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Biomedical subjects

I Martin-Kleiner

Publications and source records attributed to I Martin-Kleiner.

12 recordsLinked to original sources
PubMed2006

PMA and doxorubicin decrease viability, MTT activity and expression of CD10 marker on NALM-1 leukemic cells.

PMA (10, 20 ng/ml) and doxorubicin (5-20 ng/ml) decreased the viability and MTT-activity of NALM-1 pre-B leukemic cells (3 days' treatment). Further, CD10 was downregulated, suggesting that PMA and doxorubicin induced differentiation of NALM-1 cells. However, PMA did not alter expression of B cell markers CD20 and of mIgM. In contrast to PMA, another differentiation agent ATRA did not alter CD10 expression on NALM-1 cells but affected viability after 6 days (5, 10 ng/ml). The data in this study are the first evidence that PMA and doxorubicin inhibited viability and MTT activity and induced partial differentiation, by decreasing CD10 on NALM-1 cells.

Antibiotics, Antineoplastic↗
PubMed2004

A pilot study of mitochondrial DNA point mutation A3243G in a sample of Croatian patients having type 2 diabetes mellitus associated with maternal inheritance.

In this work, patients having type 2 diabetes mellitus and diabetic mothers were tested for the presence of mitochondrial DNA point mutation A3243G. This mutation is associated with the MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes), diabetes and deafness. Twenty-two diabetic persons were screened. DNA was isolated from peripheral blood lymphocytes and from swabs of oral mucosa. The mitochondrial DNA point mutation A3243G was detected using PCR-RFLP test. The mutation was detected in oral mucosal DNA of two patients (but not from lymphocyte DNA). One patient was a man with hearing and visual impairments and proteinuria; the other was a woman having proteinuria but no hearing impairment. The mutation was not detectable in oral mucosal DNA from the control persons: 20 diabetic patients having diabetic fathers and 22 healthy, nondiabetic volunteers. The incidence of mitochondrial DNA point mutation A3243G in this study of Croatian diabetic patients is in line with data in the literature.

Adenine↗
PubMed2002

The effect of opioid agonists of delta-class DSLET, mu-class DAMGO, kappa-class U-69593 and an opioid antagonist, naloxone, on MTT activity of NALM-1 leukemic cells.

The effects of synthetic agonists of delta-, mu-, kappa-opioid classes were studied on the proliferation of NALM-1 leukemic cells, using the MTT-test. Delta-opioid DSLET and mu-opioid DAMGO mildly and transiently decreased, in higher concentrations, the MTT-activity of NALM-1 cells after 6 h of treatment. The kappa-opioid agonist U-69593 mildly suppressed proliferation of NALM-1 cells after 48 h of treatment. Naloxone, an opioid receptor antagonist, mildly and transiently diminished MTT-activity of NALM-1 cells after 6 h of treatment. Treatment with opioid agonists, DAMGO, DSLET, U-69593, and an opioid antagonist naloxone for 6, 24, and 48 h, did not trigger DNA fragmentation, which was considered as a possible mechanism of action.

Benzeneacetamides↗
PubMed2001

The effect of the zeolite clinoptilolite on serum chemistry and hematopoiesis in mice.

Zeolites are natural or synthetic crystalline alumosilicates with ion exchanging properties. Supplied in fodder, they promote biomass production and animal health. Our aim was to assess the effects of the natural zeolite, clinoptilolite, on hematopoiesis, serum electrolytes and essential biochemical indicators of kidney and liver function in mice. Two preparations differing in particle size were tested: a powderized form obtained by countercurrent mechanical treatment of the clinoptilolite (MTCp) and normally ground clinoptilolite (NGCp). Young adult mice were supplied with food containing 12.5, 25 or 50% clinoptilolite powder. Control animals received the same food ration without the clinoptilolite. After 10, 20, 30 and 40 days, six animals from each group were exsanguinated to obtain blood for hematological and serum for biochemical measurements as well as to collect femoral bone marrow for determination of hematopoietic activity. Clinoptilolite ingestion was well tolerated, as judged by comparable body masses of treated and control animals. A 20% increase of the potassium level was detected in mice receiving the zeolite-rich diet, without other changes in serum chemistry. Erythrocyte, hemoglobin and platelet levels in peripheral blood were not materially affected. NGCp caused leukocytosis, with concomitant decline of the GM-CFU content in the bone marrow, which was attributed to intestinal irritation by rough zeolite particles. The mechanically treated clinoptilolite preparation caused similar, albeit less pronounced, changes. In a limited experiment, mice having transplanted mammary carcinoma in the terminal stage showed increased potassium and decreased sodium and chloride levels, severe anemia and leukocytosis, decreased bone marrow cellularity and diminished content of hematopoietic progenitor cells in the marrow. The clinoptilolite preparations ameliorated the sodium and chloride decline, whereas the effects on hematopoiesis were erratic.

Administration, Oral↗
PubMed2001

Chronic opioid treatment of the mouse thymoma cell lines R1.G1 and R1EGO leads to down-regulation of the kappa opioid receptor without desensitization of adenylyl cyclase activity.

Kappa opioid agonists alter some immune functions of macrophages, and T- and B-lymphocytes. The mouse thymoma cell lines R1.G1 and R1EGO express only kappa-opioid receptors and these kappa-opioid receptors are coupled to an inhibitory GTP-binding regulatory protein. Binding of kappa-opioid agonists to the opioid receptor leads to the inhibition of adenylyl cyclase activity in these cells. In this study, an acute (15 min) and chronic (24 h) treatment of R1.G1 and R1EGO cell with a potent kappa-opioid agonist (-)U50,488 (100 nM) was studied to determine if a kappa-opioid agonist altered receptor number and/or desensitization of adenylyl cyclase activity in these two cell lines. Chronic treatment of both R1.G1 and R1EGO cells with (-)U50,488 lead to down-regulation of the kappa-opioid receptor, measured as a decrease of approximately 50% in the Bmax value for the binding of [3H]U69,593. The binding affinity (Kd value) was not affected after chronic treatment either in R1.G1 or R1EGO cells. There was no difference in the magnitude of inhibition of adenylyl cyclase activity by (-)U50,488 between the acute (15 min) and chronic (24-h) treatment in both cell lines R1.G1 and R1EGO. This study indicates that chronic opioid treatment of mouse thymoma R1.G1 and R1EGO cell lines leads to down-regulation of the receptor, without desensitization. This phenomenon was observed in R1.1 parent mouse thymoma cell line and recently in CHO cells expressing kappa-opioid receptor. This study demonstrates that unlike some neuronal preparations, chronic opioid treatment of the thymoma cell lines resulted in receptor down-regulation without desensitization.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1999

The synthetic kappa-opioid agonist (-)U50,488 does not affect calcium transport into R1.1 mouse thymoma cell line.

In this paper, the effect of the synthetic kappa-opioid agonist (-)U50,488 on 45Ca2- transport into R1.1 mouse thymoma cells is presented. This thymoma cell line expresses selectively the kappa-opioid class of receptors. 45Ca2+ transport into R1.1 cells was not affected by the kappa-opioid agonist (-)U50,488 (10(-10) M-10(-4) M) alone, or in the presence of the plant lectins: PHA (250 microg/ml) and Con A (800 microg/ml), after a 60 min treatment. The plant lectins PHA and Con A stimulated 45Ca2+ transport into R1.1 cells, in high concentrations (100-800 microg/ml) and (200-1000 microg/ml) respectively, after a 60 min treatment. Thus, 45Ca2+ transport was not affected in R1.1 cells by the kappa-opioid agonist (-)U50,488 alone, or in the presence of mitogens after a 60 min treatment. This negative result does not indicate the lack of calcium channels on R1.1 cells, since the plant lectins PHA and Con A were able to stimulate 45Ca2+ transport into R1.1 cells.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Pretreatment of human peripheral blood lymphocytes with interleukin-2 or dexamethasone does not alter their response to Met-Enkephalin in a NK-cytotoxic assay.

The effect of Met-Enkephalin (MENK; 10(-12) - 10(-8) M) on NK-activity of peripheral blood lymphocytes (PBL) after in vitro treatment (18 h, 37 degrees C) was examined in 30 young, healthy male donors. In the group as a whole (n = 30), no significant effect of MENK was detected. At the individual level, 18 of 30 donors (60%) responded to MENK either by mild enhancement (up to 8%, 8 responders), or by mild attenuation (up to 12%, 10 responders) of the basal NK-activity. The effect of MENK was donor-related regarding the dose-response, E/T ratio, and direction of MENK action. The influence of pretreatment of PBL (1 h) with either graded doses of interleukin-2 (IL-2; 3, 25, 50 U/ml) or dexamethasone (Dex; 2.5 x 10(-9), 2.5 x 10(-8), 2.5 x 10(-7) M), on the effect of MENK was also tested. The idea was that pretreatment of PBL would result in predictable, and/or stronger response to MENK. In the group as a whole again no significant effect of MENK was detected on the NK-activity of PBL prestimulated by IL-2 (n = 16), or inhibited by Dex (n = 12). Further, pretreatment of PBL with IL-2/Dex did not significantly alter the intensity of modulation by MENK, which was generally mild. The data obtained have shown that pretreatment of PBL with IL-2 or Dex, regardless of their concentrations, did not significantly alter the frequency of responders to MENK being 50%, 62.5% and 64.3% with 3, 25 or 50 U/ml IL-2, respectively, and 50% with all concentration of Dex used, as compared to that observed with resting PBL (60%). However, at the individual level physiological concentrations of MENK (10(-12) - 10(-9) M) induced enhancement or/and attenuation of the NK-activity pretreated with IL-2/Dex, respectively. The effect of MENK at the individual level was donor-related regarding the dose-response, E/T ratio, and direction of MENK action. Thus, pretreatment of PBL with graded concentrations of IL-2/Dex did not alter the effect of MENK on NK-activity, regarding the frequency and intensity, as well as the direction of modulation: it remained bidirectional, of low intensity, and independent of the grade of PBL preactivation/inhibition, therefore unpredictable.

Adolescent↗
PubMed1992

Regulation of NK cell activity and the level of the intracellular cAMP in human peripheral blood lymphocytes by Met-enkephalin.

The effect of Met-enkephalin on natural killer (NK) activity and on intracellular cyclic adenosine monophosphate (cAMP) level in human peripheral blood lymphocytes was measured 1/4, 1, 2, and 24 h after incubation. Concentrations of Met-enkephalin ranged from 10(-12) to 10(-8) M. Cyclic changes in NK activity and in the intracellular cAMP level after treatment with Met-enkephalin were observed. Kinetics of changes caused by high (10(-9), 10(-8) M) and low concentrations (10(-12), 10(-11), 10(-10) M) of Met-enkephalin differed from each other. Early, nearly threefold increase in the level of intracellular cAMP was found 15 min after treating peripheral blood lymphocytes with 10(-12) M Met-enkephalin. By contrast, a nearly 75% decrease of intracellular cAMP level was found 2 h after treatment with 10(-9) M Met-enkephalin. Generally, early intensive changes in the cAMP level in peripheral blood lymphocytes, induced by Met-enkephalin, were followed by delayed, subtle changes in NK cell activity in the opposite direction.

Adolescent↗
PubMed1989

In vivo and in vitro modulation of NK and ADCC activities of mouse spleen cells by peptidoglycan monomer (PGM).

The ability of peptidoglycan monomer (PGM), an immunomodulator obtained from Brevibacterium divaricatum, to modulate NK and ADCC activities of spleen cells was tested in mice with constitutively weak (C57B1) or strong NK activity (CBA, C3H). In weak reactors, i.v. injection of PGM enhanced the NK and ADCC activity as effectively as a known stimulator, poly I.C, and the dynamics of the response was comparable. In strong reactors, PGM caused two peaks of the ADCC response, and one peak of NK stimulation (after an initial decline), whereas poly I.C caused more or less persistent stimulation of both activities. Incubation of spleen cells with PGM was generally less effective than the treatment in vivo. No alteration of NK activity was recorded at high effector-to-target ratio (E:T), and at low ones, PGM caused suppression. This was true both for weakly and strongly reactive cells. ADCC was either unchanged (CBA spleen cells), stimulated (C3H), or suppressed at high E:T and enhanced at low E:T (C57B1). PGM apparently activates an interlocked regulatory mechanism, and the final outcome probably depends on relative concentrations of regulatory and effector cells and on their per cell activities. Hence the effect varied with the time interval between treatment and assay, with strain-related constitutive reactivity, and with the E:T ratio.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1989

Defect of NK activity in children with untreated acute lymphocytic leukemia (ALL). I. Dependence on the blast count and phenotype, and response to exogenous and endogenous alpha-interferon.

Endogenous NK-activity (eNK) against K-562 cells was determined in peripheral blood of 68 children with acute lymphocytic leukemia (ALL) before treatment. In 53% of them it was depressed, and in 47% it was within the range of control children (27) and adults (104). There was a significant negative correlation between blast contamination of peripheral blood and the level of eNK-activity. In spite of this general trend, 8 patients with high blast count have had normal eNK-activity, and 10 patients with relatively low blast count (below 50%) have had depressed eNK-activity. Examples of T ALL showed significantly lower eNK-activity than CALLA ALL. The ability of exogenous alpha-interferon (IFN) to stimulate eNK-activity was impaired in 18 of 40 examples of ALL and preserved in 22. The IFN-induced NK-response was also negatively correlated to the blast burden, but again with exceptions: Six nonresponders in spite of low blast count, and six responders in spite of high blast count in peripheral blood. IFN-inducer, poly-IC, stimulated eNK-activity only in 6 of 26 ALL samples. Surprisingly, positive correlation was found between poly-IC-induced NK-stimulation and blast count in peripheral blood. Poly-IC induced significant IFN production only in one of six cultures of ALL. Impaired eNK-activity has been attributed, in part, to "dilution" of NK cells by the blasts. Defects in production of IFN, and in response to it, may be additional reasons for depressed NK-activity in about 50% of children with untreated ALL.

Adolescent↗
PubMedDate not supplied

Naloxone modulates NK-cell activity of human peripheral blood lymphocytes like an opioid agonist.

Naloxone at concentrations 10(-6) M to 10(-10) M modulated endogenous NK-activity in 11 of 14 samples of human peripheral blood lymphocytes after 18-hour incubation. The dose response usually showed two peaks, which varied with the donor. Enhancement was obtained in 6, suppression in 4, and both effects (depending on naloxone concentration) in 1 example; 3 donors were nonresponders. However, the overall effect of naloxone on endogenous NK activity was not statistically significant in the population as a whole. IL-2-stimulated NK-activity, was also altered by naloxone. The direction of the alteration depended on the degree of IL-2-induced NK-stimulation, and was donor-dependent. For example, naloxone enhanced NK-activity that had been stimulated by low IL-2 concentration (3 U/ml), but decreased NK-activity which had been stimulated by high (50 U/ml) IL-2 concentration. Naloxone 10(-7) M significantly reversed medium stimulation of NK activity, induced by 25 U/ml, in a group as a whole. Naloxone (10(-7) M to 10(-12) M) also modulated NK-activity stimulated by exogenous IFN alpha, as well as by endogenous, Poly-I.C-induced IFN. Decrease, or enhancement, depended on the degree of baseline NK-stimulation and varied with the donor. Short (2-hours) incubation with naloxone also resulted in the modulation of basal and IFN-stimulated NK-activity. Again, the effect varied with the donor and with the degree of lymphocyte activation. Thus, naloxone, the opioid receptor antagonist, modulated the NK-cell activity like opioid peptides, i.e. resembled an opioid agonist, in an individual, donor dependent fashion.

Adolescent↗