels by "hibernation induction trigger" (HIT).

A "Hibernation Induction Trigger" (HIT) isolated from plasma of winter-hibernating woodchucks induced hibernation in summer-active ground squirrels (Citellus tridecemlineatus). Effects of kappa opioid U69593 on the HIT-induced hibernation were examined. U69593 alone did not elicit marked behavioral alteration or hibernation in summer-active ground squirrels. U69593, however, antagonized hibernation induced by HIT in summer active ground squirrels. In the guinea pig ileum myenteric plexus-longitudinal muscle preparation, woodchuck HIT depressed the electrically-induced contraction. The depression was, however, neither reversed nor blocked by naloxone even when naloxone was used at high doses. This study demonstrates that kappa opioid, at least in the case of U69593, was unable to induce hibernation in the summer-active ground squirrels. The results also demonstrate that woodchuck HIT, like the bear HIT, did not act directly at opioid receptors. Together with our previous observation that naloxone blocked summer hibernation induced by HIT (Bruce et al., Life Sci.., this issue), it is tempting to suggest that HIT may not mediate its effects through kappa opioid receptors but may do so through other types of opioid receptors such as mu or delta. U69593 may antagonize HIT-induced hibernation as a mu or delta receptor antagonist.

Animals↗
PubMed1982

Lack of association between induction of dominant-lethal mutations and induction of heritable translocations with benzo[a]pyrene in postmeiotic germ cells of male mice.

Benzo[a]pyrene was tested for induction of dominant-lethal mutations in germ cells of male mice. Clear-cut dominant-lethal effects were induced in middle and early spermatozoa. In contrast to the dominant-lethal observed the study showed no detectable increase in heritable translocations for these stages over the spontaneous level. Thus, the results provide another example of a chemical mutagen that is effective in inducing dominant-lethal mutations but relatively ineffective in inducing heritable translocations in male postmeiotic germ cells.

Animals↗
PubMed1977

Elective induction of labor conducted under lumbar epidural block. I. Labor induction by amniotomy and intravenous oxytocin.

Epidural analgesia (bupivacaine) was administered during labor after amniotomy, in some cases supplemented by intravenous oxytocin. A higher incidence of transient uterine hypertonus was seen after blocking. Fetal heart rate changes mainly took the form of bradycardia (in association with uterine hypertonus). At birth, the maternal biochemical condition was characterized by a lower degree of metabolic acidosis, compared to normal unanesthetized controls. The fetuses displayed a slight degree of hypoxia and hypercapnia. The mechanisms underlying these modifications are discussed. Epidural blockade in combination with elective induction of labor, whether or not supplemented by intravenous oxytocin, may carry a risk. Its magnitude is considered acceptable for both mother and fetus provided they are constantly under close surveillance, limited amounts of bupivacaine are administered and the second stage of labor is kept short. However, some warnings against epidural analgesia apply to patients with placental insufficiency and very active labor.

Adult↗
PubMed1981

Relationship between in vivo mitomycin C exposure, sister chromatid exchange induction and in vitro mitogenic proliferation. II. Effect of aging on spleen cell mitogenesis and sister chromatid exchange induction.

In vivo administration of mitomycin C (MMC) produces an increase in both the frequencies of sister chromatid exchange (SCE) as well as inhibition of in vitro mitogenic responses. At low concentrations of MMC (2 mg/kg) spleen cell suspensions from both young and old mice showed similar patterns of mitogen inhibition and increased SCE frequencies. At high MMC concentrations (5 mg/kg) significant differences between young and old responses were observed. Spleen cells from young animals displayed mitogen-inhibition curves which plateaued with increasing doses of MMC, while the cells from old animals displayed a continuing increase in mitogenic inhibition. MMC-induced SCE frequencies revealed a complementary pattern: increasing SCE frequencies as a function of MMC concentration in young spleen cells while SCE levels plateaued in old spleen cell populations. The results of these studies suggest (1) that an inverse relationship exists between sister chromatid exchange induction and mitogenic response, (2) that cells from older animals may have an increased sensitivity to high levels of DNA damage (5 mg/kg MMC), and (3) that this sensitivity may be expressed functionally by increased inhibition of in vitro mitogenic responses.

Aging↗
PubMed1991

Comparative mutagenicity testing of bropirimine, 1. Induction of chromosome aberrations in CHO cells is not reflected in induction of mutation at the TK locus of L5178Y cells.

Bropirimine (U-54,461) is a novel compound which is being developed as a biological response modifier for use in treatment of neoplastic and viral disease. Compounds of this type exert their therapeutic effects by immuno-stimulation or other non-cytotoxic mechanisms. The purpose of the experiments described in this paper was to evaluate the hazard potential of this drug. Bropirimine was previously reported to be negative in the Ames Salmonella assay (Aaron et al., 1989a) and the in vitro UDS assay (Aaron et al., 1989b). In experiments reported here positive response was observed in a test for clastogenicity in vitro in CHO cells, but bropirimine was negative in the L5178Y mouse lymphoma TK+/- assay. A subsequent experiment demonstrated the ability of bropirimine to induce HPRT mutations in CHO cells. Interestingly, evidence for induction of chromosome aberrations in the L5178Y cells by bropirimine was also obtained. While the reason for the apparent insensitivity of the L5178Y TK+/- assay to bropirimine is unexplained by the experiments, it is clear that at high dose bropirimine is capable of clastogenesis in both CHO and L5178Y cells and can give rise to gene mutations in CHO cells but apparently not in L5178Y cells.

Animals↗
PubMed1994

Differentiation of sensorimotor neuronal structures responsible for induction of motor evoked potentials, attenuation in detection of somatosensory stimuli, and induction of sensation of movement by mapping of optimal current directions.

Transcranial magnetic stimulation (TMS) of the sensorimotor cortex can evoke motor evoked potentials (MEPs), attenuation in detection of somatosensory stimuli (ADSS), and sensation of movement (SOM) referred to the same body part. In this study we tried to differentiate the substrates responsible for these effects. In 6 normal volunteers, TMS was applied with a nearly monopolar Dantec stimulator and a butterfly coil. Optimal scalp location and current direction were determined for induction of MEPs in abductor pollicis brevis (APB), first dorsal interosseous (FDI), and adductor digiti minimi (ADM); SOM in digits 2 and 5 in an ischemically paralyzed hand; and ADSS applied to digits 2 and 5. All 3 muscles' MEPs and SOM and ADSS in both digits were optimally activated from a single scalp position. In all subjects, optimal current directions for MEPs pointed anteriorly; those for ADSS and SOM pointed posteriorly. Optimal current directions showed the same progression in all subjects for MEPs (ADM, FDI, and APB from antero-lateral to antero-medial), ADSS (digit 5 postero-medial, 2 postero-lateral), and SOM (digit 1 through 5 postero-lateral to postero-medial). We conclude that neuronal networks targeting corticospinal neurons responsible for MEPs are different from those leading to SOM and ADSS (which could not be differentiated).

Adult↗