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PubMed2006

Transcriptional regulatory networks in cellular responses and tolerance to dehydration and cold stresses.

Plant growth and productivity are greatly affected by environmental stresses such as drought, high salinity, and low temperature. Expression of a variety of genes is induced by these stresses in various plants. The products of these genes function not only in stress tolerance but also in stress response. In the signal transduction network from perception of stress signals to stress-responsive gene expression, various transcription factors and cis-acting elements in the stress-responsive promoters function for plant adaptation to environmental stresses. Recent progress has been made in analyzing the complex cascades of gene expression in drought and cold stress responses, especially in identifying specificity and cross talk in stress signaling. In this review article, we highlight transcriptional regulation of gene expression in response to drought and cold stresses, with particular emphasis on the role of transcription factors and cis-acting elements in stress-inducible promoters.

Adaptation, Physiological↗
PubMed2006

Role of oxidative stress in the extremely salt-tolerant yeast Hortaea werneckii.

Eukaryotic halotolerant microorganisms are important as model organisms to understand the general mechanisms of resistance to environmental salinity. The ability of the extremely halotolerant black yeast Hortaea werneckii to combat oxidative stress was addressed, using hydrogen peroxide to generate the reactive oxygen species. Increasing environmental salinity was found to have no effect on its high ability to degrade hydrogen peroxide but resulted in a decrease in viability in response to externally added hydrogen peroxide, suggesting that the latter property determines the upper limit of the salt tolerance of H. werneckii. A refinement of the model of adaptation of H. werneckii to high-salinity environments is proposed.

Adaptation, Physiological↗
PubMed1999

Tolerance to morphine-induced antinociception is decreased by chronic sucrose or polycose intake.

Chronic intake of palatable fluids alters morphine-induced antinociception. Two experiments were conducted to evaluate how long-term access to palatable fluids alters the development of tolerance to morphine-induced antinociception. In Experiment 1, 40 adult male Long-Evans rats were used. In addition to ad lib chow and water, 10 rats were given a 0.15% saccharin solution, 10 were given a 32% sucrose solution, and 10 were given a 32% Polycose solution to drink for 3 weeks. Ten rats were given chow and water alone, and served as dietary controls. Morphine-induced antinociception was assessed using the radiant-heat tail-flick method (TF). Half of the animals in each dietary condition were given preexposure to 7.5 mg/kg morphine; the other half received saline. All rats were given a TF 30-min postinjection. To determine whether tolerance developed, a cumulative dose paradigm (0.625, 1.25, 2.5, 5.0, 10.0 mg/kg) was employed 1 week after initial morphine injections, and was repeated at weekly intervals for 3 weeks. Antinociception was significantly lower in rats preexposed to morphine relative to rats preexposed to saline. Although all rats displayed decreased antinociception relative to the first morphine injection, rats that drank saccharin showed greater reductions in morphine-induced antinociception relative to rats that drank sucrose or Polycose. Experiment 2 was conducted to determine whether initial pairing of the TF with morphine preexposure produced differences in the development of opioid tolerance. All conditions and procedures were identical to Experiment 1, except that the initial morphine and saline injections were not followed by TF. As in Experiment 1, rats that drank saccharin showed less antinociception than rats that drank sucrose or Polycose. The present results suggest that long-term intake of palatable nutritive solutions curbs tolerance to morphine-induced antinociception, whereas long-term intake of a nonnutritive, sweet saccharin solution does not.

Analgesics, Opioid↗
PubMed1981

Facilitation of morphine-induced tolerance and physical dependence by prolyl-leucyl-glycinamide.

The pretreatment of mice with 30 mg/kg morphine s.c. did not alter the analgesic effect of morphine in mice pretreated with saline but decreased the analgesic effect of morphine in mice pretreated with prolyl-leucyl-glycinamide (PLG). Tolerance was evaluated by the effect of PLG on morphine-induced enhancement of naloxone potency which is a measure of the capacity of naloxone to antagonize morphine-induced analgesia and is postulated to be an indicator of tolerance development. The naloxone potency of PLG-treated mice was 2-fold greater than that of control mice. PLG did not alter the whole brain levels of morphine, nor did it alter the naloxone potency in mice which were not pretreated with 30 mg/kg morphine. In mice treated with 100 mg/kg morphine or implanted with 50 mg morphine pellets for 24 or 72 h, the amount of naloxone required to induce jumping was not altered by PLG. However, PLG treatment did increase the hypothermia and body weight loss seen after naloxone-induced withdrawal. Administration of PLG to morphine-dependent mice 1 h prior to naloxone did not modify the resultant hypothermia or body weight loss. These results indicate that PLG facilitated the development of morphine tolerance and dependence.

Analgesia↗
PubMed2000

Subcutaneous administration of amifostine during fractionated radiotherapy: a randomized phase II study.

PURPOSE: Amifostine (WR-2721) is an important cytoprotective agent. Although intravenous administration is the standard route, pharmacokinetic studies have shown acceptable plasma levels of the active metabolite of amifostine (WR-1605) after subcutaneous administration. The subcutaneous route, due to its simplicity, presents multiple advantages over the intravenous route when amifostine is used during fractionated radiotherapy. PATIENTS AND METHODS: Sixty patients with thoracic, 40 with head and neck, and 40 with pelvic tumors who were undergoing radical radiotherapy were enrolled onto a randomized phase II trial to assess the feasibility, tolerance, and cytoprotective efficacy of amifostine administered subcutaneously. A flat dose of amifostine 500 mg, diluted in 2.5 mL of normal saline, was injected subcutaneously 20 minutes before each radiotherapy fraction. RESULTS: The subcutaneous amifostine regimen was well tolerated by 85% of patients. In approximately 5% of patients, amifostine therapy was interrupted due to cumulative asthenia, and in 10%, due to a fever/rash reaction. Hypotension was never noted, whereas nausea was frequent. A significant reduction of pharyngeal, esophageal, and rectal mucositis was noted in the amifostine arm (P <.04). The delays in radiotherapy because of grade 3 mucositis were significantly longer in the group of patients treated with radiotherapy alone (P <.04). Amifostine significantly reduced the incidence of acute perineal skin and bladder toxicity (P <.0006). CONCLUSION: Subcutaneous administration of amifostine is well tolerated, effectively reduces radiotherapy's early toxicity, and prevents delays in radiotherapy. The subcutaneous route is much simpler and saves time compared with the intravenous route of administration and can be safely and effectively applied in the daily, busy radiotherapy practice.

Abdominal Neoplasms↗
PubMed1989

Failure of aminophylline and salbutamol to improve respiratory muscle function and exercise tolerance in healthy humans.

We investigated the effects of intravenously administered aminophylline (A; 6 mg/kg over 20 min, followed by 0.9 mg/kg/h), salbutamol (S; 4 micrograms/kg over 20 min, followed by 3 micrograms/kg/h) and placebo (P; saline solution) on the strength of the respiratory muscles, the ventilatory endurance and the exercise tolerance in 7 healthy humans. Neither A nor S caused bronchodilation, as shown by the lack of change in FEV1. The strength of respiratory muscles, as measured by maximal inspiratory pressure (MIP), and the ventilatory endurance, as measured by sustainable inspiratory pressure (SIP), were not statistically different after A (MIP: 136.5 +/- SE 11.6 cm H2O; SIP: 104.2 +/- 8.4 cm H2O or after S (MIP: 135.7 +/- 11.5; SIP: 107.1 +/- 10.4) compared to after P (MIP: 127.1 +/- 10.1; SIP: 105.0 +/- 5.9). Significant changes in 12-min walking distance, perceived exertion rate, anaerobic threshold, maximal work output, maximal O2 uptake were observed neither after A nor after S. The exchange ratio and heart rate were higher after A and S than after P at some steps of a progressive, symptom-limited, treadmill-based exercise test. This might be the result of metabolic or cardiovascular adaptations elicited by these drugs. We conclude that A or S at therapeutic concentrations have no clinically relevant beneficial effects on ventilatory muscle function and exercise tolerance in healthy subjects.

Adult↗
PubMed1978

Induction and mechanism of tolerance to bovine serum albumin in mice given total lymphoid irradiation (TLI).

BALB/c mice given total lymphoid irradiations (TLI) were injected i.p. with bovine serum albumin (BSA) in saline, and challenged with DNP-BSA in complete Freund's adjuvant 6 weeks later. The latter animals made no anti-DNP antibody response as measured by a modified Farr assay, but made a normal anti-DNP response after challenge with DNP-BGG in adjuvant. Normal mice or mice given whole body irradiation were not tolerized by the i.p. injection of BSA in saline. Spleen cells from unresponsive mice (TLI + BSA in saline) suppressed the adoptive secondary anti-DNP response of sublethally irradiated syngeneic hosts given BSA-primed T cells, DNP-BSA-primed B cells, and DNP-BSA in saline. The suppressor cells were antigen specific, and were inactivated by in vitro treatment with anti-Thy 1.2 antiserum and complement. The findings suggest that soluble antigens administered to mice after TLI evoke a state of tolerance that is maintained by antigen-specific suppressor T cells. A similar mechanism may be involved in the maintenance of tolerance to allografts. These findings may have important clinical implications for patients treated with TLI for lymphoid malignancies.

Animals↗
PubMed1998

Long-term alterations in opiate antinociception resulting from infant fentanyl tolerance and dependence.

Postnatal day-14 (P14) infant rats remained naive or were implanted with osmotic minipumps infusing saline or fentanyl (50 microg kg(-1) h(-1)). Fentanyl was administered 72 h later for measurement of antinociception in the tail-flick test. The potency of fentanyl was 3.0-fold lower in fentanyl-infused compared to saline-infused P17 rats. Fentanyl-infused P17 rats injected with naloxone underwent withdrawal characterized by increases in spontaneous activity, wall climbing, diarrhea, abdominal stretching, forepaw treading/tremors, wet-dog shakes, jumping, ptosis, rhinorrhea and hypothermia. Other naive, saline-infused and fentanyl-infused P17 rats not challenged with fentanyl or naloxone were housed until maturing into P42 juveniles. Fentanyl's potency was equal among each treatment group. However, morphine's potency was reduced in juveniles tolerant to fentanyl as infants. Morphine was also less potent in P90 adults tolerant to fentanyl as infants. Thus, chronic opiate exposure during infancy may affect the developing central nervous system, and desensitize animals and humans to opiate analgesia throughout life.

Analgesics, Opioid↗
PubMed1997

Magnitude of tolerance to fentanyl is independent of mu-opioid receptor density.

The effect of a mu-opioid receptor irreversible antagonist on the development of tolerance to fentanyl was determined in mice. Mice were injected with saline or clocinnamox (3.2 mg/kg, i.p.) and 4 h later mice implanted s.c. with a placebo pellet or an osmotic minipump that infused fentanyl (0.165 mg/kg per day) for 3 days. Fentanyl pumps and placebo pellets were removed on the third day following implantation and 4 h later mu-opioid receptor saturation binding studies in whole brain ([3H][D-Ala2,MePhe4,Gly-ol5]enkephalin: DAMGO) or fentanyl analgesic dose-response studies (tailflick assay) were conducted. Fentanyl infusions and clocinnamox both significantly reduced the potency of fentanyl by 2.8- and 2.4-fold, respectively. When fentanyl and clocinnamox were administered together, a significant 5.0-fold reduction in fentanyl potency relative to the saline-placebo group was observed, which represents an additive effect of clocinnamox and fentanyl. The ED50 of fentanyl in clocinnamox-treated mice was shifted 2.1-fold by fentanyl infusion relative to the clocinnamox-placebo group. This is comparable to the 2.8-fold shift in the ED50 produced by fentanyl infusion in saline-treated mice. In binding studies, fentanyl produced a small (-9%) reduction in Bmax, while clocinnamox significantly reduced (-41%) mu-opioid receptor density without altering affinity (Kd). In the clocinnamox-fentanyl group, there was a 50% reduction in Bmax, which is similar to the additive effect observed in analgesia studies. These data indicate that changes in mu-opioid receptor density prior to the development of tolerance to fentanyl do not impact on the magnitude of tolerance.

Analgesics↗
PubMed1994

Osmoprotective compounds in the Plumbaginaceae: a natural experiment in metabolic engineering of stress tolerance.

In common with other zwitterionic quarternary ammonium compounds (QACs), glycine betaine acts as an osmoprotectant in plants, bacteria, and animals, with its accumulation in the cytoplasm reducing adverse effects of salinity and drought. For this reason, the glycine betaine biosynthesis pathway has become a target for genetic engineering of stress tolerance in crop plants. Besides glycine betaine, several other QAC osmoprotectants have been reported to accumulate among flowering plants, although little is known about their distribution, evolution, or adaptive value. We show here that various taxa of the highly stress-tolerant family Plumbaginaceae have evolved four QACs, which supplement or replace glycine betaine-namely, choline O-sulfate and the betaines of beta-alanine, proline, and hydroxyproline. Evidence from bacterial bioassays demonstrates that these QACs function no better than glycine betaine as osmoprotectants. However, the distribution of QACs among diverse members of the Plumbaginaceae adapted to different types of habitat indicates that different QACs could have selective advantages in particular stress environments. Specifically, choline O-sulfate can function in sulfate detoxification as well as in osmoprotection, beta-alanine betaine may be superior to glycine betaine in hypoxic saline conditions, and proline-derived betaines may be beneficial in chronically dry environments. We conclude that the evolution of osmoprotectant diversity within the Plumbaginaceae suggests additional possibilities to explore in the metabolic engineering of stress tolerance in crops.

Aldehyde Oxidoreductases↗
PubMed1980

Effect of morphine and naloxone on intestinal transit in mice.

Morphine caused a dose-dependent slowing of the rate of intestinal transit in mice. This inhibitory effect of morphine was antagonised by naloxone administration. Pretreatment with a single dose of morphine did not induce any detectable tolerance to the inhibitory effect of a second dose of morphine given 5 h later. However, naloxone was more effective in antagonising this inhibitory effect of morphine in morphine-pretreated mice than in saline-pretreated animals. Molecular sieve morphine pellet implantation for 24 h induced detectable tolerance to the inhibitory effect of morphine administered 3 h after removal of the pellet. In addition, the antagonistic effect of naloxone was also augmented when compared with blank pellet-implanted control animals. The present study has shown that the enhanced naloxone potency against the inhibitory effect of morphine was intestinal transit was observalbe before the development of overt tolerance, and that tolerance to the effect of morphine on the small intestine could be induced by implantation of a molecular sieve morphine pellet for 24 h.

Animals↗
PubMed2001

Early neonatal experience of Long-Evans rats results in long-lasting changes in morphine tolerance and dependence.

RATIONALE: Daily, 3-h separations from the dam on postnatal days 2-14 produce long-lasting changes in behavioral and neuroendocrine responses to stressors and sensitivity to acute morphine in Long-Evans rats. OBJECTIVE: We tested whether offspring that were separated from their dam for 3 h daily (MS) on postnatal days 2-14 exhibit altered sensitivity to chronic morphine, compared to animals that experienced only brief (15 min) separations (H) from the dam or that were left undisturbed (NH) during the same period. METHODS: Subjects received 1 week SC infusion of either morphine, or saline via osmotic pumps. Twenty-hours after pump removal, the global opioid withdrawal scores were recorded. Four hours later, animals were tested for antinociception (tail-flick and hot-plate tests) during cumulative morphine administration. RESULTS: MS males and MS females undergoing withdrawal from chronic morphine had higher global withdrawal scores compared to NH controls. MS males (but not MS females) were less sensitive to the antinociceptive effects of morphine compared to H and NH controls, primarily in the hot-plate test, regardless of whether they had received a saline or a morphine infusion. MS males consistently exhibited significant morphine tolerance, whereas control males failed to exhibit tolerance either in the hot-plate test (NH group) or in both antinociception assays (H group). In contrast, tolerance was exhibited by all females in both tests for antinociception. CONCLUSIONS: These data indicate that repeated neonatal maternal separation alters sensitivity to chronic morphine administration in a sex-dependent manner.

Analgesics, Opioid↗
PubMedDate not supplied

[Efficacy of topical administration of lidocaine through a Malinckrodt Hi-Lo Jet tube in lessening cough during recovery from general anesthesia].

To achieve tracheal anesthesia during intubation, an endotracheal tube was purposely designed. The tube had multiple laser-induced perforations in its lower portion produced that allowed administration of the local anesthetic in a pulverized form. We evaluated the efficacy of lidocaine 2% in preventing cough during recovery from general anesthesia. The goal of this study was to perform a topical anesthesia of the hypopharynx, larynx, and trachea. This attenuates the laryngeal reflex occurring during anesthesia recovery and therefore, prevents from potential complications. Sixteen patients ASA I-II underwent surgery with general anesthesia. They were prospectively studied following a randomized double blind protocol. The control group received saline infusion (n = 6) whereas the experimental group (n = 10) was treated with lidocaine. At the end of the anesthesia period, the presence of cough was treated with the test solution. In 90% of cases treated with lidocaine, cough disappeared in about 30 seconds and patients tolerated the endotracheal tube until extubation was performed. All patients who received saline solution presented cough until extubation.

Administration, Topical↗
PubMed1998

Differential tolerance to morphine's immunomodulatory effects following continuous administration.

Rats were continuously infused with either morphine or saline via an osmotic minipump for 20 consecutive days. Effects on immune status were assessed on the twentieth day of the chronic administration period following a bolus injection of morphine administered 1 h prior to sacrifice. The morphine injection suppressed measures of splenic natural killer (NK) cell activity, mitogen-stimulated T-cell proliferation, and gamma-interferon (IFN) production in rats that received saline via the minipump. In rats that received chronic morphine via the minipump, the morphine injection also suppressed mitogen-stimulated splenocyte proliferation and gamma-IFN production but did not suppress NK cell activity. These data indicate that chronic morphine administration via osmotic minipumps leads to differential tolerance to the immunomodulatory effects of morphine. These findings support previous results indicating differential tolerance development within the immune system following chronic morphine administration via the drinking water.

Animals↗
PubMedDate not supplied

Interactive effect of exercise training and growth hormone administration on glucose tolerance and muscle GLUT4 protein expression in rats.

The insulin-resistance effect of growth hormone (GH) administration has been frequently reported. The present study investigated the effect of GH administration on glucose tolerance and muscle GLUT4 protein expression in exercise-trained and untrained rats. Forty-eight rats were weight-matched and assigned to the following 4 groups: control, GH, exercise training, and exercise training + GH groups. After 2 weeks of GH injections (65 microg/kg/day) and exercise training, the glucose tolerance and insulin response were measured in these rats. The GLUT4 protein level, glycogen storage, and citrate synthase activity were determined in red gastrocnemius and plantaris muscles. Daily GH administration elevated the curves of the oral glucose tolerance test and insulin response compared with those of saline-injected control rats. Furthermore, exercise training completely eliminated this GH-induced insulin resistance as determined 18 h after the last bout of exercise training. Additionally, exercise training significantly increased muscle glycogen storage and GLUT4 protein levels. GH administration did not affect the GLUT4 protein and glycogen storage increases induced by exercise training, but the citrate synthase activity in the plantaris muscle was further elevated by GH administration to a level above that induced by training. In conclusion, this is the first study that demonstrates that regular exercise training prevents GH-induced insulin-resistance side effect in rats.

Analysis of Variance↗
PubMed1983

Arginine vasopressin enhances retention of morphine tolerance.

The hot plate method was used to assess tolerance in rats following daily injections of morphine. Following analgesia assessment, or a time equated rest period, rats were injected with either saline or a pituitary peptide. Arginine vasopressin, but not ACTH 4-10, prolonged the retention of morphine tolerance when assessed five weeks after the last injection. Neither the rate nor the degree of tolerance development were influenced by either peptide. These hormones had no effect on retention of tolerance development were influenced by either peptide. These hormones had no effect on retention of tolerance in rats not assessed for analgesia during the period of tolerance development. The effects of pituitary peptides on morphine tolerance are analogous to the effects they have on learning and memory processes, suggesting that similar adaptational processes are occurring in both phenomena.

Adrenocorticotropic Hormone↗
PubMed2004

The effects of intrathecal gabapentin on spinal morphine tolerance in the rat tail-flick and paw pressure tests.

Analgesic tolerance to opioids has been described in both experimental and clinical conditions and may limit the clinical utility of these drugs. We have previously shown that systemic gabapentin (GBP), a non-opioid drug, prevents and reverses tolerance to systemic morphine in the rat. In this study, we investigated the effect of intrathecal GBP on spinal morphine tolerance. Studied rats were given 7 days of intrathecal injections with saline (10 microL), GBP (300 microg), morphine (15 microg), or a GBP-morphine combination, and analgesic testing using tail-flick and paw-pressure tests was conducted before and 30 min after the drug injection. On Day 8, an antinociceptive dose-response curve was constructed and the 50% effective dose (ED(50)) values for morphine (given alone) were calculated for each study group. Coinjection of GBP with morphine blocked the development of tolerance, as shown by the preservation of morphine analgesia over 7 days as well as by a concomitant decrease in ED(50) values on Day 8, as compared with the morphine-alone group. Although additive analgesia over Days 1-7 cannot be ruled out, ED(50) reductions in the GBP-morphine combination group indeed suggest some suppression of tolerance. These data support previous evidence that GBP prevents opioid tolerance and, more specifically, indicate that intrathecal GBP prevents the development of spinal opioid tolerance. Future studies are required to examine the respective roles of supraspinal and peripheral sites of GBP-morphine interaction and to investigate the mechanisms underlying the action of GBP on opioid tolerance.

Acetates↗
PubMed1986

Conditional tolerance to haloperidol-induced catalepsy is not caused by striatal dopamine receptor supersensitivity.

The purpose of this study was to determine if non-pharmacological stimuli influence behavioural tolerance to haloperidol via striatal postsynaptic dopamine receptors. Rats received daily haloperidol and saline in two different environments for a period of 28 days. After this conditioning period half of the rats received haloperidol in the haloperidol-associated environment, whereas the other half received haloperidol in the saline-associated environment. All rats were tested for catalepsy and at the end of the last catalepsy test, striatal DOPAC, HVA and ACh were determined. Only the rats tested in the haloperidol-associated environment were behaviourally tolerant to haloperidol. In contrast, both groups were biochemically tolerant to haloperidol. These results indicate that environmental cue factors govern the development of behavioural tolerance to haloperidol, rather than biochemical factors (striatal DA super-sensitivity). In addition, these factors do not exert their influence on behavioural tolerance via striatal DA receptors.

3,4-Dihydroxyphenylacetic Acid↗