Disease relevance of Ppox

• The impregnation of tissue blocks with PPO (2,5-Diphenyloxazole) and POPOP (1,4-bis-2-(5-phenyloxazolyl)-benzene) during dehydration, infiltration and Epon embedding produced a 20% increase of reaction intensity in light microscope radioautographs using NTB2 emulsion and a 75% increase in electron microscope radioautographs using L4 emulsion [1].
• Administration of the protoporphyrinogen oxidase inhibitor oxadiazon (12.5 mg/kg/day) for four days to male Wistar rats caused a partial block of porphyrin biosynthesis, thus mimicking the condition of quiescent variegate porphyria [2].

High impact information on Ppox

• In this cell line, addition of 2% DMSO to growing cultures results in the normal induction of PBG deaminase and coproporphyrinogen oxidase but not in the induction of the terminal two enzymes, protoporphyrinogen oxidase and ferrochelatase [3].
• Kinetic studies on protoporphyrinogen oxidase inhibition by diphenyl ether herbicides [4].
• Mouse protoporphyrinogen oxidase. Kinetic parameters and demonstration of inhibition by bilirubin [5].
• Ubiquinone-6, ubiquinone-10 and dicoumarol stimulate protoporphyrinogen oxidase activity at low concentrations (less than 15 microM), whereas coenzyme Q0 and menadione show no activation at these concentrations [5].
• The penultimate enzyme of the heme biosynthetic pathway, protoporphyrinogen oxidase (EC 1.3.3.4), has been purified to apparent homogeneity from mouse liver mitochondria [6].

Biological context of Ppox

• Purified mouse protoporphyrinogen oxidase (EC 1.3.3.4) and ferrochelatase (EC 4.99.1.1), the two terminal enzymes of the heme biosynthetic pathway, have been reconstituted into phospholipid vesicles, and the kinetics of the enzymes in the reconstituted systems were compared with the values obtained with the free enzymes [7].
• In contrast, PS conjugated with RGD via endgroup-activated PEO/PPO/PEO copolymers supported cell adhesion and spreading [8].

Anatomical context of Ppox

• Hepatocyte COH activity was increased also by the ferrochelatase inhibitor griseofulvin and the protoporphyrinogen oxidase inhibitor acifluorfen (about 9-fold induction) [9].
• Metabolism of diphenyloxazole (PPO) by mouse liver microsomes [10].

Associations of Ppox with chemical compounds

• To test this possibility, the content of brain mitochondrial cytochrome a3 was determined after intracerebroventricular administration of the protoporphyrinogen oxidase-inhibiting herbicide fomesafen [11].
• Protoporphyrinogen oxidase: high affinity tetrahydrophthalimide radioligand for the inhibitor/herbicide-binding site in mouse liver mitochondria [12].
• Denaturation of PPO with urea resulted in a biphasic curve when ellipticity is plotted against urea concentration, typical of amphipathic proteins [13].
• Acifluorfen resistant cells do not have increased levels of PPO activity, nor does the PPO made by these cells have increased resistance to acifluorfenin, but these cells accumulate porphyrin and have elevated levels of heme [14].
• PS modified with PEO/PPO/PEO copolymers alone was found to be inert to cell adhesion both in the presence of serum proteins and when exposed to activated RGD peptide [8].

Analytical, diagnostic and therapeutic context of Ppox

• Photodynamic therapy using a protoporphyrinogen oxidase inhibitor [15].

References