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4-Hydroxyphenyl pyruvate dioxygenase

Johnson-Winters K, VM Purpero, M Kavana, T Nelson, GR Moran (2003) (4-Hydroxyphenyl)pyruvate dioxygenase from Streptomyces avermitilis the basis for ordered substrate addition. Biochemistry 42 2072-2080. [Pg.140]

Hall MG Wilks ME, Provan WM, Eksborg S, Lumholtz B. (2001) Pharmaco-kinetics and pharmacodynamics of NTBC [2-(2-nitro-4-fluo-romethyl-benzoyl)-l,3-cyclohexanedione] and mesotrione, inhibitors of 4-hydroxyphenyl pyruvate dioxygenase (HPPD) following a single dose to healthy male volunteers. Br J Clin Pharmacol 52 169-177. [Pg.157]

Kavana M, Moran GR. (2003) Interaction of (4-hydroxyphenyl)pyruvate dioxygenase with the specific inhibitor 2-[2-nitro-4-(trifluoromethyl) benzoyl]- ,3-cyclohexanedione. Biochemistry 42 10238-10245. [Pg.157]

We end this section on enzyme inhibition with a case study about 4-hydroxyphenyl-pyruvate dioxygenase (HPPD) and disorders in tyrosine catabolism. After transamination of tyrosine, 4-hydroxyphenylpyruvate (148) is formed which is then decarboxylated, isomerized and oxygenated by HPPD to yield homogentisate (149) or by hydroxyman-delate synthase (HMS) to yield p-hydroxymandelate (150). 149 serves as the precursor for plastoquinones and tocopherols in plants . Thus, inhibitors of HPPD have been designed... [Pg.661]

C3a4b. Inhibition of 4-hydroxyphenyl-pyruvate-dioxygenase (F2) C3a4c. Inhibition of carotenoid biosynthesis (unknown target) (F3)... [Pg.2060]

Hydroxyphenyl-pyruvate dioxygenase (D 22) Hydroxylation, oxidative decarboxylation Fe +, ascorbic acid, requires a-ketoglutarate... [Pg.95]

Fig. 4.2. Increased tyrosine concentration is caused by inborn or acquired deficiency of the first two enzymes of the tyrosine degradation pathway (the increased tyrosine concentration of tyrosinemia type I is caused by secondary deficiency of 4-hydroxyphenyl-pyruvate dioxygenase). Hypertyrosinemia in the newborn is in most instances not due to inborn errors of tyrosine metabolism, but rather to liver immaturity or other unspecific liver affections. However, whenever hypertyrosinemia is found, the pathognomonic sign of tyrosinemia type I should be excluded by a sufficiently sensitive analysis of suc-cinylacetone and related metabolites. Decreased activity of porphobilinogen synthase activity in RBC is a sensitive and easily performed marker for increased concentrations of succinylacetone, which may be used as a first line diagnostic test before positive identification of succinylacetone and related metabolites by GC-MS can be achieved. It should also be noted that increased excretion of phenolic tyrosine metabolites is always found in hypertyrosinemia and is of no differential diagnostic value... Fig. 4.2. Increased tyrosine concentration is caused by inborn or acquired deficiency of the first two enzymes of the tyrosine degradation pathway (the increased tyrosine concentration of tyrosinemia type I is caused by secondary deficiency of 4-hydroxyphenyl-pyruvate dioxygenase). Hypertyrosinemia in the newborn is in most instances not due to inborn errors of tyrosine metabolism, but rather to liver immaturity or other unspecific liver affections. However, whenever hypertyrosinemia is found, the pathognomonic sign of tyrosinemia type I should be excluded by a sufficiently sensitive analysis of suc-cinylacetone and related metabolites. Decreased activity of porphobilinogen synthase activity in RBC is a sensitive and easily performed marker for increased concentrations of succinylacetone, which may be used as a first line diagnostic test before positive identification of succinylacetone and related metabolites by GC-MS can be achieved. It should also be noted that increased excretion of phenolic tyrosine metabolites is always found in hypertyrosinemia and is of no differential diagnostic value...
Neidig, M.L. et al. (2005). Spectroscopic and computational studies of NTBC bound to the non-heme iron enzyme (4-hydroxyphenyl) pyruvate dioxygenase active site contributions to drug inhibition. Biochem. Biophys. Res. Commun. 338, 206-214... [Pg.379]

Nitisinone (59 Qrfadin ) Leptospermone 2-[2-Nitro-4-(trifluoromethyl) benzoyl] cyclohexane-1,3-dione NP-derived Plant Antityrosinaemia Inhibits /5-hydroxyphenyl-pyruvate dioxygenase (HPPD) activity 208-210, 518-524... [Pg.20]

Nitisinone (59 Orfadin Swedish Orphan, 2002) is a derivative of lepto-spermone, an important new class of herbicides from the bottlebmsh plant (Callistemon citrinus), and exerts an inhibitory effect for /7-hydroxyphenyl-pyruvate dioxygenase (HPPD) involved in plastoquinone synthesis the... [Pg.58]

Expression of an herbicide insensitive target has also been reported to provide resistance to diclofop and sethoxydim (ACCase inhibitors), various dinitroani-lines, and inhibitors of phytoene desaturase, lycopene cyclase and hydroxyphenyl-pyruvate dioxygenase. None of these traits are currently incorporated into commercial products. [Pg.285]

With carotenoid biosynthesis, plastoquinone is involved as an electron acceptor, which we encounter further in photosynthetic electron transport [2]. An important precursor in the synthesis of plastoquinone, which also serves as a cofactor for the PDS enzyme, is homogentisic acid, which is formed from 4-hydroxyphenyl-pyruvate by 4-hydroxyphenylpyruvate dioxygenase (HPPD)... [Pg.187]

See other pages where 4-Hydroxyphenyl pyruvate dioxygenase is mentioned: [Pg.524]    [Pg.29]    [Pg.85]    [Pg.7]    [Pg.145]    [Pg.141]    [Pg.142]    [Pg.144]    [Pg.554]    [Pg.524]    [Pg.29]    [Pg.85]    [Pg.7]    [Pg.145]    [Pg.141]    [Pg.142]    [Pg.144]    [Pg.554]    [Pg.268]    [Pg.197]   
See also in sourсe #XX -- [ Pg.241 , Pg.242 ]



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4-hydroxyphenyl

Dioxygenases

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