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PubMed2006

Immunological hormone atrophy by gonadotropin-based drug.

Luteinizing hormone releasing hormone-Pseudomonas aeruginosa exotoxin A (LHRH-PE40) and sequence-modified LHRH-PE40 (mLHRH-PE40) are two anti-tumour drugs developed by fusing either native or modified LHRH with the same PE40. This study was designed to evaluate their toxicity on the male genital tract. Male rats were treated intravenously or intraperitoneally with either LHRH-PE40 or mLHRH-PE40 on alternate days for 12 weeks. Serum and testes were examined to detect anti-LHRH, anti-LHRH-PE40 or anti-mLHRH-PE40 using an ELISA assay, testosterone level was measured by radioimmunoassay, and testicular morphology was evaluated. Rats receiving LHRH-PE40 intraperitoneal injections had higher anti-LHRH antibody titres, lower serum testosterone concentration and remarkable testicular atrophy, whereas those administrated with intravenous injections of either LHRH-PE40 or mLHRH-PE40 demonstrated no such changes. We concluded that the testicular atrophy can be attributed to higher titre of anti-LHRH antibodies, which was affected by both drug delivery and the LHRH motif of the chimeric protein.

ADP Ribose Transferases↗
PubMed1969

Anti-inflammatory activity of the steroid alkaloid glycoside, toatine.

1. Tomatine, isolated from extracts of crown gall-infected tomato plants or obtained commercially, was tested for anti-inflammatory activity using three different methods.2. Tomatine administered to intact rats intramuscularly in a dose range of 1-10 mg/kg or orally in doses of 15-30 mg/kg exerted a significant dose dependent inhibition of carrageenan induced paw oedema. The inhibitory effect of tomatine when given in a dose of 10 mg/kg intramuscularly to intact rats lasted more than 24 hr.3. In adrenalectomized rats significant dose-related inhibition of paw oedema was obtained with tomatine and the inhibition at each dose level (0.5-10 mg/kg) was found to be greater than that found in intact animals.4. Tomatine administered subcutaneously to intact rats daily for 7 days in doses of 5 or 10 mg/kg exerted a significant, dose dependent inhibition of granulation tissue formation induced by the subcutaneous implantation of carrageenan impregnated cotton pellets.5. Tomatine administered to intact mice in a dose of 10 mg/kg subcutaneously 1 hr before the intraperitoneal injection of acidified saline and intravenous pontamine sky blue significantly decreased the leakage of the protein bound dye into the peritoneal cavity.6. Tomatidine, the aglycone of tomatine, was not effective at dose levels of 10-20 mg/kg in any of the three tests.

Adrenalectomy↗
PubMed1973

Seizures induced by allylglycine, 3-mercaptopropionic acid and 4-deoxypyridoxine in mice and photosensitive baboons, and different modes of inhibition of cerebral glutamic acid decarboxylase.

1. DL-C-Allyglycine, 4-deoxypyridoxine hydrochloride and 3-mercaptopropionic acid have been studied with reference to their convulsant effects in mice and in baboons (Papio papio) with photosensitive epilepsy, and their action on the cerebral enzyme synthesizing gamma-aminobutyric acid (L-glutamate-1-carboxy-lyase).2. In mice, the ED(50) values for seizures following intraperitoneal injection were allylglycine 1.0 mmol/kg body weight, 4-deoxypyridoxine 1.1 mmol/kg and 3-mercaptopropionic acid 0.27 mmol/kg. Latency to seizure onset was longest after allylglycine (44-240 min), intermediate after 4-deoxypyridoxine (9-114 min) and shortest after 3-mercaptopropionic acid (2.5-8 min).3. In Papio papio intravenous administration of subconvulsant doses of allylglycine (0.87-3.1 mmol/kg), or of 4-deoxypyridoxine (0.21-0.53 mmol/kg) enhanced the occurrence and persistence of myoclonic responses to intermittent photic stimulation, and augmented the associated electroencephalographic abnormalities, without modifying their character or distribution. Higher doses produced brief seizures recurring at regular intervals, between 2-14 h after allylglycine (4.0-4.3 mmol/kg) or 1-4 h after 4-deoxypyridoxine (0.53-0.87 mmol/kg). Electroencephalographically these seizures originated unilaterally in the occipital or posterior parietal cortex.4. In Papio papio photically-induced epileptic responses were enhanced 5-10 min after the intravenous injection of 3-mercaptopropionic acid (0.09-0.28 mmol/kg). A sequence of brief generalized seizures followed by complete recovery occurred 4-17 min after the injection of 3-mercaptopropionic acid (0.28-0.38 mmol/kg). Fatal status epilepticus followed the injection of 3-mercaptopropionic acid (0.57-0.75 mmol/kg). E.E.G. records showed generalized cortical involvement at the onset of the seizures.5. L-Glutamate 1-carboxy-lyase (GAD) activity was determined in whole brain homogenates from mice killed at various intervals after receiving i.p. a convulsant dose of one of the compounds. Inhibition of GAD activity was evident 30-60 min before seizure onset following allylglycine or 4-deoxypyridoxine administration, and was maximal (40-60%) just before or during seizure activity. Addition of pyridoxal phosphate to the brain homogenate relieved inhibition produced by 4-deoxypyridoxine but not that produced by allylglycine. Inhibition of GAD activity in brain homogenates from animals killed 2 or 4 min after injection of a convulsant dose of 3-mercaptopropionic acid varied from 0-49% depending on the dose of 3-mercaptopropionic acid and the concentration of substrate in the assay system.6. Kinetic analysis of the inhibition of GAD activity following direct addition of the compounds to mouse brain homogenates indicated that 3-mercaptopropionic acid (0.01-0.5 mM) was competitive with respect to the substrate. A comparable percentage inhibition of GAD activity was obtained only with much higher concentrations of 4-deoxypyridoxne, i.e. 10-50 mM. Allylglycine in vitro was a very weak inhibitor of GAD activity.7. Three biochemically different mechanisms underlie the inhibition of cerebral GAD activity that precedes seizures induced by ailylglycine, 4-deoxypyridoxine and 3-mercaptopropionic acid. The data are consistent with a critical reduction in the rate of synthesis of gamma-aminobutyric acid being responsible for the onset of seizures.

Allyl Compounds↗
PubMed1990

Induction of tumoricidal activated macrophages by a liposome-encapsulated glycolipid, trehalose 2,3,6'-trimycolate from Gordona aurantiaca.

A mycolic acid-containing glycolipid, trehalose 2,3,6'-trimycolate, prepared from a non-pathogenic acid-fast bacterium Gordona aurantiaca, was shown to induce strong tumoricidal activity in peritoneal exudate cells by intravenous or intraperitoneal injection of liposome-encapsulated preparations. The mycolic acid derivative containing a high proportion of unsaturated fatty acids rendered macrophages cytotoxic against syngeneic mastocytoma cells in the absence of endotoxin, for over 14 days after the injection. The macrophages were ascertained to be at low intracellular levels of a lysosomal enzyme beta-galactosidase and an ectoenzyme alkaline phosphodiesterase, a specific pattern as previously described for "primed macrophages". However the culture supernatants of the peritoneal exudate cells were not cytotoxic.

Adjuvants, Immunologic↗
PubMed1979

Interactions between 1,2--propanediol (propylene glycol) and hexobarbital.

The interaction between 1,2--propanediol and hexobarbital was studied with an anaesthesia threshold method, where hexobarbital is infused intravenously. The dose needed to obtain a burst suppression of one second or more is determined and given as per cent of a pre-experimental value obtained in the same rat. The effect of varying the interval between the intraperitoneal injection of 1,2--propanediol (2.06 g/kg) and the threshold determination was investigated. In the intervals, 10--50 min., the hexobarbital threshold doses were significantly decreased by 13--27% (n = 7--18). Four different doses between 0.25 and 2.06 g/kg of 1,2--propanediol were then tested after a fixed interval of 30 min. As in the time interval study the thresholds after 2.06 g/kg were significantly decreased. No certain depressant effect was seen with 1.03 and 0.52 g/kg. With the lowest tested dose of 1,2-propanediol (0.25 g/kg) there was instead a significant increase in the threshold dose (13%). This might be an excitatory effect, which could correspond to the well-known effect, seen with low doses of other depressants for instance ethanol.

Animals↗
PubMed1987

Similar effects of acetylsalicylic acid and morphine on immediate responses to acute noxious stimulation.

The formalin and writhing tests in mice were employed to investigate a possible delay in the onset of antinociceptive action of acetylsalicylic acid (ASA). Drugs were given 30 min. before the noxious stimulation by either formalin or acetic acid. In the formalin test, the difference between the drug treated groups and the control group reach statistical significance within 30 sec. of noxious stimulation. ASA (400 mg/kg intraperitoneally) and morphine (5 mg/kg intraperitoneally) treated groups were not significantly different in any of the ten periods (30 sec. each) that were analysed during the first 5 min. In the writhing test, the number of writhings in response to intraperitoneal injection of acetic acid was counted during the first 20 min. The difference between the drug treated groups and the control group reached statistical significance after 3 min. both for ASA (400 mg/kg subcutaneously) and morphine (2 mg/kg subcutaneously) and no significant differences between the drug treated groups were found in any of the one min. periods that were analysed. Thus no delay of onset in the action of ASA compared to morphine could be demonstrated, and ASA seems to be antinociceptive also in acute non-inflammatory pain. Actions apart from inhibition of the synthesis of prostaglandins are suggested for this effect of ASA.

Analgesics↗
PubMed2006

Heroin-administered mice involved in oxidative stress and exogenous antioxidant-alleviated withdrawal syndrome.

Heroin has been shown to elevate dopamine (DA) level. It is well known that an increase in DA oxidative metabolism leads to increased reactive oxygen species (ROS) formation, and thus, ROS have been frequently associated with neuronal cell death due to damage to carbohydrates, amino acids, phospholipids, and nucleic acids. This study investigated whether there are oxidative stress and effects of exogenous antioxidants in heroin-administered mice. The heroin-dependent mice model was made via intraperitoneal injection. Oxidative damage of DNA, protein, and lipid was measured by analysis of single cell electrophoresis, the 2,4-dinitrophenylhydrazine method, and thiobarbituric acid method respectively. The activities of antioxidative enzymes and total antioxidant capacity were assayed by spectrophotometry. After administration with heroin, the mice not only showed decrease of total antioxidant capacity in serum and antioxidant enzymes such as superoxide dismutase, catalase, and glutathione (GSH) peroxidase in brain, but also exhibited the oxidative damages of DNA, protein and lipid. On the other hand, exogenous antioxidants could restrain the oxidative stress, even alleviate withdrawal syndrome in heroin-administered mice. Our results also imply a possibility that ROS may participate in the whole process of dependence and withdrawal of heroin. Therefore, strategies of blocking oxidative stress may be useful in the development of therapy for opiate abuse.

Animals↗
PubMed1989

Bromocriptine-induced decrease in blood pressure in conscious spontaneously hypertensive rats: evidence for a peripheral site of action.

The aim of the study was to discover whether the dopamine agonist bromocriptine has a central or peripheral site of action on blood pressure. An intraperitoneal injection of bromocriptine (0.5 mg kg-1) induced a long-lasting decrease in blood pressure in conscious spontaneously hypertensive rats (SHR). This effect was blocked by peripheral pretreatment with haloperidol or domperidone, but not by central treatment with haloperidol. A central injection of bromocriptine had only minor effects on blood pressure. These results suggest that primarily peripheral, rather than central, mechanisms are involved in the hypotensive effects of bromocriptine.

Animals↗
PubMed1969

Simple isolation of antimycin A1 and some of its toxicological properties.

An unidentified actinomycete, RTI 246, was found to produce antimycin A(1) in high yield on a high protein cereal medium. The antibiotic compound was extracted from the cells and isolated in pure form by crystallization. It was identified by ultraviolet, infrared, nuclear magnetic resonance, and mass spectroscopy and by alkaline hydrolysis to antimycic acid and a neutral lactone. The intravenous LD(50) was 1.0 mg/kg in white mice, whereas the intraperitoneal LD(50) was 1.50 +/- 0.19 mg/kg. Animals receiving an intraperitoneal injection displayed an incoordination of the hind limbs and impaired reflexes before showing signs of respiratory distress. These findings indicated that antimycin A(1) possesses a neurotoxic property separate from its well-documented property as a respiratory poison.

Actinomycetales↗
PubMed1980

Lipophilic derivative of muramyl dipeptide is more active than muramyl dipeptide in priming macrophages to release superoxide anion.

Mouse peritoneal macrophages, when treated with a lipophilic derivative of muramyl dipeptide either in vitro or in vivo by intraperitoneal injection, showed a more than fivefold increase in their ability to generate superoxide anion after stimulation of the macrophages with phorbol myristate acetate. This response was more than twice that observed with the parent molecule, muramyl dipeptide (MDP). Unlike MDP, which has a systemic effect, the lipophilic derivative, [B30]-MDP, did not alter the response of peritoneal macrophages when given subcutaneously in the flank, suggesting that [B30]-MDP remains localized at the site of injection. The enhanced effect of [B30]-MDP over MDP appeared to be due to the inherent lipophilicity of the molecule, and was probably not due to either stimulation of T lymphocytes or activation of the alternative pathway of complement.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1994

Immunization against experimental coccidiosis produces contrasting results in inbred mice of differing susceptibility to infection.

Pretreatment of inbred mice with intravenous and/or intraperitoneal injection of an antigen prepared from sporozoites of Eimeria vermiformis modulated the course of infection with the parasite in a manner that depended on the resistance-susceptibility phenotype of the host. Mice with a resistant background (BALB) produced more oocysts and those with a susceptible background (C57BL) produced fewer oocysts than their respective controls. The optimum conditions for producing these effects were established, and evidence is presented which suggests that the phenomenon might also apply in the target host, the chicken.

Animals↗
PubMed1999

Efficient gene delivery to the inflamed colon by local administration of recombinant adenoviruses with normal or modified fibre structure.

BACKGROUND/AIMS: Replication deficient recombinant adenoviruses represent an efficient means of transferring genes in vivo into a wide variety of dividing and quiescent cells from many different organs. Although the gastrointestinal tract is a potentially attractive target for gene therapy approaches, only a few studies on the use of viral gene transfer vehicles in the gut have been reported. The prospects of using recombinant adenoviruses for gene delivery into epithelial and subepithelial cells of the normal and inflamed colon are here analysed. METHODS: An E1/E3 deleted recombinant adenovirus (denoted AdCMVbetaGal) and an adenovirus with modified fibre structure (denoted AdZ.F(pk7)) both expressing the bacterial lacZ gene under the control of a human cytomegalovirus promoter were used for reporter gene expression in vitro and in vivo. beta-Galactosidase activity was determined by specific chemiluminescent reporter gene assay. RESULTS: Intravenous or intraperitoneal injection of AdCMVbetaGal into healthy Balb/c mice caused strong reporter gene expression in the liver and spleen but not in the colon. In contrast, local administration of AdCMVbetaGal resulted in high reporter gene expression in colonic epithelial cells and lamina propria mononuclear cells. A local route of adenovirus administration in mice with experimental colitis induced by the hapten reagent trinitrobenzenesulphonic acid was next evaluated. Interestingly, rectal administration of AdCMVbetaGal caused a higher beta-galactosidase activity in isolated lamina propria cells from infected mice with experimental colitis than in those from controls. Furthermore, isolated lamina propria cells from mice with colitis infected in vitro showed a significant increase in reporter gene activity compared with controls. Finally, AdZ.F(pk7) adenoviruses with modified fibre structure produced 10- to 40-fold higher reporter gene activity in spleen T cells and lamina propria mononuclear cells of colitic mice compared with standard AdCMVbetaGal vectors. CONCLUSIONS: Local administration of recombinant adenoviruses with normal or modified fibre structure could provide a new reliable method for targeted gene expression in the inflamed colon. Such gene delivery could be used to specifically express signal transduction proteins with therapeutic potential in inflamed colonic tissue. In particular, adenoviruses with modified fibre structure may be useful in T cell directed therapies in intestinal inflammation.

Adenoviridae↗
PubMed1978

Regional distribution of ethanol in the rat brain.

The regional distribution of ethanol in selected areas of the rat brain was studied after single intravenous and intraperitoneal injections. Ethanol concentrations (measured by gas-liquid chromatography) in cortex, striatum, and hippocampus were compared with arterial and venous blood alcohol concentrations. As previously reported, equilibrium between tissue and arterial blood occurred within 3 min and followed simple diffusion kinetics. At shorter time intervals (1 min) after injection, regional ethanol concentrations differed, possibly because of regional blood flow and tissue mass. Equilibrium between tissue and venous blood required 10--15 min and coincided with the disappearance of the arterial-venous difference. These findings suggest that tissue ethanol concentrations cannot be determined from venous blood samples until brain arteriovenous equilibrium has occurred. They also support the argument that alcohol concentrations in tissue perfusates do not necessarily provide a reliable guide to those in the tissue.

Animals↗
PubMed1977

Distribution of 99mTc-1-thioglucose in rats: effect of administration route on pancreatic specificity.

Tissue distribution of 99mTc-1-thioglucose was studied in inbred albino Fisher rats. High levels of radioactivity were observed in the kidney with concurrent low pancreatic levels and pancreas/liver ratios of 0.4 following intravenous administration of the agent. High pancreatic concentration were observed with pancreas/liver ratios of 4.0 after intraperitoneal administrations. Future studies on pancreatic radiopharmaceuticals should avoid production of artificially high pancreatic values by intraperitoneal injection.

Animals↗
PubMed2006

Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst.

Thirst and sodium appetite are both critical for restoring blood volume. Because these two behavioral drives can arise under similar physiological conditions, some of the brain sensory sites that stimulate thirst may also drive sodium appetite. However, the physiological and temporal dynamics of these two appetites exhibit clear differences, suggesting that they involve separate brain circuits. Unlike thirst-associated sensory neurons in the hypothalamus, the 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite (16). Here, we tested whether the HSD2 neurons are also activated in response to either of the two physiological stimuli for thirst: hyperosmolarity and hypovolemia. Hyperosmolarity, produced by intraperitoneal injection of hypertonic saline, stimulated a large increase in water intake and a substantial increase in immunoreactivity for the neuronal activity marker c-Fos within the medial NTS, but not in the HSD2 neurons. Hypovolemia, produced by subcutaneous injection of hyperoncotic polyethylene glycol (PEG), stimulated an increase in water intake within 1-4 h without elevating c-Fos expression in the HSD2 neurons. The HSD2 neurons were, however, activated by prolonged hypovolemia, which also stimulated sodium appetite. Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity. In summary, the HSD2 neurons are activated specifically in association with sodium appetite and appear not to function in thirst.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed1982

Cholecystokinin suppresses food intake by inhibiting gastric emptying.

In a search for the physiological mechanisms that could mediate and characterize a satiety function for the hormone cholecystokinin (CCK), we examined in Macaca mulatta the effect of intraperitoneal injections (0.1-0.8 microgram/kg) and intravenous infusions (60-240 ng.kg-1.h-1) of the C-terminal octapeptide of CCK on gastric emptying of saline test meals. Within these dose ranges, gastric emptying was inhibited by this hormone to a degree comparable with that produced by intraintestinal nutrient. The onset of the inhibition is rapid and its effect brief. At the doses of CCK that produce gastric inhibition, CCK would not affect feeding in a fasted monkey unless the stomach was filled with saline. This result suggests that a satiety influence of circulating CCK is an indirect one. The satiety effect depends upon inhibition of gastric emptying, which then leads to gastric distention with further food injection. CCK thus can be considered a link in a chain of physiological elements producing the short-term satiety that leads to the appropriate interruption of a meal or bout of feeding behavior.

Animals↗
PubMed1997

Central noradrenergic system modulates plasma interleukin-6 production by peripheral interleukin-1.

The role of the central noradrenergic system in systemic interleukin-6 (IL-6) production induced by intravenously administered recombinant human interleukin-1 beta (IL-1 beta) was examined in rats. Pretreatment of rats intracerebroventricularly with 6-hydroxydopamine (6-OHDA, 100 or 200 micrograms/rat) significantly attenuated the increase in plasma IL-6 levels caused by IL-1 beta (2 micrograms/kg i.v.). A modest inhibition of the IL-1 beta-induced plasma IL-6 production was observed following pretreatment with prazosin (20 micrograms/rat i.c.v.) but not after administration of idazoxan or propranolol. There were no significant increases in the IL-6 content in the hypothalamus, medulla oblongata, and cortex of the brain after intravenous IL-1 beta. Adrenalectomy produced an augmented plasma IL-6 response to intravenous IL-1 beta, whereas chemical sympathectomy with intraperitoneal injection of 6-OHDA (50 or 100 mg/kg) decreased the IL-1 beta-induced plasma IL-6 levels. Nor-epinephrine (NE), in the dose range 10(-6)-10(-4) M, significantly increased the IL-6 levels in the rat spleen lymphocyte culture media. At doses of 10(-9)-10(-7) M, NE enhanced the effect of IL-1 beta on the IL-6 release by spleen lymphocytes in a dose-dependent manner. These findings suggest that the plasma IL-6 response to intravenous IL-1 beta is partially mediated through the activation of the central noradrenergic system and a consequent increase in the sympathetic outflow to the peripheral tissues and that the NE released from the sympathetic terminals may function as a mediator and/or modulator to facilitate the synthesis/release of IL-6 in the sympathetic nerve-innervated organs.

Adrenergic Antagonists↗
PubMed1999

Long-term CCK-leptin synergy suggests a role for CCK in the regulation of body weight.

The gut peptide CCK is a nutrient-related signal important to the control of food intake. In the present studies, we observed that a single intraperitoneal injection of CCK (1-2 microgram/kg) given 2-3 h after intracerebroventricular leptin (2-5 microgram) reduced body weight and chow intake over the ensuing 48 h more than did leptin alone. CCK alone had no effect on either 48-h chow intake or body weight but significantly reduced feeding during a 30-min sucrose test. However, reduction of 30-min sucrose intake by CCK was not enhanced by prior intracerebroventricular leptin. The present data suggest that CCK can contribute to the regulation of body weight when central leptin levels are elevated.

Animals↗