RESUMO
Agricultural burning is used in farm management operations; however, information about the impact of fire cues on the release and/or induction of secondary dormancy in crop seeds is scarce. Seeds from two oilseed rape cultivars were induced for high (HD) or low (LD) secondary dormancy using polyethyleneglycol (PEG) pre-treatment, and their germination after exposure to various fire cues was compared to control PEG pre-treated and non-dormant seeds. Non-dormant seed germination was unaffected by various fire cues. Low doses of aerosol smoke released secondary dormancy in HD seeds, while higher doses increased dormancy of LD seeds. Dilute smoke water also released HD seed secondary dormancy, but concentrated smke water enhanced dormancy in both LD and HD seeds. The concentrated aqueous extracts from charred oilseed rape straw only promoted germination of HD seeds, while dilution inhibited LD seed germination. Heat shock (80 °C, 5 min) released secondary dormancy in HD seeds; however, higher temperatures and/or increased exposure time was associated with seed death. GC-MS analyses of smoke water revealed two butenolides and an array of monoaromatic hydroxybenzene compounds with potential germination inhibitor or promoter activity. The extent of secondary dormancy induction in seeds affects their subsequent responses to fire cues. Both aerosol smoke and smoke water have both germination promoter and inhibitor activity. Lacking any butenolides, aqueous extracts of charred straw contain a potential germination stimulating steroid, i.e. ergosterol. The significance of fire-derived cues on behaviour of oilseed rape seeds in the soil seed bank is discussed.
Assuntos
Brassica napus , Incêndios , Germinação , Dormência de Plantas , Sementes , Brassica napus/fisiologia , Sinais (Psicologia) , Germinação/fisiologia , Sementes/fisiologiaRESUMO
BACKGROUND: Pre-pubertal varicocele can result in hypotrophy of testes, progressive deterioration of Sertoli cells and spermatogonia cell number, decrease in seminiferous diameter and cause to sperm damage. AIMS: Because of detrimental time-dependent effects of varicocele, this study describes the effects of varicocele on the levels of interleukin-6 (IL-6) and interferon-gamma in serum and testis tissue, seminiferous tubules diameter, number of Sertoli and spermatogonia cells, testis and epididymis weight and volume and sperm indices in immature rats. METHODS: Thirty-six immature rats (5-6 weeks) were assigned into six groups: three sham groups and three varicocele groups. Serum, testis, and sperm samples were collected at 9, 11, and 13 weeks after induction of varicocele or sham operation to evaluate histological parameters and levels of cytokines. RESULTS: Varicocele significantly caused an increase in serum and testis IL-6 and interferon-gamma, compared to related sham groups and previous varicocele groups (P < 0.05). Varicocele significantly decreased Sertoli cells and spermatogonia cell number with increasing varicocele time (P < 0.05). In the evaluation of seminiferous tubules diameter, the external, internal, and epithelium diameter were decreased compared to sham-related groups and previous varicocele groups. In the all varicocele groups, all types of sperm motility decreased compared to the related sham-operated group (P < 0.05). CONCLUSIONS: This study suggests varicocele has a detrimental, time-dependent effect on cytokines levels and decreases Sertoli cells, spermatogonia cell number, seminiferous tubules diameter, and sperm indices.
Assuntos
Epididimo/patologia , Interferon gama/análise , Interleucina-6/análise , Túbulos Seminíferos/patologia , Testículo/química , Testículo/patologia , Varicocele/sangue , Animais , Contagem de Células , Humanos , Interferon gama/sangue , Interleucina-6/sangue , Masculino , Tamanho do Órgão , Ratos , Análise do Sêmen , Células de Sertoli/patologia , Espermatogônias , Varicocele/patologiaRESUMO
BACKGROUND: Ischemia-reperfusion (IR)-induced nephrotoxicity is associated with proteinuria. There are reports on the involvement of inducible nitric oxide synthase (iNOS) in proteinuria in conjunction with renal disease. This study was designed to investigate the effect of N6-(1-iminoethyl)-L-lysine hydrochloride (L-Nil), a selective inhibitor of iNOS, to prevent proteinuria in IR injury. METHODS: Ischemia was induced by 40-minute clamping of the renal arteries followed by 6-hour reperfusion. Rats were administered either L-Nil (3 mg/kg intravenous bolus followed by infusion of 1 mg/kg/h) or saline. To monitor glomerular and tubular functional changes before and after treatment, we measured blood urea nitrogen, plasma creatinine, and urinary N-acetyl-beta-D-glucosaminidase activity. Total protein (TP), albumin, and low- (LMW) and high-molecular-weight (HMW) protein excretion rates were determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis of urine samples. Kidney ultrastructure was examined through a transmission electron microscope (TEM). RESULTS: IR resulted in significant LMW and HMW proteinuria. L-Nil significantly prevented the IR-induced increases in TP, albumin, and alpha1-microglobulin excretion. TEM showed loss of microvilli of the proximal tubule cells, injured mitochondria, and foamy changes in the structure of nuclear and cytoplasm in IR group. L-Nil reduced IR-mediated renal ultrastructural changes and tubular proteinuria. DISCUSSION: This study suggested possible differences in the mechanism(s) of nephrotoxicity induced by iNOS in the glomeruli and tubular cells. The types of proteins excreted in the urine should be considered in the treatment strategy. In conclusion, this study suggested the involvement of iNOS in IR-induced tubular proteinuria.
Assuntos
Inibidores Enzimáticos/uso terapêutico , Lisina/análogos & derivados , Óxido Nítrico Sintase Tipo II/antagonistas & inibidores , Óxido Nítrico Sintase/antagonistas & inibidores , Proteinúria/prevenção & controle , Traumatismo por Reperfusão/fisiopatologia , Animais , Pressão Sanguínea , Frequência Cardíaca , Lisina/uso terapêutico , Masculino , Ratos , Ratos Sprague-Dawley , Artéria Renal/efeitos dos fármacos , Artéria Renal/fisiopatologiaRESUMO
In the present study, the effects of intra-locus coeruleus (LC) injection of GABA(B) receptor-interacting agents on naloxone-induced withdrawal signs of morphine-dependent rats were examined. The GABA(B) receptor agonist and antagonists were injected 5 min prior to naloxone injection. Baclofen, a GABA(B) receptor agonist, decreased the TWS in a dose-dependent manner but CGP35348, a GABA(B) receptor antagonist, alone had no effect. On the other hand, baclofen effects were reversed by CGP35348. It may be concluded that activation of GABA(B) receptor mechanisms in the LC reduces precipitated withdrawal symptoms from chronic morphine treatment.
Assuntos
Agonistas GABAérgicos/farmacologia , Locus Cerúleo/efeitos dos fármacos , Morfina/toxicidade , Atividade Motora/efeitos dos fármacos , Síndrome de Abstinência a Substâncias/tratamento farmacológico , Análise de Variância , Animais , Baclofeno/administração & dosagem , Baclofeno/farmacologia , Baclofeno/uso terapêutico , Relação Dose-Resposta a Droga , Quimioterapia Combinada , Agonistas GABAérgicos/administração & dosagem , Agonistas GABAérgicos/uso terapêutico , Antagonistas GABAérgicos/administração & dosagem , Antagonistas GABAérgicos/farmacologia , Injeções Subcutâneas , Locus Cerúleo/fisiopatologia , Masculino , Morfina/administração & dosagem , Dependência de Morfina/tratamento farmacológico , Dependência de Morfina/fisiopatologia , Dependência de Morfina/psicologia , Atividade Motora/fisiologia , Naloxona/administração & dosagem , Naloxona/farmacologia , Naloxona/uso terapêutico , Antagonistas de Entorpecentes/administração & dosagem , Antagonistas de Entorpecentes/uso terapêutico , Entorpecentes/administração & dosagem , Entorpecentes/toxicidade , Compostos Organofosforados/administração & dosagem , Compostos Organofosforados/farmacologia , Ratos , Ratos Wistar , Síndrome de Abstinência a Substâncias/fisiopatologia , Síndrome de Abstinência a Substâncias/psicologiaRESUMO
In the present study, the effects of low-intensity laser therapy (LILT) on naloxone-induced withdrawal signs of morphine-dependent rats were examined. Low-intensity lasers with a power density of 12.5J/cm(2) have been used by a Ga-Al-As laser. One-way ANOVA showed that the LILT which applied immediately or 15min prior to naloxone injection significantly decreased total withdrawal score (TWS). These results suggest that LILT prior to naloxone injection attenuates the expression of withdrawal signs in morphine-dependent rats. Further studies may elucidate the likely role of LILT in clinical management of opioid withdrawal syndrome.
Assuntos
Analgésicos Opioides , Terapia com Luz de Baixa Intensidade , Morfina , Síndrome de Abstinência a Substâncias/terapia , Animais , Comportamento Animal/efeitos dos fármacos , Interpretação Estatística de Dados , Masculino , Naloxona/farmacologia , Antagonistas de Entorpecentes/farmacologia , Ratos , Ratos WistarRESUMO
BACKGROUND AND PURPOSE: Relaxation of corpus cavernosum, which is mediated by nitric oxide (NO) released from non-adrenergic non-cholinergic (NANC) neurotransmission, is critical for inducing penile erection and can be affected by many pathophysiological conditions. However, the peripheral effect of liver cirrhosis on erectile function is as yet unknown. The aim of the present study was to investigate the effect of biliary cirrhosis on NANC-mediated relaxation of rat corpus cavernosum and the possible roles of endocannabinoid and nitric oxide systems in this model. EXPERIMENTAL APPROACH: Cirrhosis was induced by bile duct ligation. Controls underwent sham operation. Four weeks later, strips of corpus cavernosum were mounted in a standard organ bath and NANC-mediated relaxations were obtained by applying electrical field stimulation. KEY RESULTS: The NANC-mediated relaxation was enhanced in corporal strips from cirrhotic animals. Anandamide potentiated the relaxations in both groups. Either AM251 (CB(1) antagonist) or capsazepine (vanilloid VR(1) antagonist), but not AM630 (CB(2) antagonist), prevented the enhanced relaxations of cirrhotic strips. Either the non-selective NOS inhibitor L-NAME or the selective neuronal NOS inhibitor L-NPA inhibited relaxations in both groups, but cirrhotic groups were more resistant to the inhibitory effects of these agents. Relaxations to sodium nitroprusside (NO donor) were similar in tissues from the two groups. CONCLUSIONS AND IMPLICATIONS: Cirrhosis potentiates the neurogenic relaxation of rat corpus cavernosum probably via the NO pathway and involving cannabinoid CB(1) and vanilloid VR(1) receptors.
Assuntos
Moduladores de Receptores de Canabinoides/fisiologia , Endocanabinoides , Cirrose Hepática Biliar/fisiopatologia , Óxido Nítrico/fisiologia , Pênis/fisiopatologia , Transdução de Sinais/fisiologia , Animais , Ácidos Araquidônicos/farmacologia , Arginina/análogos & derivados , Arginina/farmacologia , Western Blotting , Canabinoides/farmacologia , Estimulação Elétrica , Inibidores Enzimáticos/farmacologia , Técnicas In Vitro , Masculino , Relaxamento Muscular/efeitos dos fármacos , Relaxamento Muscular/fisiologia , NG-Nitroarginina Metil Éster/farmacologia , Doadores de Óxido Nítrico/farmacologia , Óxido Nítrico Sintase Tipo I/antagonistas & inibidores , Óxido Nítrico Sintase Tipo I/metabolismo , Nitroprussiato/farmacologia , Pênis/inervação , Fenilefrina/farmacologia , Alcamidas Poli-Insaturadas/farmacologia , Ratos , Canais de Cátion TRPV/antagonistas & inibidores , Vasoconstritores/farmacologiaRESUMO
Significant potentiation of analgesic effects of opioids can be achieved through selective blockade of their stimulatory effects on intracellular signaling pathways by ultra-low doses of opioid receptor antagonists. However, the generality and specificity of this interaction is not well understood. The bimodal modulation of pentylenetetrazole-induced seizure threshold by opioids provide a model to assess the potential usefulness of this approach in seizure disorders and to examine the differential mechanisms involved in opioid anti- (morphine at 0.5-3 mg/kg) versus pro-convulsant (20-100 mg/kg) effects. Systemic administration of ultra-low doses of naltrexone (100 fg/kg-10 ng/kg) significantly potentiated the anticonvulsant effect of morphine at 0.5 mg/kg while higher degrees of opioid receptor antagonism blocked this effect. Moreover, inhibition of opioid-induced excitatory signaling by naltrexone (1 ng/kg) unmasked a strong anticonvulsant effect for very low doses of morphine (1 ng/kg-100 microg/kg), suggesting that a presumed inhibitory component of opioid receptor signaling can exert strong seizure-protective effects even at very low levels of opioid receptor activation. However, ultra-low dose naltrexone could not increase the maximal anticonvulsant effect of morphine (1-3 mg/kg), possibly due to a ceiling effect. The proconvulsant effects of morphine on seizure threshold were minimally altered by ultra-low doses of naltrexone while being completely blocked by a higher dose (1 mg/kg) of the antagonist. The present data suggest that ultra-low doses of opioid receptor antagonists may provide a potent strategy to modulate seizure susceptibility, especially in conjunction with very low doses of opioids.
Assuntos
Morfina/uso terapêutico , Naltrexona/uso terapêutico , Antagonistas de Entorpecentes/uso terapêutico , Entorpecentes/uso terapêutico , Convulsões/prevenção & controle , Animais , Limiar Diferencial/efeitos dos fármacos , Limiar Diferencial/fisiologia , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Sinergismo Farmacológico , Masculino , Camundongos , Pentilenotetrazol , Tempo de Reação/efeitos dos fármacos , Convulsões/induzido quimicamenteRESUMO
There is a marked elevation of endogenous opioid levels in plasma of human subjects with biliary cirrhosis as well as animal model of cholestasis. In addition, development of morphine tolerance and dependence has been shown to be inhibited by drugs which reduce brain serotonin levels. However, intracerebroventricular injection of serotonin increases the morphine analgesia. In the present study we have investigated the role of the serotonergic pathway in determining the withdrawal syndrome in a mouse model of cholestasis. There were three experimental groups: unoperated mice, sham operated mice and mice in which the main bile duct was ligated. Physical dependency was assessed by precipitating a withdrawal syndrome (writing, climbing, rearing, grooming and jumping) by naloxone (2 mg/kg) 5 days after induction of cholestasis. In separate experimental same groups, the antinociception was evaluated by the tail flick latency (TFL) test. Administration of serotonin receptors antagonists, cyproheptadine (10 mg/kg), methysergide (6 mg/kg) and ondansetron (10 mg/kg) attenuated withdrawal signs and decreased the antinociception. However, treatment by fluoxetine (15 mg/kg), an inhibitor of serotonin reuptake, increased the withdrawal signs and antinociception. These experiments lead us to conclude that the naloxone-precipitated withdrawal signs which occur in the mouse model of cholestasis are potentially dependent on the serotonergic pathway. Copyright 2000 John Wiley & Sons, Ltd.
RESUMO
1. In endothelium-containing rings of rat aorta, precontracted by phenylephrine, addition of acetylcholine (Ach), resulted in a concentration-dependent relaxation through the release of endothelial dependent relaxing factors, including nitric oxide (IC50 = 8.41 microM). 2. Pretreatment of the tissues with 20 microM indomethacin, significantly decreased the relaxation. 3. Preincubation of the preparations in medium solution in which sodium has been partially replaced by 0.5 mM lithium, significantly reduced Ach-induced endothelial dependent relaxation (EDR). 4. Lithium (2 mM) in medium, significantly increased Ach-induced relaxation. 5. As is shown in this study, lithium has two opposite actions of EDR, with the dose of 0.5 mM inhibiting, while the dose of 2 mM potentiates EDR. Thus it seems that the action of lithium on EDR is mediated through two separate mechanisms.