Identification and Phytotoxicity of a New Glucosinolate Breakdown Product from Meadowfoam (Limnanthes alba) Seed Meal

2014 ◽  
Vol 62 (30) ◽  
pp. 7423-7429 ◽  
Author(s):  
Suphannika Intanon ◽  
Ralph L. Reed ◽  
Jan F. Stevens ◽  
Andrew G. Hulting ◽  
Carol A. Mallory-Smith
2009 ◽  
Vol 57 (5) ◽  
pp. 1821-1826 ◽  
Author(s):  
Jan F. Stevens ◽  
Ralph L. Reed ◽  
Susan Alber ◽  
Larry Pritchett ◽  
Stephen Machado

Weed Science ◽  
2015 ◽  
Vol 63 (1) ◽  
pp. 302-311 ◽  
Author(s):  
Suphannika Intanon ◽  
Andrew G. Hulting ◽  
Carol A. Mallory-Smith

Meadowfoam seed meal (MSM), a by-product after oil extraction, has potential uses for crop growth enhancement or weed control. The herbicidal effect of MSM is the result of a secondary metabolite, glucosinolate glucolimnanthin (GLN). Field evaluations were conducted using concentrations of 3, 5, and 7% by weight and two forms (nonactivated and activated) of MSM applied as soil amendments. No injury was observed on lettuce transplanted 7 d after MSM incorporation in 2011. Activated MSM at 7% reduced weed emergence up to 71%. Lettuce leaf N content was at least 8.5-fold greater in MSM treatments compared to the untreated control. Greater soil nitrate levels correlated with greater weed biomass in MSM-amended plots. Isothiocyanate, a potent herbicidal compound, was detected in soil incorporated with 7% activated MSM. In 2012, 2.86 g m−2 of activated MSM, applied as a split or single dose, was evaluated for weed control efficacy and crop injury response. The split MSM application provided weed control similar to that from the single MSM application. The split and single MSM applications inhibited spiny sowthistle emergence more than 95% compared to the untreated control. A single application of activated MSM as a PRE soil amendment suppressed weeds and increased lettuce yield.


2011 ◽  
Vol 60 (1) ◽  
pp. 339-345 ◽  
Author(s):  
Inga A. Zasada ◽  
Jerry E. Weiland ◽  
Ralph L. Reed ◽  
Jan F. Stevens

Plant Disease ◽  
2014 ◽  
Vol 98 (9) ◽  
pp. 1253-1260 ◽  
Author(s):  
Yurdagül Şimşek Erşahin ◽  
Jerry E. Weiland ◽  
Inga A. Zasada ◽  
Ralph L. Reed ◽  
J. Fred Stevens

Meadowfoam (Limnanthes alba) is a commercial oilseed annual crop grown in Oregon. After extracting oil from seed, the remaining seed meal is rich in the secondary plant metabolite glucolimnanthin, which can be converted into pesticidal compounds such as 3-methoxybenzyl isothiocyanate (ITC) and 3-methoxyphenylacetonitrile (nitrile) in the presence of the enzyme myrosinase. In previous studies, we demonstrated that ITC and nitrile, produced by mixing freshly ground meadowfoam seed with meadowfoam seed meal, are toxic to the plant-parasitic nematode Meloidogyne hapla and the plant pathogen Pythium irregulare. In this study, we evaluated factors that might influence the implementation of meadowfoam seed meal into agricultural production systems for soilborne pathogen and nematode control. Rate-finding experiments demonstrated that a minimum 1.0% seed/seed meal formulation (wt/wt) was necessary to achieve nematode and pathogen suppression; seed meal alone was insufficient for complete control of M. hapla and stimulated the growth of P. irregulare. When this 1.0% seed/seed meal formulation was used, a greater soil amendment rate was required to cause 100% mortality of P. irregulare (1.0% wt/wt) than for M. hapla (0.5% wt/wt). In phytotoxicity experiments, soil amended with the 1.0% seed/seed meal formulation was consistently phytotoxic to wheat, cucumber, and tomato. However, phytotoxic effects were mitigated by a delayed planting into the amended soil. A final assay to monitor concentrations of ITC and nitrile in conjunction with assessing M. hapla and P. irregulare mortality was conducted over a 6-day period in soils amended at 0.5 and 1.0% (wt/wt) with the 1.0% seed/seed meal formulation. The response was rapid, with 100% mortality of both organisms within 2 h after exposure to amended soil. Concentrations of nitrile remained relatively constant over the 6-day period (approximately 0.017 and 0.032 mg/ml at 0.5 and 1.0% amendment rates, respectively), whereas ITC production increased rapidly and peaked 12 to 24 h after amendment (0.083 and 0.171 mg/ml at 0.5 and 1.0% amendment rates, respectively) before returning to near undetectable levels.


2007 ◽  
Vol 74 ◽  
pp. 37-45 ◽  
Author(s):  
James W. Putney

The original hypothesis put forth by Bob Michell in his seminal 1975 review held that inositol lipid breakdown was involved in the activation of plasma membrane calcium channels or ‘gates’. Subsequently, it was demonstrated that while the interposition of inositol lipid breakdown upstream of calcium signalling was correct, it was predominantly the release of Ca2+ that was activated, through the formation of Ins(1,4,5)P3. Ca2+ entry across the plasma membrane involved a secondary mechanism signalled in an unknown manner by depletion of intracellular Ca2+ stores. In recent years, however, additional non-store-operated mechanisms for Ca2+ entry have emerged. In many instances, these pathways involve homologues of the Drosophila trp (transient receptor potential) gene. In mammalian systems there are seven members of the TRP superfamily, designated TRPC1–TRPC7, which appear to be reasonably close structural and functional homologues of Drosophila TRP. Although these channels can sometimes function as store-operated channels, in the majority of instances they function as channels more directly linked to phospholipase C activity. Three members of this family, TRPC3, 6 and 7, are activated by the phosphoinositide breakdown product, diacylglycerol. Two others, TRPC4 and 5, are also activated as a consequence of phospholipase C activity, although the precise substrate or product molecules involved are still unclear. Thus the TRPCs represent a family of ion channels that are directly activated by inositol lipid breakdown, confirming Bob Michell's original prediction 30 years ago.


1980 ◽  
Vol 43 (02) ◽  
pp. 099-103 ◽  
Author(s):  
J M Whaun ◽  
P Lievaart ◽  

SummaryBlood from normal full term infants, mothers and normal adults was collected in citrate. Citrated platelet-rich plasma was prelabelled with 3H-adenine and reacted with release inducers, collagen and adrenaline. Adenine nucleotide metabolism, total adenine nucleotide levels and changes in sizes of these pools were determined in platelets from these three groups of subjects.At rest, the platelet of the newborn infant, compared to that of the mother and normal adult, possessed similar amounts of adenosine triphosphate (ATP), 4.6 ± 0.2 (SD), 5.0 ± 1.1, 4.9 ± 0.6 µmoles ATP/1011 platelets respectively, and adenosine diphosphate (ADP), 2.4 ± 0.7, 2.8 ± 0.6, 3.0 ± 0.3 umoles ADP/1011 platelets respectively. However the marked elevation of specific radioactivity of ADP and ATP in these resting platelets indicated the platelet of the neonate has decreased adenine nucleotide stores.In addition to these decreased stores of adenine nucleotides, infant platelets showed significantly impaired release of ADP and ATP on exposure to collagen. The release of ADP in infants, mothers, and other adults was 0.9 ± 0.5 (SD), 1.5 ± 0.5, 1.5 ± 0.1 umoles/1011 platelets respectively; that of ATP was 0.6 ± 0.3, 1.0 ± 0.1,1.3 ± 0.2 µmoles/1011 platelets respectively. With collagen-induced release, platelets of newborn infants compared to those of other subjects showed only slight increased specific radioactivities of adenine nucleotides over basal levels. The content of metabolic hypoxanthine, a breakdown product of adenine nucleotides, increased in both platelets and plasma in all subjects studied.In contrast, with adrenaline as release inducer, the platelets of the newborn infant showed no adenine nucleotide release, no change in total ATP and level of radioactive hypoxanthine, and minimal change in total ADP. The reason for this decreased adrenaline reactivity of infant platelets compared to reactivity of adult platelets is unknown.Infant platelets may have different membranes, with resulting differences in regulation of cellular processes, or alternatively, may be refractory to catecholamines because of elevated levels of circulating catecholamines in the newborn period.


1965 ◽  
Vol 14 (03/04) ◽  
pp. 490-499 ◽  
Author(s):  
S Niewiarowski ◽  
R Farbiszewski ◽  
A Popławski

SummaryIt has been found that fibrinogen breakdown product – antithrombin VI – is neutralized by the purified preparation of platelet factor 4, obtained by means of zinc acetate precipitation and DEAE chromatography column. It has been suggested that antiheparin activity of platelet factor 4 and its ability to neutralize antithrombin VI may be related to the same protein.The purified preparation of platelet factor 4 does not influence the fibrinogen – fibrin conversion by thrombin. This means that platelet factor 2 and platelet factor 4 are not the same substance.Crude platelet extracts neutralize antithrombin III and V. However, the purified product did not interferes with the action of these antithrombins.


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