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PubMed2005

[Effects of glutamine on alpha-sarcomeric actin and its mRNA expression of myocardium in rats with endotoxemia].

OBJECTIVE: Endotoxemia is a serious syndrome resulting in multi-organ failure. Once it happens, the penetration of small intestine epithelium increases, body liquid losses, then effective circulating blood decreases and serious metabolic acidosis, serious hypotension, systolic failure, and even shock may occur. In this pathological process, endotoxin, tumor necrosis alpha and systolic dysfunction play important roles. Nowadays, many studies have been done to resolve the systolic dysfunction, but too much attention had been paid to the followings: the depressions of myocardium caused by tumor necrosis alpha, other inflammatory factors, endotoxin and metabolic acidosis; the disturbance of blood vessel-nerve regulations; nitric oxide (NO)/inducible nitric oxide synthase (iNOS) over-synthesis and the decreased density of beta-receptors in the myocardium and/or their activities. Little attention has been paid to the relationship between alpha sarcmeric actin (alpha-SA) and systolic dysfunction during endotoxemia. Glutamine (Gln) can be metabolized into glutathione, an eliminator of free radical. It has been used in preventing myocardial damage from reperfusion. This study aimed to observe the dynamic changes of alpha-SA and mRNA expressions in rats with endotoxemia and examine the effects of Gln on them. METHODS: Classical rat model of endotoxemia was established by intraperitoneal injection of LPS (4 mg/kg, Escherichia coli O55:B5, Sigma). 121 Wistar 18-day-rats were divided into three groups randomly, (1) 0 h control group (normal saline: 1 ml/kg, n = 11). (2) LPS group (LPS: 4 mg/kg, n = 55). (3) Gln group (LPS: 4 mg/kg and immediately 13.64%; Gln: 1 ml/kg, Fresenus, n = 55), Furthermore, LPS and Gln groups were divided into 2, 4, 6, 24 and 72 h time points (n = 11). Each time point of LPS and Gln as well as control rats were anaesthetized at each time point with 1% chloral hydrate injected intraperitoneally at the dosage of 1 ml/kg. Then rats were sacrificed at appoint time, and the hearts were isolated. Eight of them were put in 76 degrees C liquid nitrogen and then frozen in minute 80 degrees C icebox in order to measure the expression of alpha-SA mRNA by RT-PCR. Three of them were fixed in 4% formaldehydum polymerisatum for 12 to 16 h, then the expression of alpha-SA was detected by immunohistochemistry. RESULTS: (1) Compared to 0 h, the expressions of alpha-SA and mRNA in LPS group were significantly depressed (P < 0.01). In LPS group, the lowest was at 6 - 24 h, while in Gln group, it was postponed to 24 h. At 72 h, there was no difference in expressions of alpha-SA between Gln and 0 h group (P > 0.05). (2) Comparing at same time point, the expressions of alpha-SA were significant higher in Gln group than those in LPS group, while the expressions of alpha-SA mRNA in Gln group were high at 4-72 h. There was, however, no significant difference at early phase (P > 0.05). CONCLUSION: Alpha-SA and its mRNA expression were depressed in LPS-induced endotoxemia, especially from 6 to 24 h. It could damage the systolic function. alpha-SA decrease in endotoxemia was due to the inhibited synthesis other than the promoted degradation. Glutamine could inhibit the effects of LPS on both alpha-SA and its mRNA expressions.

Actins↗
PubMed2006

[Therapeutic effect of glucose-6-phosphate polyclonal antibody on vasogenic brain edema in rats].

OBJECTIVE: To observe the therapeutic effect of glucose-6-phosphate polyclonal antibody (G-6-P pAb) on vasogenic brain edema (VBE) in rats. METHODS: Sixty Wistar rats were randomly divided into normal control group, VBE group, mannitol-treated edema group, and G-6-P pAb-treated edema group. After establishment of rat models of VBE by intraperitoneal injection of phenylephrine in the latter 3 groups, mannitol was injected through the femoral vein in mannitol group and G-6-P pAb injected intraperitoneally in G-6-P pAb group. The permeability of the blood-brain barrier (BBB) was determined by Evans blue (EB) extravasation method, and the brain water content in the gray and white matter measured with a moisture analyzer. RESULTS: G-6-P pAb administration significantly reduced the permeability of BBB as well as the water content in the white matter in comparison with mannitol treatment (P<0.01), but the two treatments showed no obvious difference in reducing the water content in the gray matter (P>0.05). CONCLUSION: Changes in G-6-P activity results in BBB permeability alteration in the condition of VBE, and G-6-P pAb has a selective therapeutic effect against VBE, especially white matter edema.

Animals↗
PubMed2006

[Effects of glutamine on matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-3 expressions in myocardium of rats with sepsis].

OBJECTIVE: The underlying mechanisms for cardiac dysfunction in sepsis include the inhibitory effect of endotoxin and inflammatory factors on myocardium and the decrease in cardiac myocardial cells in number. However, whether there is ventricular remodeling resulted from the abnormalities of extracellular collagen metabolism and whether glutamine (Gln) can protect myocardium from LPS-induced damage as in reperfusion are unknown. The aim of the present study was to examine the effects of Gln on the expressions of matrix metalloproteinase-3 (MMP-3), tissue inhibitor of metalloproteinase-3 (TIMP-3) and their mRNA in myocardium of rats with sepsis. METHODS: Classical rat model of sepsis was established by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg, from Escherichia coli O(55): B(5), Sigma). from 121 Wistar rats aged 18 days were divided into three groups randomly, 0 h control group (normal saline: 1 ml/kg, n = 11), LPS group (LPS: 4 mg/kg, n = 55) and Gln group (LPS: 4 mg/kg and immediately 13.64% glutamine 1 ml/kg, Fresenus, n = 55). Furthermore, LPS and Gln groups were examined at 2 h, 4 h, 6 h, 24 h and 72 h time points (n = 11). On each time point, rats of LPS and Gln groups as well as control group were anesthetized with 1% chloral hydrate injected intraperitoneally at a dosage of 1 ml/kg. Then, rats were sacrificed, and the hearts were isolated. Eight of them were frozen at minus 80 degrees C to measure the expression of TIMP-3 mRNA by using RT-PCR. The expressions of MMP-3 and TIMP-3 were observed with immunohistochemistry and the expression of MMP-3 mRNA was observed by using in situ hybridization. RESULTS: (1) Compared to 0 h, the mRNA expressions of MMP-3 and TIMP-3 in LPS group significantly increased (P < 0.01) with the peak at 6 - 24 h. While, in Gln group, they were significantly higher than those in controls but significantly lower than those in LPS group with the peak at 24 h (P < 0.01). Even at 72 h, they were still higher than those at 0 h (P < 0.05 and P < 0.01). (2) Compared to 0 h, the expressions of MMP-3 and TIMP-3 in LPS group were significantly lower at any other time point with the lowest at 6 h (P < 0.01). In Gln group, these expressions were also significantly lower than those in controls, but significantly higher than those in LPS group with the lowest being postponed to 24 h (P < 0.01). (3) The ultra structure changed obviously. Z line was unclear and the ridge of mitochondrion disappeared. While, in Gln group, the myocardial injury was slight compared to that in LPS group. CONCLUSIONS: MMP-3 mRNA expression was increased and TIMP-3 mRNA expression was depressed in LPS-induced sepsis. Myocardial extracellular matrix was damaged in sepsis. Glutamine might decrease the effects of LPS on MMP-3 and TIMP-3 expressions and postpone the time of myocardial matrix injury.

Animals↗
PubMed1991

Neutralization of the activity of vipera ammodytes ammodytes snake venom on myocardium of rats by antitoxinum viperinum: a histopathological study.

Antitoxinum viperinum was tested for its ability to prevent alteration of the myocardium induced by Vipera ammodytes ammodytes venom. Antivenom was injected intraperitoneally either immediately, 30 min or 2 hr after the intraperitoneal injection of venom. The light microscopic examination showed that the antiserum neutralized the effects of venom and antivenom might be useful in treating V.a. ammodytes venom poisoning.

Animals↗
PubMed1990

Acute obstructive parasternal lymphedema produced in rats without surgery.

Although rat red blood cells (RBC) were altered by pretreatment with glutaraldehyde, they nonetheless were well absorbed into mediastinal lymphatics of Lewis rats after intraperitoneal injection. Unlike normal RBC, they did not pass freely through the draining mediastinal lymph nodes. Instead, clumps of free and phagocytosed glutaraldehyde-treated RBC distended and obstructed the afferent lymphatics and the sinuses of draining lymph nodes. The lymphatic obstruction caused edema in a clearly defined compartment of fatty connective tissue between the muscle layers of the ventral chest wall. The obstructive lymphedema interfered with the immunizing effect of small doses of sheep RBC injected intraperitoneally. This study emphasizes the potential utility of the rat's mediastinal lymphatics for studies of lymphatic leakage and obstruction.

Animals↗
PubMedDate not supplied

[Experimental hypervitaminosis A in the rat. 14. Morphological and morphometric study of changes in the esophageal epithelium].

Male rats were subjected to hypervitamin A treatment by daily intraperitoneal injections of 150 UI Arovit per g body weight. Another group of rats were injected intraperitoneally with saline solution for ten days and were used as controls. The results indicated that: 1) the body weight of animals treated with excess vitamin A was decreased; 2) histological analysis of the esophageal epithelium in treated animals showed increased thickness, characterizing a picture of hyperplasia and hypertrophy. On the basis of the results obtained, we suggest that excess vitamin A may act on the esophageal epithelium by direct action on the epithelial structures, stimulating and increase of the mitosis, and on the epithelium (mediated by the adrenals), resulting in increased thickness due to the concentration of a larger number of more immature cells. These alterations were more evident in the lower esophageal third.

Animals↗
PubMed1987

Detection of mutagenic compounds in the urine of mice administered pyrene during exposure to NO2.

The urine of mice injected intraperitoneally with pyrene during exposure to NO2 was found to contain highly mutagenic compounds by means of the Ames test using Salmonella typhimurium strain TA98. The mice were exposed to 20 ppm NO2 for 3 days before intraperitoneal injection of pyrene (800 mg/kg of body weight). The pyrene-treated mice were further exposed to NO2 for an additional 24 hr, and the urine from the mice was collected in ice-cooled containers and stored frozen in the dark. The collected samples were treated with beta-glucuronidase and passed through activated Sep-Pack C18 cartridges. After elution with methanol, the effluent was concentrated and the residue was dissolved in dimethyl sulfoxide (DMSO). The DMSO solution was fractionated by high-performance liquid chromatography and the mutagenicity of each fraction was assayed with S. typhimurium strain TA98. The mutagenic compounds 3-hydroxy-1-nitropyrene, 6-hydroxy-1-nitropyrene, 8-hydroxy-1-nitropyrene, and 1-hydroxypyrene were identified in the mutagenic fractions by mass spectrometry and UV-visible spectrophotometry with synthetic reference substances. These mutagenic compounds may have been formed by either nitration of hydroxylated pyrene, or hydroxylation of 1-nitropyrene, which is formed in vivo from pyrene and NO2, or the simultaneous occurrence of these two reactions in the mouse body.

Animals↗
PubMed1987

Interleukin-1 and the acute-phase response: induction of mouse liver serum amyloid A mRNA by murine recombinant interleukin-1.

Traumatic tissue injury of infection provokes a systemic inflammatory response, termed the acute-phase response, which is accompanied by hepatic synthesis of certain plasma proteins. Increased levels of serum amyloid A (SAA), C-reactive protein (CRP), and fibrinogen have been observed during the acute-phase response. One possible mediator of the acute-phase response is interleukin-1, a pro-inflammatory monokine released in response to traumatic tissue injury or infection. There is evidence that partially purified macrophage supernatants containing interleukin-1 activity stimulate hepatocyte secretion of SAA, CRP, and fibrinogen. The effect of interleukin-1 on mouse liver serum amyloid A mRNA levels was investigated. The acute-phase response was induced in mice by intraperitoneal injection of interleukin-1 obtained from cloned murine recombinant DNA. We monitored SAA mRNA levels using DNA/RNA dot blot hybridization. Interleukin-1 stimulated a dose-dependent increase in SAA mRNA levels compared to unstimulated controls. In contrast, mRNA levels for apolipoprotein E (a constitutive hepatic protein not produced as part of the acute-phase response) were unchanged under identical conditions. Interleukin-1 also induced SAA mRNA in an endotoxin-resistant strain of mice (C3H/HeJ), indicating that this stimulation was not due to endotoxin contamination since endotoxin alone was unable to induce SAA mRNA in these mice. These results indicate that recombinant interleukin-1, when injected intraperitoneally into mice, induced specific production of SAA mRNA and hence one phase of the acute-phase response.

Acute-Phase Reaction↗
PubMed1987

[Experimental study on the development of endotoxemia in peritonitis with special reference to route of absorption of endotoxin].

As endotoxemia develops and presents marked symptoms in severe peritonitis, the absorption route of endotoxin from the peritoneal cavity was studied in this study. Twenty-four adult mongrel dogs were divided into 4 groups as follows. Group 1: Physiological saline solution was injected intraperitoneally with thoracic duct (TD) lymph drainage. Group 2: Peritonitis was induced without lymph drainage. Group 3: Peritonitis was induced with TD lymph drainage. Group 4: Peritonitis was induced with right lymph duct (RLD) and TD lymph drainage. Peritonitis was induced by intraperitoneal injection of endotoxin (Difco 055 B5 LPS) at 0.5 mg/kg. In Group 4, the endotoxin level in lymph from RLD reached a maximum value of 4.19 X 10(7) +/- 2.32 X 10(7) pg/ml (mean +/- S.E.), while that from TD was only 7203 +/- 5022 pg/ml. The endotoxin level in the portal venous blood three hours after administration was almost within normal limits throughout the experiment. In conclusion the route of endotoxin absorption in peritonitis is considered to be via the lymphatic system and in particular RLD is assumed to play an important role.

Absorption↗
PubMed1977

A study of maternal lymphoid organs and the progeny following treatment with immunomodulating agents during pregnancy.

Whether differences in foetoplacental weight and post-implantation mortality in rodents are secondary to heterosis and inbreeding depression or antigenic differences between mother and foetus has been a continuing controversy. To determine whether non-specific depression or stimulation of the maternal immune system affects the success of the foetoplacental allograft, groups of virgin Fischer (Ag-B1) females of similar age and weight mated with DA (Ag-B4) males were treated with daily intraperitoneal injections of: (a) saline, (b) methylprednisolone (MP), 1-0 mg/kg, (c) cyclophosphamide (CY), 3.0 mg/kg, or (d) azathioprine (AZ), 3.0 mg/kg; or they were injected intraperitoneally on the fifth day of gestation with: (a) B. pertussis, 1.0 ml, (b) C. parvum, 0.2 ml, or (c) BCG, 0.1 ml. None of the immunostimulating agents were detrimental to the progeny, but the immunosupprissive drugs caused an increased percentage of foetal deaths and foetoplacental growth retardation. The reduced foetal and placental size induced by CY or AZ could be partially blocked by simultaneous maternal treatment with BCG. Analysis of mean maternal weight gain, spleen weight assays, changes in the lymph nodes draining the uterus and comparison of data from non-pregnant animals and syngeneic pregnancies treated with these agents suggest that immunosuppressive drugs reduce foetal survival rates and produce foetoplacental growth retardation via a combination of immunological and cytotoxic mechanisms.

Adjuvants, Immunologic↗
PubMed1987

[The effects of hyperglycemia on ischemic brain edema].

The effects of hyperglycemia on ischemic brain edema in rats were studied by measuring the local changes in water content of brain and cerebrovascular permeability using a transient middle cerebral artery (MCA) occlusion model. Rats, fasted except for water for 12-16 hours, were used. They were anesthetized with halothane and the stem of the left MCA was occluded for 2 hours by a microclip. Reperfusion was performed by removal of the clip. The rats were allowed to awake from anesthesia after removal of the clip. Hyperglycemia was induced by intraperitoneal injection of 50% glucose and same volume of physiological saline was injected intraperitoneally 20 minutes before MCA occlusion in control rats. Cerebrovascular permeability was measured by quantitative autoradiography using 14C-alpha-amino-isobutyric acid (14C-AIB) 2 hours after reperfusion. The specific gravity of cerebral tissue, determined by the gradient column with bromobenzene and kerosene, was used to study local changes in brain water content 2 hours after MCA occlusion and 2 hours after reperfusion. In hyperglycemic rats, plasma glucose content-ration rose to over 500 mg/dl at the peak and then declined. A hyperglycemic state around 300 mg/dl was maintained during the experiments. Elevation of hematocrit and plasma osmolarity were observed in hyperglycemic rats. At 2 hours after MCA occlusion, specific gravity of the brain was decreased in the left MCA territory, especially in the frontal cortex, in both groups. The decrease in the frontal cortex in hyperglycemic rats was statistically significant compared with that in the control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Antitumor activity of peritoneal exudate cells induced by cell-wall skeleton of Mycobacterium bovis BCG.

Peritoneal exudate cells (PEC) induced by oil-attached cell-wall skeleton of Mycobacterium bovis BCG (BCG-CWS) in ACI/N rats were tested for their effect on both in vivo and in vitro growth of syngeneic fibrosarcoma cells (AMC-60). Treatment of rats with intraperitoneal injections of BCG-CWS induced regression of syngeneic ascites tumor and increased the number of survivals. Whole PEC and adherent PEC from rats injected intraperitoneally with BCG-CWS inhibited the uptake of tritiated thymidine into the fibrosarcoma cells in an in vitro cytostasis test. This in vitro cytostatic effect was more marked as the ratio of effector to target cells increased. In addition, when tumor cells were inoculated subcutaneously with BCG-CWS activated PEC, tumor takes decreased markedly. Oil-stimulated PEC and normal peritoneal resident cells were inactive in inhibition of tumor growth in vivo and in vitro.

Animals↗
PubMed1986

[The effect of hyperglycemia on ischemic brain damage: relevance to the local cerebral blood flow].

The effect of hyperglycemia on ischemic brain damage in rats was studied by measuring the local cerebral blood flow (LCBF) using a transient middle artery (MCA) occlusion model. Rats, fasted except for water for 12-16 hours, were used. They were anesthetized with halothane and the stem of the left MCA was occluded for 2 hours by a microclip. Reperfusion was performed by removal of the clip. The rats were awaken from anesthesia after removal of the clip. Hyperglycemia was induced by intraperitoneal injection of 50% glucose and same volume of 50% D-mannitol or physiological saline were injected intraperitoneally 20 minutes before MCA occlusion in control rats. LCBF was measured by quantitative autoradiography using 14C-iodoantipyrine 2 hours after clipping and 2 hours after reperfusion. Some rats were prepared for neuropathological observation 72 hours after reperfusion. In hyperglycemic rats, plasma glucose concentration rose to over 500 mg/dl at the peak. A hyperglycemic state around 300 mg/dl was maintained during the experiments. Elevation of hematocrit and plasma osmolarity to the same degree were observed in both hyperglycemic and mannitol pretreated rats. On histological study ischemic neuronal cell damage was found to be more extensive in hyperglycemic rats than in the saline pretreated rats. At 2 hours after MCA occlusion, LCBF in the ischemic focus decreased significantly in hyperglycemic rats compared with the control. The reduction of LCBF was observed also in the contralateral non-ischemic side (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effect of theophylline treatment on the functional hyperaemic and hypoxic responses of cerebrocortical microcirculation.

The purpose of the present study was to elucidate the importance of extracellular adenosine (ADO) in the regulation of cerebrocortical microcirculation during rest, hypoxia, and brain activation. Cerebrocortical microcirculation and fluorescence of reduced nicotinamide adenine dinucleotide (NADH) were measured by surface fluororeflectometry through a cranial window. Arterial hypoxia and brain activation were produced by respirating the animals with a gas mixture containing 6-7% O2 and by injecting 4-6 mg/kg metrazol into the lingual artery, respectively. These reactions were used as test before and after theophylline (THEO) treatment. In some of the experiments only the cortical area beneath the cranial window was treated with THEO (10(-4) M), in others 2 X 10(-4) mol/kg THEO was injected intraperitoneally. Potency of THEO in antagonizing the cerebral blood flow (CBF) increasing effect of topically applied ADO was also tested. It was found that superfusion of the brain cortex with artificial cerebrospinal fluid (mock CSF) containing 10(-4) M THEO does not alter resting CBF, but inhibits the CBF increasing effect of 10(-6) M and 10(-5) M ADO by approximately 70% and 40%, respectively. Intraperitoneally injected THEO increased CBF by approximately 60%, which has been attributed mostly to its action on the systemic circulation. Under control conditions, arterial hypoxia and epileptic seizures increased CBF by approximately 150% and 300%, respectively. Since neither topical nor systemic THEO treatment altered the vasodilatory and CBF increasing potency of arterial hypoxia and attenuated these effects of epilepsy slightly, it was concluded that extracellular ADO is not a critical factor in the regulation of cerebrocortical microcirculation.

Adenosine↗
PubMed1985

Effects of regenerating liver cytosol on drug-induced hepatic failure.

Despite various interventions, the mortality rate after acute hepatic failure remains extremely high. Although it has been shown that administration of regenerating liver cytosol (RLC) after hepatic failure improves the survival rate of animals, the sequence in which various hepatic functions are altered after acute hepatic failure and their improvement by RLC remain unknown. To study this, fulminant hepatic failure in rats was produced by intraperitoneal injection of 1.5 gm/kg D-galactosamine (GAL). Twenty-four hours after 68% hepatectomy in normal rats, RLC was prepared and 4 ml of this solution (40 to 50 mg protein) was injected intraperitoneally in other animals at 6 or 24 hours after GAL administration. The long-term survival rate was 19.4% in the GAL-vehicle (control) group, 26.7% in the GAL-treated rats given liver cytosol from normal rats, and 72.2% (p less than 0.01 compared with both groups) in rats given RLC even 24 hours after GAL administration. Reticuloendothelial function was depressed at 24 and 48 hours after GAL administration; however, treatment with RLC but not vehicle or normal liver cytosol at 6 or even 24 hours after GAL administration significantly improved reticuloendothelial function 24 hours after GAL administration. DNA synthesis (an indicator of cell proliferation) did not increase in any group 24 hours after GAL administration; however, it increased strikingly at 48 hours in the GAL-RLC groups. Serum bilirubin levels were also lower in the RLC group 48 hours after GAL administration. Thus RLC administration improved survival, reticuloendothelial function, DNA synthesis, and hepatocyte function after GAL-induced acute hepatic failure. Improvement of reticuloendothelial function by RLC occurred before stimulation of DNA synthesis and appears to play an important role in improving survival after hepatic failure.

Animals↗
PubMed1985

[Influencing factors in the leakage of liposome and arabinoside cytosine (ARA-C) entrapped in liposomes in treatment of L1210 mouse leukemia].

Ara-c entrapped into multilamella vesicles (MLV's) composed of PC:C (2:1) (phosphotidylcholine, cholesterol) or PC:SM (1:4) (sphingomyelin) was incubated in the simple salt medium at 37 degrees C for one hour. Its leakage from the liposomes was 5.6-17.6% but, in the presence of serum, the leakage was 35.7-49.1%. Having been incubated at 37 degrees C overnight, the leakage significantly increased but the leakage rate was the highest within the 1st hour. When ara-c entrapped into reverse evaporation vesicles (REV's) composed of PC:C (2:1) or PC:SM (1:4) was incubated in the simple salt medium at 37 degrees C for one hour, its leakage was 2.4-4.1% but, in the presence of serum, the leakage was 10.9-8.2%. When the liposomes were incubated at 37 degrees C overnight, the leakage gradually increased. Whether in the presence of serum or not, the leakage from REV's was much less than that from MLV's. There was no effect on the survival of L1210 leukemia mice when free ara-c was injected intraperitoneally once at the dose of 10 mg/kg, but when the same dose was given for five times, the increase rate in life span was 43.2--51.3%. When ara-c, entrapped into MLV's or REV's composed of PC:C (2:1) and PC:SM (1:4), was given at the dose of 10 mg/kg only once, the effect of intraperitoneal injection was more marked than that of intravenous injection. No effect was observed when free ara-c was continuously infused at the dose of 2 mg/kg once everyday for five days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

In vivo activity of spleen cells from untreated syngeneic mice against Ehrlich ascites carcinoma.

Inbred CFW/L1 or BALB/c male mice were injected intraperitoneally with 1 X 10(5) EAC cells. They died in 98.6 or 100%, respectively, within 100 days of observation. Intraperitoneal injection of 6 X 10(7) syngeneic spleen cells from 6--9-week-old CFW/L1 or BALB/c donors 2.5--4 h after tumour inoculation significantly prolonged MST and 16.7 or 23.5% of mice, respectively, survived for 100 days. Smaller amounts of spleen cells, thymus cells, mixed spleen and thymus cells, or spleen cells from older donors did not show this effect. Homogenized spleen cells were also inactive. Antitumour activity of spleen cells was still evident when they were isolated from irradiated (2 000R) donors or were given 24 h after tumour inoculation. Spleen cells used for in vivo studies showed spontaneous cytotoxic activity in vitro against EAC cells in the 51Cr-release cell-mediated cytotoxicity test. The possible participation of NK cells in the observed in vivo antitumour activity of normal spleen cells is discussed.

Animals↗
PubMed1977

Macrophage disappearance reaction in Rana esculenta induced by specific antigen and rabbit lymphokines.

Macrophage disappearance reaction was induced by intraperitoneal injections of specific antigens in Rana esculenta sensitized by bovine gamma globulin and Mycobacterium bovis BCG. Rabbit lymphokines derived from concanavalin A stimulated blood lymphocytes injected intraperitoneally were able to induce macrophage disappearance reaction in normal Rana esculenta. This suggests that mammalian lymphokines are capable of acting in amphibia. Mammalian lymphokines have not an exclusive class-specificity in vertebrates.

Animals↗