Disease relevance of 2,4,5-trichlorophenoxyacetic acid

• An investigation of the rate of birth malformations in the Northland region of New Zealand provides no evidence to associate spraying of 2,4,5-trichlorophenoxyacetic acid with the occurrence of any malformation of the central nervous system, including spina bifida [1].
• 2,4,5-T, trichlorophenol, and soft tissue sarcoma [2].
• When the animals were killed, 7 months after initiation, the incidence of hepatocellular carcinoma was 83, 33 and 16% in the animals treated with NAF, PFOA or 2,4,5-T respectively [3].
• Cloning and characterization of a chromosomal DNA region required for growth on 2,4,5-T by Pseudomonas cepacia AC1100 [4].
• Substrate diversity and expression of the 2,4,5-trichlorophenoxyacetic acid oxygenase from Burkholderia cepacia AC1100 [5].

Psychiatry related information on 2,4,5-trichlorophenoxyacetic acid

• Suggestions are made concerning the possible long-term effects on food preferences among wild-living animals as a result of large-scale application of 2,4,5-T-containing herbicides [6].

High impact information on 2,4,5-trichlorophenoxyacetic acid

• Bioavailability of dioxin in soil from a 2,4,5-T manufacturing site [7].
• PURPOSE: The objective of this study was to determine whether the blood serum levels of TCDD in a group of professional 2,4,5-T applicators in New Zealand were greater than those of a matched control group not involved in 2,4,5-T spraying [8].
• Phenoxyherbicides, including (2,4,5-trichlorophenoxy)acetic acid (CAS: 93-76-5), have been widely used in New Zealand for over 30 years [9].
• Various environmental isolates of B. cepacia are, however, capable of degrading environmental pollutants, such as trichloroethylene, 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), etc., and are also highly effective in controlling plant diseases caused by nematodes and fungi [10].
• Induction of the multispecific organic anion transporter (cMoat/mrp2) gene and biliary glutathione secretion by the herbicide 2,4,5-trichlorophenoxyacetic acid in the mouse liver [11].

Chemical compound and disease context of 2,4,5-trichlorophenoxyacetic acid

• Combined cell suspensions of the 2,4,5-trichlorophenoxyacetic acid (2,4,5-T)-metabolizing organism Pseudomonas cepacia AC1100, and the 2,4-dichlorophenoxyacetic acid (2,4-D)-metabolizing organism Alcaligenes eutrophus JMP134 were shown to effectively degrade either of these compounds provided as single substrates [12].
• Pseudomonas aeruginosa cells transformed with this DNA acquired the ability to convert 2,4,5-T to 2,4,5-TCP [4].
• Purification of hydroxyquinol 1,2-dioxygenase and maleylacetate reductase: the lower pathway of 2,4,5-trichlorophenoxyacetic acid metabolism by Burkholderia cepacia AC1100 [13].
• Resting cells of 2,4,5-trichlorophenoxyacetic acid-grown Pseudomonas cepacia AC1100 were able to completely and rapidly dechlorinate several chlorine-substituted phenols, including 2,4,5-trichlorophenol, 2,3,4,6-tetrachlorophenol, and pentachlorophenol [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].

Biological context of 2,4,5-trichlorophenoxyacetic acid

• The nucleotide sequence of a 5.5-kb chromosomal fragment from B. cepacia AC1100 which complemented PT88 for growth on 2,4,5-T was determined [16].
• ORF5, which encoded an 11-kDa polypeptide, was essential for growth on 2,4,5-T, but the amino acid sequence did not show homology to those of any known proteins [16].
• Complementation analyses of RHC22 with a series of subcloned fragments and spontaneously deleted derivatives of the recombinant cosmid pRHC21 showed the 2,4,5-T (tft) genes to occur within an 8.9-kb region [4].
• Two of these mutants, RHC22 and RHC23, were complemented for growth on 2,4,5-T using an AC1100 genomic library constructed in the cosmid vector pCP13 [4].
• Sequence analysis of a gene cluster involved in metabolism of 2,4,5-trichlorophenoxyacetic acid by Burkholderia cepacia AC1100 [16].

Anatomical context of 2,4,5-trichlorophenoxyacetic acid

• P-glycoprotein traffic ATPase content increased in the canalicular domain of hepatocyte of mice treated with the herbicide 2,4,5-trichlorophenoxyacetic acid and with partially hydrogenated fish oil (108% and 87%, respectively, p<0.05) as well as biliary phospholipid output (106% and 74%, respectively, p<0.05) [17].
• As with certain other peroxisome proliferators, 2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid increased total cytochrome oxidase activity as well [18].
• Transport of the anionic herbicide, 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) across the blood-cerebrospinal fluid barrier was investigated using the isolated choroid plexus of the adult rabbit in vitro and ventriculocisternal perfusion in vivo [19].
• Together, these data indicate that 2,4,5-T is cleared from the brain and cerebrospinal fluid by the organic anion transport system and that alterations in such transport may have a significant impact on the toxicity of this agent in the central nervous system [19].
• Trace analysis of 2,4,5-trichlorophenoxyacetic acid, its glycineamide, and their alkaline hydrolyzable conjugates in mouse blood, urine, and feces [20].

Associations of 2,4,5-trichlorophenoxyacetic acid with other chemical compounds

• In comparison with controls, NAF and PFOA caused a 60-and 24-fold increase inthe peroxisomal beta-oxidation of fatty acids respectively, but only about a 2-fold increase in the catalase activity, 2,4-D and/or 2,4,5-T were much less active in this respect, giving approximately a doubling in the rate of fatty acid oxidation [3].
• The pesticides considered include: DDT, hexachlorobenzene (HCB), 2,4,5-T, pentachlorophenol, and various herbicidal precursors (e.g., carbamates, triazines) of nitrosamines and nitroso derivatives [21].
• Four herbicides, namely propanil, maleic hydrazide, glyphosate, and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), were investigated for genotoxicity in the wing spot test of Drosophila melanogaster [22].
• Endogenously added alpha-, beta-, and gamma-HCH, o,p'-DDT, 2,2'-dichlorobiphenyl (2,2'-PCB), and 2,4,5-T at 100 nM were found to promote foci formation in postconfluent cultures of this cell line [23].
• 1. The effect of pretreatment of rats with the peroxisome proliferator 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) on sulphobromophthalein excretion from the isolated perfused rat liver has been investigated and compared with the effect of clofibrate which is also a peroxisome proliferator [24].

Gene context of 2,4,5-trichlorophenoxyacetic acid

• In 2,4,5-trichlorophenoxyacetic acid-fed mice we found five-fold increase on mdr2 transcription rate, assessed by nuclear run-off assay [17].
• In the current study, we also found that 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) at 1 nM and alpha-HCH isomers at 100 nM could also significantly activate protein tyrosine kinase of Neu immunoprecipitates in a cell-free system [23].
• Induction of total microsomal cytochrome P-450 was obtained after dietary exposure to clofibrate, clofibric acid, 2,4-dichlorophenoxyacetic acid, 2,4,5-trichlorophenoxyacetic acid, nafenopin, Wy-14.643, di(2-ethylhexyl)phthalate and di(2-ethylhexyl)phosphate [25].
• Retarded development of fetal renal alkaline phosphatase in mice given 2,4,5-trichlorophenoxyacetic acid [26].
• Spectrophotometric tests for the presence of a lysozyme-like principle in the serum also revealed similar trends with a significant loss of enzyme activity in 2,4,5-T-treated insects [27].

Analytical, diagnostic and therapeutic context of 2,4,5-trichlorophenoxyacetic acid

• Spectrophotometry and gas chromatography reveal various intermediates during growth of the culture with 2,4,5-T [28].
• The technique of plasmid-assisted molecular breeding has led to the development of bacterial strains capable of totally degrading 2,4,5-T by using it as their sole source of carbon at high concentrations (greater than 1 mg/ml) [28].
• A clinical epidemiologic study was conducted to determine the long-term health effects of workplace exposure to the process of manufacturing the herbicide (2,4,5-trichlorophenoxy)acetic acid including contaminants such as 2,3,7,8-tetrachlorodibenzo-rho-dioxin [29].
• A randomized biomechanical study was carried out by installing 13-mm-long meniscus arrows into fresh porcine menisci with the Crossbow and with the standard manual inserter trocar system [30].
• Reversed-phase high-performance liquid chromatography (HPLC) analysis of bile indicated that more than 85% of compound excreted in bile was unchanged 2,4,5-T [31].

References