Disease relevance of Decamine

• In addition, the risk of canine malignant lymphoma rose to a twofold excess with four or more yearly owner applications of 2,4-D [1].
• The findings in this study are consistent with occupational studies in humans, which have reported modest associations between agricultural exposure to 2,4-D and increased risk of non-Hodgkin's lymphoma, the histology and epidemiology of which are similar to those of canine malignant lymphoma [1].
• The available data from animal studies of acute, subchronic, and chronic exposure to 2,4-D, its salts, and esters show an unequivocal lack of systemic toxicity at doses that do not exceed renal clearance mechanisms [2].
• In Alcaligenes eutrophus JMP134, pJP4 carries the genes coding for 2,4-dichlorophenoxyacetate (2,4-D) and 3-chlorobenzoate (3-Cba) degradation plus mercury resistance [3].
• Ralstonia eutropha JMP134 carries a 22 kb DNA region on plasmid pJP4 necessary for the degradation of 2,4-D (2,4-dichlorophenoxyacetate) [4].

Psychiatry related information on Decamine

• This response time was not dependent on the 2,4-D concentration [4].
• Spontaneous locomotor activity decreased dramatically 4 h after 2,4-D treatment [5].
• Severe mental retardation and multiple congenital anomalies of uncertain cause after extreme parental exposure to 2,4-D [6].
• Formulation and food deprivation affects 2,4-D neurobehavioral toxicity in rats [7].
• Stereotyped behaviors were observed earlier and were more prolonged in 2,4-D treated and amphetamine challenged rats than in rats treated only with 5 or 10 mg/kg amphetamine [8].

High impact information on Decamine

• 2,4-D plasmids and persistence [9].
• Canine malignant lymphoma and 2,4-dichlorophenoxyacetic acid herbicides [10].
• A defect in beta-oxidation has been confirmed by demonstrating the resistance of the aim1 mutant to 2,4-diphenoxybutyric acid, which is converted to the herbicide 2,4-D by the beta-oxidation pathway [11].
• Accordingly a significant increase of GST activity was detected in the tobacco mesophyll protoplasts cultured in the presence of 2,4-dichlorophenoxyacetic acid [12].
• Pinus taeda suspension cultures grown in medium containing 2,4-dichlorophenoxyacetic acid showed only primary cell wall formation and essentially no lignification, as determined by histochemical, ultrastructural, chemical, and NMR spectroscopic analyses [13].

Chemical compound and disease context of Decamine

• The first step in catabolism of the broadleaf herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) is catalyzed by 2,4-D/alpha-ketoglutarate (alpha-KG)-dioxygenase (TfdA) in Ralstonia eutropha (formerly Alcaligenes eutrophus) JMP134 [14].
• Sinorhizobium meliloti Rm1021 cells containing cadRABKC transformed several phenoxyacetic acids, including 2,4-D and 2,4,5-T, to corresponding phenol derivatives [15].
• The expression of the genes for ERD11 and ERD13 was induced by dehydration, but was not affected by the application of four plant growth regulators, 2,4-dichlorophenoxyacetic acid 6-benzylaminopurine, abscisic acid, or gibberellic acid [16].
• Potassium deficiency, salt stress and hormonal treatments (ABA, BA, 2,4-D) were found to differentially affect channel mRNA levels, each channel displaying its own regulation pattern [17].
• Here, the cadmium-resistant isolate Pseudomonas strain H1 enhanced degradation of 2,4-D in reactors inoculated with R. eutropha JMP134 in the presence of 60 microg of cadmium g(-1) [18].

Biological context of Decamine

• The degradation of phosphatidylinositol (PI) in such membranes is enhanced in the presence of the synthetic auxin, 2,4-dichlorophenoxyacetic acid (2,4-D), measured as the hydrolysis of PI or by an enhancement of [3H]inositol incorporation into membrane-associated PI stimulated by Mn2+, but not dependent upon added CTP, Mg2+, or diglyceride [19].
• The growth regulator 2,4-D (2,4-dichlorophenoxyacetic acid) has been used to investigate the inter-relationship between cell elongation and cell division in carrot suspension cells [20].
• In vivo recombinants of pYG1010 and a cloned tfdS gene rescued the 2,4-D phenotype, indicating that TfdS is a positive regulator of tfdA expression, but not for tfdCDEF expression [3].
• We show that arcA3 transcription is induced at cell cycle entry but not directly by the 2,4-D treatment [21].
• Despite several thorough in vitro and in vivo animal studies, no experimental evidence exists supporting the theory that 2,4-D or any of its salts and esters damages DNA under physiologic conditions [2].

Anatomical context of Decamine

• Phosphatidylinositol turnover in isolated soybean membranes stimulated by the synthetic growth hormone 2,4-dichlorophenoxyacetic acid [19].
• There is no evidence that 2,4-D in any of its forms activates or transforms the immune system in animals at any dose [2].
• This conclusion is confirmed by immuno- and electron-microscopy which show that development of elaborate arrays of cytoplasmic microtubules is unaffected by 1 mg/l. 2,4-D when FUdR is present [20].
• Vectorial transport of 2,4-dichlorophenoxyacetate was observed in the basal-to-apical direction in rat organic anion transporter 3-expressing LLC-PK1 cells (rOat3-LLC); however, coexpression of mouse RST in rOat3-LLC caused a 1.3-fold increase in the basal-to-apical transport [22].
• At high doses, 2,4-D damages the liver and kidney and irritates mucous membranes [2].

Associations of Decamine with other chemical compounds

• Two forms of beta-1,4-glucan 4-glucanohydrolase (EC 3.2.1.4) were extracted from growing regions of Pisum sativum epicotyls which had been treated with the auxin, (2,4-dichlorophenoxy)acetic acid [23].
• Furthermore, transcription of the as-1/GUS reporter gene activated by the synthetic auxin 2,4-dichlorophenoxyacetic acid and by methyl jasmonate was also inhibited by DRB [24].
• Similarly, the agravitropic phenotype of inhibitor-treated seedlings was rescued by the auxin 1-naphthaleneacetic acid, but not by 2,4-dichlorophenoxyacetic acid, again resembling the relative abilities of these two auxins to rescue the phenotype of aux1 [25].
• Mutations in an Auxin Receptor Homolog AFB5 and in SGT1b Confer Resistance to Synthetic Picolinate Auxins and Not to 2,4-Dichlorophenoxyacetic Acid or Indole-3-Acetic Acid in Arabidopsis [26].
• The present results show that the callus tissues maintained at 4.0 mg/L 2,4-D and 8.0 mg/L kinetin can be used as a matrix for in vitro selection programs [27].
• Since melatonin was able to counteract most of redox changes produced by 2,4-D in CGC in culture, the experimental evidence reported further support the efficacy of melatonin to act as a neuroprotector [28].

Gene context of Decamine

• This transporter (ANT1, aromatic and neutral transporter) also transports indole-3-acetic acid and 2,4-dichlorophenoxyacetic acid [29].
• Since SPI1 deletion leads to the higher beta-1,3-glucanase sensitivity of 2,4-D-stressed cells, it was hypothesized that adaptation may involve an Spi1p-mediated increase in the diffusional restriction of the liposoluble acid form of the herbicide across the cell envelope [30].
• Adaptation of Saccharomyces cerevisiae to the herbicide 2,4-dichlorophenoxyacetic acid, mediated by Msn2p- and Msn4p-regulated genes: important role of SPI1 [30].
• Within the 5.9-kb DNA region between the tfdR and tfdK genes on the 2,4-dichlorophenoxyacetic acid (2,4-D) catabolic plasmid pJP4 from Ralstonia eutropha JMP134, we identified five open reading frames (ORFs) with significant homology to the genes for chlorocatechol and chlorophenol metabolism (tfdCDEF and tfdB) already present elsewhere on pJP4 [31].
• One reason why the tfd(II) genes do not disappear from plasmid pJP4 might be the necessity for keeping the regulatory genes for the 2,4-D pathway expression tfdR and tfdS [31].

Analytical, diagnostic and therapeutic context of Decamine

• Case-control study of canine malignant lymphoma: positive association with dog owner's use of 2,4-dichlorophenoxyacetic acid herbicides [1].
• An increase in the level of the ribosomal protein mRNAs can be detected 1 h after treatment with (2,4-dichlorophenoxy)acetic acid [32].
• The experimental data and sequence analysis lead us to conclude that His-113, Asp-115, and His-262 are likely metal ligands in TfdA and that His-213 may aid in catalysis or binding of 2,4-D [33].
• Overall, the available evidence from epidemiologic studies is not adequate to conclude that any form of cancer is causally associated with 2,4-D exposure [2].
• That the aar1 mutation alters 2,4-D responsiveness specifically was confirmed by analysis of GUS expression in the DR5:GUS and HS:AXR3NT-GUS backgrounds, as well as by real-time PCR quantification of IAA11 expression [34].

References