In vivo 31P NMR spectrum of Hymenolepis diminuta and its change on short-term exposure to mebendazole

1987 ◽  
Vol 22 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Stewart N. Thompson ◽  
Edward G. Platzer ◽  
Robert W.K. Lee
Keyword(s):  
31P Nmr ◽  
Hymenolepis Diminuta ◽  
Short Term ◽  
Nmr Spectrum ◽  
Short Term Exposure

A method for calculating the distribution of pH in tissues and a new source of pH error from the 31P-NMR spectrum

1994 ◽  
Vol 266 (2) ◽  
pp. R638-R645 ◽  
Author(s):  
R. A. Graham ◽  
A. H. Taylor ◽  
T. R. Brown
Keyword(s):  
31P Nmr ◽  
Significant Error ◽  
Nonlinear Relationship ◽  
Ph Responsive ◽  
Nmr Spectrum ◽  
Ph Distribution ◽  
Morris Hepatoma ◽  
Intensity Axis ◽  
Hasselbalch Equation

The true distribution of the pH in tissues can be determined from the in vivo 31P-nuclear magnetic resonance (NMR) spectrum by converting the parts per million (PPM) axis of the pH responsive resonance to pH using the Henderson-Hasselbalch equation. In addition, the intensity axis of the resonance must be divided by the derivative of the Henderson-Hasselbalch equation to correct for the nonlinear relationship between pH and PPM. This nonlinear relationship causes the apparent center of the resonance in PPM to be dependent not only on the center of the pH distribution but also on its width and distance from the pKa, where Ka is the association constant. Therefore, the pH determined from uncorrected spectra may be in significant error, particularly if the pH distribution is distant from the pKa and is broad. The method was applied to the isolated perfused Morris hepatoma 5123C to determine the distribution of intracellular pH (pHi) using resonances from two intracellular compounds. The two resonances did not report the same pHi unless the spectral data were properly corrected. The method should be of interest to anyone interested in pHi.

Dietary protection by iron against clastogenic effects of short-term exposure to arsenic in mice in vivo

2000 ◽  
Vol 38 (8) ◽  
pp. 735-737 ◽  
Author(s):  
S Poddar ◽  
P Mukherjee ◽  
G Talukder ◽  
A Sharma
Keyword(s):  
Short Term ◽  
Short Term Exposure

Short-term exposure to homocysteine depresses rat aortic contractility by an endothelium-dependent mechanism

2000 ◽  
Vol 78 (6) ◽  
pp. 500-506 ◽  
Author(s):  
S Wang ◽  
G Wright ◽  
J Harrah ◽  
R Touchon ◽  
W McCumbee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Contractile Response ◽  
Fold Increase ◽  
No Production ◽  
Short Term ◽  
Short Term Exposure ◽  
Oxide Synthase

The effect of short-term exposure to homocysteine (Hcy) on the contractile characteristics of rat aortic tissue was assessed both in vitro and in vivo. The contractile response of Hcy-treated aortic rings in culture for 1 or 4 days was unchanged from control responses. By comparison, aortic rings from animals injected with Hcy showed marked attenuation of response compared with controls injected with saline, cysteine or methionine. The contractile response to K+ was decreased within 24 hours of Hcy injection, whereas the response to both K+ (-27%) and noradrenaline (-56%) was significantly decreased by 4 days. In contrast, the contractile response to phorbol-12,13-dibutyrate was not different between Hcy and control groups. Intimal rubbing completely restored the responsiveness of Hcy-treated tissue to K+ and noradrenaline. By comparison, L-NAME only partially restored contractile responsiveness, while the cyclooxygenase inhibitor indomethacin had no effect on contractile attenuation induced by Hcy. Western blot analysis showed a 2-fold increase of endothelial nitric oxide synthase (eNOS) and a 3-fold increase in inducible nitric oxide synthase (iNOS) protein expression in the aortic endothelial cells from Hcy-injected rats. The results indicate an early detectable effect of Hcy on the in vivo contractile properties of vascular smooth muscle. The effect is endothelium-mediated and may vary depending on the agonist studied. The mechanism is uncertain but appears to involve increased nitric oxide (NO) production. Finally, the data suggest that attenuation of contraction may not be due to a direct effect of Hcy but that the compound is modified or acts indirectly in vivo.Key words: nitric oxide, nitric oxide synthase, in vivo, smooth muscle.

Apoptosis signal ceramide c6 synergizes anti-tumor effects of paclitaxel oxaliplatin & cisplatin on growth of pancreatic cancer in SCID mice

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 13135-13135
Author(s):  
D. Shrayer ◽  
H. J. Wanebo ◽  
M. Resnick
Keyword(s):  
Body Weight ◽  
Caspase 3 ◽  
Combined Therapy ◽  
Drug Dose ◽  
Scid Mice ◽  
Short Term ◽  
Short Term Exposure ◽  
Chemical Studies

13135 Background: Ceramide (C6) is an analog of endogenous ceramides, which are a major signaling pathway for apoptosis in cells undergoing stress, exposure to chemotherapy. Current report documents in vivo anti tumor effects combining C6 with oxaliplatin & cisplatin on L3.6 human pancreatic adenocarcinoma implanted in the SCID mouse. Correlative histologic studies provide additional mechanistic insights. Methods: SCID/Beige/ Taconicmale mice were inoculated subcutaneously (S.C.) w/2×106 L3.6 pancreatic cells. Chemotherapy doses were based on clinical & in vitro data. Treatment began 4 days post tumor implant with 3 weekly 3×/wk) intraperitoneal (IP) injections of Paclitaxel (P) 3.0 m/kg, oxaliplatin (OX) 2.5 mg/kg, cisplatin (CP) 2.5 mg/kg, with/without ceramide 10 mg/kg. Mice were observed for 6 weeks & were autopsied when near death, or at 6 week level. (All controls died by 3rd week). Data recovered included maximum tumor volume, tumor weight, body weight & survival. Histopathology studies were carried out in a separate group of 40 mice treated by the same drug dose levels & autopsied at 4 hours & 24 hours. Tumors were bi-valved & fixed in buffered formalin or frozen in hexane/acetone bath. Major focus was effects on tumor necrosis, apoptosis, mitotic index & Apoptosis (caspase 3 expression) index. Results: Combination w/C6 ceramide augmented the tumor reduction obtained by chemotherapy alone by 57% (while preserving body weight), & increased 6 wk survival from 0% (Chemotherapy alone) to 60% w/combined therapy. Mean survival was increased from 25 to 37 days. Preliminary short term immunohisto chemical studies showed enhancement of apoptotic index by increased and caspase 3 expression at 4 & 24 hr by ceramide combinations. Conclusion: Combination therapy w/C6 Ceramide significantly enhanced anti tumor response to Paclitaxel, Oxaliplatin & Cisplatin in SCID Mice bearing L3.6 pancreatic tumor implants. Early development of enhanced apoptosis by caspase 3 expressions was shown in preliminary short term exposure experiments. No significant financial relationships to disclose.

Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver

1996 ◽  
Vol 81 (3) ◽  
pp. 1395-1403 ◽  
Author(s):  
Z. F. Xia ◽  
J. W. Horton ◽  
P. Y. Zhao ◽  
E. E. Babcock ◽  
A. D. Sherry ◽  
...  
Keyword(s):  
Nmr Spectroscopy ◽  
Atomic Absorption ◽  
Rat Liver ◽  
Absorption Spectroscopy ◽  
Atomic Absorption Spectroscopy ◽  
31P Nmr ◽  
Ischemic Injury ◽  
Nmr Spectrum ◽  
23Na Nmr

Metabolic factors that influence the transition form reversible to irreversible ischemic injury were studied in the rat liver in vivo with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hepatic ischemia for 15, 35, or 65 min was produced by occlusion of the hepatic artery and portal vein in rats. Ischemia caused a rapid decrease in the ATP concentration ([ATP])-to-P(i) concentration ratio and pH within 5 min, but there was little change in these variables detectable by 31P-NMR with longer periods of ischemia. After reperfusion, the [ATP] and P(i) concentration returned toward normal values in livers exposed to 15 or 35 min of ischemia, but 65 min of ischemia were associated with only modest recovery in [ATP], and the [ATP] later decreased. Because the 31P-NMR spectrum was similar after brief compared with prolonged ischemia, it appears that neither ATP depletion, P(i) accumulation, nor acidosis predicts metabolic recovery. Hepatic intracellular NA+ was also measured in separate groups of animals by 23Na-NMR in the presence of a shift agent, thulium (III) 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrakis (methylene-phosphonate) (TmDOTP5-), and by atomic absorption spectroscopy. Under baseline conditions, the concentration of intracellular Na+ was 15.2 mM by atomic absorption spectroscopy and 16.5 mM by 23Na-NMR. Although the 31P-NMR spectrum responded very rapidly to the onset of ischemia, intracellular Na+ concentration measured by 23Na-NMR increased gradually but steadily at approximately 1.0 mM/min during early (up to 15 min) ischemia. These observations demonstrate that a rise in intracellular Na+ does occur early ischemia, that TmDOTP5- can be applied in vivo for analysis of intracellular Na+ in the ischemic liver, and that 31P-NMR spectroscopy is very sensitive to early ischemic injury.

Effects ofPseudomonas aeruginosaendotoxin on vasodilation in the intact spinotrapezius muscle

2001 ◽  
Vol 91 (1) ◽  
pp. 351-356 ◽  
Author(s):  
Hideyuki Suzuki ◽  
Hiroyuki Ikezaki ◽  
Rinku Chandiwala ◽  
Dennis Hong ◽  
Israel Rubinstein
Keyword(s):  
Methyl Ester ◽  
Skeletal Muscles ◽  
Peripheral Circulation ◽  
Sepsis Syndrome ◽  
Short Term ◽  
Short Term Exposure ◽  
Synthase Inhibitor ◽  
Vasomotor Dysfunction

The purpose of this study was to determine whether short-term exposure to clinically relevant concentrations of Pseudomonas aeruginosa lipopolysaccharide (LPS) impairs vasoreactivity of resistance arterioles in the intact spinotrapezius muscle microcirculation and, if so, to determine the mechanisms mediating this response. Using intravital microscopy, we found that 60-min suffusion of P. aeruginosa LPS (0.03–3.0 μg/ml) on the in situ hamster spinotrapezius muscle elicited an immediate, profound, and prolonged concentration-dependent vasodilation ( P < 0.05). This response was reversible once suffusion of P. aeruginosa LPS was stopped. Pretreatment with NG-nitro-l-arginine methyl ester (10.0 μM), a nonselective nitric oxide (NO) synthase inhibitor, but not NG-nitro-d-arginine methyl ester, abrogated P. aeruginosa LPS-induced vasodilation and elicited a small, albeit significant, vasoconstriction. Indomethacin had no significant effects on P. aeruginosa LPS-induced responses. P. aeruginosa LPS had no significant effects on acetylcholine- and nitroglycerin-induced vasodilation in the spinotrapezius muscle. Collectively, these data indicate that short-term exposure to clinically relevant concentrations of P. aeruginosa LPS evokes an immediate, potent, prolonged, and reversible NO-dependent, prostaglandin-independent vasodilation in skeletal muscles in vivo. We suggest this response could play an important role in the pathophysiology of the profound vasomotor dysfunction observed in the peripheral circulation of patients with P. aeruginosa sepsis syndrome.

scholarly journals Short-Term Nose-Only Water-Pipe (Shisha) Smoking Exposure Accelerates Coagulation and Causes Cardiac Inflammation and Oxidative Stress in Mice

2015 ◽  
Vol 35 (2) ◽  
pp. 829-840 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Badreldin H Ali
Keyword(s):  
Oxidative Stress ◽  
Platelet Aggregation ◽  
Plasma Concentrations ◽  
Cardiovascular Effects ◽  
Water Pipe ◽  
Short Term ◽  
Cardiac Inflammation ◽  
Short Term Exposure ◽  
And Oxidative Stress

Background/Aim: Water-pipe smoking (WPS) has acquired worldwide popularity, and is disseminating particularly rapidly in Europe and North America. However, little is known about the short-term cardiovascular effects of WPS. Methods: Presently, we assessed the short-term cardiovascular effects of nose-only exposure to mainstream WPS in BALB/c mice for 30 min/day for 5 consecutive days. Control mice were exposed to air. At the end of the exposure period, several cardiovascular endpoints were measured. Results: WPS did not affect the number of leukocytes and the plasma concentrations of C-reactive protein, tumor necrosis factor α (TNFα) and interleukin-6 (IL-6). Likewise, plasma levels of lipid peroxidation (LPO), reduced glutathione (GSH) and catalase were not affected by WPS. By contrast, WPS aggravated in vivo thrombosis by shortening the thrombotic occlusion time in pial arterioles and venules. The number of circulating platelets was reduced by WPS suggesting the occurrence of platelet aggregation in vivo. Elevated concentrations of fibrinogen and plasminogen activator inhibitor-1 were seen after the exposure to WPS. Blood samples taken from mice exposed to WPS and exposed to adenosine diphosphate showed more platelet aggregation. The heart concentrations of IL-6 and TNFα were augmented by WPS. Likewise, heart levels of LPO, reactive oxygen species and the antioxidants catalase and GSH were increased by WPS. However, the systolic blood pressure and heart rate were not affected by WPS. Conclusion: It can be concluded that short-term exposure to WPS exerts procoagulatory effects and induce cardiac inflammation and oxidative stress. At the time point investigated, there was no evidence for blood inflammation or oxidative stress.

Positron emission tomography studies of healthy volunteers-no effects on the dopamine terminals and synthesis after short term exposure to toluene

1997 ◽  
Vol 16 (3) ◽  
pp. 171-176 ◽  
Author(s):  
C. Edling ◽  
B. Hellman ◽  
B. Arvidson ◽  
G. Johansson ◽  
J. Andersson ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Healthy Volunteers ◽  
Emission Tomography ◽  
Dopamine Synthesis ◽  
Decarboxylase Activity ◽  
Short Term ◽  
Positron Emission ◽  
Short Term Exposure ◽  
Before And After

Despite extensive research, the mechanisms for the effects of organic solvents on the central nervous system are still unknown. One mechanism proposed is that solvents interfere with the synthesis of neurotransmitters. In the present study 11 male healthy volunteers were exposed during 15 min to 100 p.p.m. toluene at light physical exercise, and the dopamine decarboxylase activity and number of terminals in putamen were measured before and after exposure by positron emission tomography. Two different tracers were used, [β-11C]L-DOPA for decarbox ylase activity during the in vivo synthesis of dopamine, and [11C] nomifensine to estimate the number of terminals. Although there was a slight increase in the rate of dopamine synthesis in the putamen after the exposure, this difference was not statistically significant (P=0.4). No effect was observed with regard to the uptake of nomifensine. There was no significant relationship between the dose of toluene and rate of dopamine synthesis, and no significant correlation between the time from end of exposure to start of the PET-camera and DOPA. Our findings indicate that short term exposure to 100 p.p.m. of toluene does not affect the rate of dopamine synthesis or the number of presynaptic terminals.

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