Impacts of fire cues on germination of Brassica napus L. seeds with high and low secondary dormancy.

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.

Increases in interleukin-6 and interferon-gamma levels is progressive in immature rats with varicocele.

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.

Proteinuria is reduced by inhibition of inducible nitric oxide synthase in rat renal ischemia-reperfusion injury.

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.

Attenuation of morphine withdrawal signs by low level laser therapy in rats.

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.

Attenuation of morphine withdrawal signs by a GABAB receptor agonist in the locus coeruleus of rats.

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.

The effect of the serotonergic system on opioid withdrawal-like syndrome in a mouse model of cholestasis.

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.

The effect of lithium on endothelial-dependent relaxation in rat isolated aorta.

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.