A high yield of oilseed rape can be achieved provided an adequate supply of magnesium and sulfur in critical stages of yield formation. The magnesium status in canopy was studied in the 2008, 2009 and 2010 growing seasons. A one factorial experiment consisting of six treatments, set up to verify the research hypothesis, was as follows: control (C), NP, NPK, NPK+ MgS - 1/3 of total planned dose applied in spring (NPKMgS1), NPK+1.0 MgS dose in autumn (NPKMgMgS2), NPK+MgS - 2/3 in autumn + 1/3 in spring (NPKMgS3). Plant samples were taken at three stages: rosette (BBCH 30), the onset of flowering (BBCH 61) and maturity (BBCH 89). An entire sample was partitioned in accordance with the growth stage into main plant organs: leaves, stems, straw and seeds. The yield of biomass, magnesium concentration and its content was determined in each part of the plant. The magnesium concentration in leaves at the onset of flowering can be used as the first predictor of yield. The predictive strength of the magnesium content in seeds as the final yield predictor corroborated the hypothesis of the importance of magnesium for the seed sink build-up. An analysis of relationships between the magnesium content in plant parts during the growing season and yield of seeds can be used to make an ex-post analysis of factors disturbing the development of yield structural components. The main cause of yield reduction in 2009 as compared to 2008 was the insufficient supply of magnesium to vegetative organs of oilseed plants since the onset of flowering. It was documented that the degree of magnesium supply to a growing silique is critical for the seed yield performance, as noted in 2008. It was also found that any disturbance in the magnesium supply to oilseed rape since the onset of flowering led to reduction in the seed density, which in turn decreased the magnesium seed sink capacity, as the study clearly demonstrated.
The present study investigated the involvement of endogenous melatonin in the prevention of pancreatic damage provoked by caerulein-induced pancreatitis (CIP) by using the luzindole, the antagonist of melatonin MT2 receptors. CIP was produced by subcutaneous infusion of caerulein to conscious rats (25 µg/kg). Luzindole (1, 2 or 4 mg/kg) was given as an intraperitoneal bolus injection 30 min prior to the start of CIP. Lipid peroxidation products, malondialdehyde (MDA) and 4- hydroxynonenal (4-HNE) were measured in the pancreas by LPO-584 commercial kit. CIP was confirmed by histological examination and manifested by significant increases of plasma activities of amylase, lipase and tumor necrosis factor a (TNFalpha) (by 500%, 1000% and 600%, respectively) comparing to the control values. This was accompanied by a 40% limitation in pancreatic blood flow (PBF) and by 200% increase of MDA+4-HNE in the pancreas of CIP rats. Administration of luzindole to the CIP rats reduced PBF, aggravated the histological manifestations of pancreatitis, resulted in the significant augmentation of pancreatic MDA + 4-HNE content, and produced the marked increases of plasma levels of lipase, amylase and TNFalpha, comparing to the values observes in the rats with CIP alone. These results suggest that endogenous melatonin through its receptor MT2 plays an important role in the attenuation of pancreatic damage produced by overstimulation with caerulein.
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Central nervous system affects pancreatic secretion of enzymes however,the neural modulation of acute pancreatitis has not been investigated.Leptin and melatonin have been recently reported to affect the inflammatory response of various tissues.The identification of specific receptors for both peptides in the pancreas suggests that leptin and melatonin could contribute to the pancreatic protection against inflammation.The aim of this study was:1/to compare the effect of intracerebroventricular (i.c.v.)or intraperitoneal (i.p.) administration of leptin or melatonin on the course of caerulein-induced pancreatitis (CIP) in the rat,2/to examine the involvement of sensory nerves (SN)and calcitonin gene-related peptide (CGRP)in pancreatic protection afforded by leptin or melatonin,3/to assess the effect of tested peptides on lipid peroxidation products (MDA +4-HNE)in the pancreas of CIP rats,4/to investigate the influence of leptin or melatonin on nitric oxide (NO)release from isolated pancreatic acini and 5/to determine the effects of caerulein and leptin on leptin receptor gene expression in these acini by RT-PCR.CIP was induced by subcutaneous (s.c.)infusion of caerulein (25 µg/kg)to the conscious rats,confirmed by the significant increases of pancreatic weight and plasma amylase and by histological examination.This was accompanied in marked reduction of pancreatic blood flow and significant rise of MDA +4-HNE in the pancreas.Leptin or melatonin were administered i.p.or i.c.v.30 min prior to the start of CIP.Deactivation of SN was produced by s.c.capsaicin (100 mg/kg).An antagonist of CGRP,CGRP8-37 (100 µg/kg i.p.),was given together with leptin or melatonin to the CIP rats.MDA +4-HNE was measured using LPO commercial kit.NO was determined using the Griess reaction.Pretreatment of CIP rats with i.p.leptin (2 or 10 µg/kg)or melatonin (10 or 50 mg/kg)significantly attenuated the severity of CIP.Similar protective effects were observed following i.c.v.application of leptin (0.4 or 2 µg/rat)but not melatonin (10 or 40 µg/rat)to the CIP rats.Capsaicin deactivation of SN or administration of CGRP8-37 abolished above beneficial effects of leptin on CIP,whereas melatonin-induced protection of pancreas was unaffected.Pretreatment with i.p.melatonin (10 or 50 mg/kg),but not leptin,significantly reduced MDA +4-HNE in the pancreas of CIP rats.Leptin (10–9 -10–6 M)but not melatonin (10–8 -10–5 M)significantly stimulated NO release from isolated pancreatic acini.Leptin receptor gene expression in these acini was significantly increased by caerulein and leptin. We conclude that 1/central or peripheral pretreatment with leptin protects the pancreas against its damage induced by CIP,whereas melatonin exerts its protective effect only when given i.p.,but not following its i.c.v.adminstration,2/activation of leptin receptor in the.pancreatic acini appears to be involved in the beneficial effects of leptin on acute pancreatitis, 3/the protective effects of leptin involve sensory nerves,CGRP and increased generation of NO whereas melatonin-induced protection of the pancreas depends mainly on the antioxidant local effect of this indole,and scavenging of the radical oxygen species in the pancreatic tissue.
Melatonin, produced from L-tryptophan, protects the pancreas against acute damage by improving the antioxidative status of tissue. Melatonin receptors have been detected in the brain, but the contribution of these receptors to the pancreatic protection is unknown. The aim of our study was to compare the effects of melatonin precursor; L-tryptophan given intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) on the course of acute pancreatitis. Acute pancreatitis was induced by subcutaneous infusion of caerulein (5µg/kg-h x 5h). L-tryptophan was given i.p. (2.5, 25 or 250 mg/kg) or administered into right cerebral ventricle (0.02, 0.2 or 2.0 mg/rat) 30 min prior to the start of caerulein infusion. Plasma amylase, lipase and TNF alpha activities were measured to determine the severity of caerulein-induced pancreatitis (CIP). The lipid peroxidation products: malonylodialdehyde and 4-hydroksynonenal (MDA + 4-HNE) and activity of superoxide dismutase (SOD) were measured in the pancreas of intact or CIP rats with or without L-tryptophan pretreatment. Melatonin blood level was measured by RIA. CIP was confirmed by histological examination and manifested as an edema and rises of plasma levels of amylase, lipase and TNF alpha (by 550%, 1000% and 600%). MDA + 4-HNE was increased by 600%, whereas SOD activity was reduced by 75% in the pancreas of CIP rats. All manifestations of CIP were significantly reduced by pretreatment of the rats with L-tryptophan given i.c.v. at doses of 0.2 or 2.0 mg/rat, or by peripheral administration of this amino acid used at dose of 250 mg/kg i.p. In control rats plasma level of melatonin averaged about 40 ± 2 pg/ml and was not significantly affected by CIP, by central application of L-tryptophan (0.02, 0.2 or 2.0 mg/rat) or by peripheral administration of this melatonin precursor used at doses of 2.5 or 25 mg/kg i.p. Plasma melatonin level was markedly increased by pretreatment of the rats with L-tryptophan given i.p. at dose of 250 mg/kg. We conclude that central administration of melatonin precursor; L-tryptophan, as well as peripheral application of high dose of this melatonin precursor prevented the pancreatic damage produced by CIP. The favorable effect of peripherally administered L-tryptophan could be related to the rise of melatonin plasma level and to pancreatoprotective action of this indoleamine. The beneficial effect of centrally administered L-tryptophan could be mediated through activation of central receptors for locally produced melatonin.
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