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BACKGROUND AND AIMS: Amphetamine, besides its well known psychological and behavioral effects, was found to influence the immune functions. However, the mechanism of amphetamine-induced changes in the immune system remains unknown. In search of a possible mechanism of immunomodulating effect of amphetamine, in the present study we tested the involvement of sympathetic nervous system in that effect. RESULTS: After pretreatment with 6-hydroxydopamine (3×75 mg/kg, ip), we evaluated the effect of acute amphetamine (1 mg/ kg, ip) administration on natural killer cell cytotoxicity (NKCC; Cr-51 release assay) and the number of NK (LGL) cells in the peripheral blood and spleen in male Wistar rats. Amphetamineinduced stimulation of blood and splenic NKCC was completely blocked by chemical sympathectomy. Blood NKCC in amphetamine-injected rats was 260% higher in comparison to a control group. Rats pretreated with 6-hydroxydopamine before amphetamine administration showed over 70% lower NKCC then rats which received amphetamine without chemical sympathectomy. Similarly to the peripheral blood, over 190% increase in NKCC in rats injected with amphetamine was observed in the spleen. Splenic NKCC in rats pretreated with 6-hydroxydopamine was about 60% lower after amphetamine in comparison with rats without chemical sympathectomy. The similar effects were observed in the case of LGL number. CONCLUSIONS: The data clearly show that AMPH-induced stimulation of NK cells numbers and function both in the peripheral blood and spleen are mediated by peripheral sympathetic nervous system.
It is well known that the main site of the action of amphetamine (AMPH) are the catecholaminergic neurons located both in central nervous system and in the sympathetic nervous system (SNS). To analyse the potential role of the SNS in the mechanism of AMPHinduced changes in natural killer cells cytotoxicity (NKCC) rats were sympathectomized by 6-hydroxydopamine (6-OHDA, 3 × 50 mg/kg, i.p.) prior to AMPH (1 mg/kg, i.p.) administration. In a separate experiment, rats were pretreated with a α-adrenergic receptor antagonist phentolamine (5 mg/kg, i.p.), β-adrenergic receptor antagonist propranolol (5 mg/kg, i.p.) or both. NKCC (51Cr-release assay) and the number of LGL (NK cells) were evaluated in the peripheral blood and spleen. In the peripheral blood AMPH-induced stimulation of NKCC was completely blocked by 6-OHDA. The increase in LGL number in the peripheral blood evoked by AMPH was partially inhibited by sympathectomy. In the spleen both effects of AMPH i.e. reduction of NKCC and decrease in LGL number were completely reversed by 6-OHDA. β-antagonist attenuated the AMPH-induced changes in NKCC and LGL number in the peripheral blood and spleen. In contrast, changes in NKCC and LGL number were not affected by α-blockade. These data clearly show that both AMPH-induced stimulation of the peripheral blood NKCC and suppression of spleen NKCC are mediated by the SNS. Furthermore, catecholamines elevated by AMPH modulate the NKCC via β-adrenergic, but not α-adrenergic mechanism.
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Although addiction to amphetamine (AMPH) is a serious social and medical problem, the data concerning AMPH – immune interactions are still not numerous. To analyze the mechanism of AMPH-induced changes in the function of the immune system, rats were pretreated with ß-adrenergic receptor antagonist propranolol (PROP; 5 mg/kg, i.p.) prior to AMPH (1 mg/kg, i.p.) administration. Natural Killer cells cytotoxicity (NKCC) (51Cr-release assay), the number of LGLs (NK cells) (Timonen method), leukocytes, lymphocytes and monocytes, and plasma corticosterone level (CORT) (RIA) were evaluated in the peripheral blood and spleen. In the peripheral blood increases in NKCC (+331%), as well as in LGL (+33%) and monocyte (+65%) number observed after AMPH were partially inhibited by PROP (respectively by 30%, 19%, and 30%) in contrast to lymphopenia (-19%) and granulocytosis (+65%) which were not affected by ß-blockade. In the spleen AMPH-induced decreases in NKCC (-25%) and in all the leukocyte populations number (approximately -30%) were completely blocked by PROP. Plasma CORT level, highly elevated by AMPH (+337%), was attenuated nearly by 50% under ß-adrenergic blockade. These data indicate that AMPH-induced enhancement of cytotoxic activity of NK cell is related to ß-adrenergic mechanism.
The medial septal nucleus (MS) is a forebrain limbic structure involved in learning and memory mechanisms. In previous study we found that electrolytic lesion of the medial septal nucleus caused depression of the peripheral blood natural killer cell cytotoxicity (NKCC) and the leukocyte number. In the sham operated group mere insertion of electrodes into the MS evoked transient NKCC enhancement, probably resulting from mechanical MS stimulation. To check this effect in the present study, we evaluated both spleen and blood NKCC (51Cr-release assay) and large granular lymphocytes (LGL) number (a morphological method) after chronic electrical stimulation (constant current 0.1 ms duration cathodal pulses delivered at a frequency of 50 Hz during 30-min daily session for 14 consecutive days) of MS in conscious, freely moving rats (n=12). Additionally, peripheral blood leukocyte, lymphocyte and neutrophile number was mesaured. Chronic MS stimulation caused signifi cant blood NKCC augmentation and LGL number (25.86 ± 9.31% vs. 15.75 ± 4.75%, P<0.01) in comparison to the sham group (n=13). No signifi cant effect was found in the spleen (27.14 ± 9.99% vs. 28.58 ± 8.04%). A week after termination of the stimulation procedure all measured parameters returned to the baseline. The results obtained indicate that such limbic structure as medial septum enhances antitumor and antiviral function and number of NK cells.
63 congeners of chloronaphthalene represented by 53 peaks fractionated and separated using two-dimensional HPLC and DB-17 capillary column were quantified using HRMS in ten samples of pine needles collected in 1999 around Tokyo Bay in Japan. Similarities and differences of chloronaphthalene concentrations and patterns between 10 sampling sites were studied using multivariate analysis. Total PCN concentrations ranged from 250 to 2100 pg/g wet weight. Except for one site, tri- and tetra-CNs highly dominated (from 54 to 80%) in CN homologue patterns of pine needles. At the easternmost site near the town of Tateyama in Chiba Prefecture the contribution from octaCN was ~20 %, while that of tri- and tetra-CNs ~42 %. Pine needles sampled from the sites around the innermost part of Tokyo Bay showed the highest load of PCNs. A multivariate analysis using the three most significant principal components explained 91% of the total variance in the measurement data. The greatest positive loading to PC1 is from the CN congeners nos. 13, 14/21/24, 15, 16, 17, 18, 19, 20, 22/23, 25, 26, 27, 28/36, 29, 30/32, 31, 33/34/37, 35, 40, 42, 43/45, 44, 47, 49, 50, 51, 52/60, 53, 57, 58, 59, 61, 62, 64, 65, 66/67, 68, 69, 71 and 72, and explains 65% variance in the data set. For PC2 the largest positive loading is from CNs nos.74 and 75, and negative load from CN nos. 38, 41, 46 and 48, which explains 17% of the variance. In case of PC3 the largest negative load is from CNs nos. 54, 56, 63, 70 and 73. A profile of the combustion process related CN congeners measured such as nos. 44, 48 and 54 didn’t show any specific trend implying pollution from diffused sources of various types.
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