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S S Lau et al.
Drug metabolism and disposition: the biological fate of chemicals, 15(6), 801-807 (1987-11-01)
Homogenates from rat renal papillae, a rich source of the prostaglandin (PG) H synthase system (PHS), metabolized [14C]2-bromohydroquinone, in the presence of arachidonic acid, to products which are covalently bound to protein. The co-oxidation of 2-bromohydroquinone caused a concentration-dependent stimulation
T J Monks et al.
Toxicology and applied pharmacology, 103(3), 557-563 (1990-05-01)
Glutathione (GSH) conjugates of 2-bromohydroquinone are more difficult to oxidize than the parent hydroquinone. Hydrolysis catalyzed by gamma-glutamyl transpeptidase (gamma-GT), however, results in the formation of the corresponding cysteine conjugate which is more readily oxidized than the parent hydroquinone. N-Acetylation
S S Lau et al.
The Journal of pharmacology and experimental therapeutics, 230(2), 360-366 (1984-08-01)
2-Bromohydroquinone was identified as a metabolite of both bromobenzene and o-bromophenol in the rat in vivo and in vitro. Identification was based on high-pressure liquid chromatography and gas chromatography-mass spectrometry. Formation of 2-bromohydroquinone by rat liver microsomes from both bromobenzene
S S Lau et al.
Toxicology, 64(3), 291-311 (1990-12-03)
Administration of 2-bromo-(diglutathion-S-yl)hydroquinone (2-Br-[diGSyl]HQ) (10-30 mumol/kg; i.v.) to rats causes severe renal proximal tubular necrosis. gamma-Glutamyl transpeptidase (gamma-GT) catalyses the first step in the metabolism of glutathione (GSH) and its S-conjugates and the toxicity of 2-Br-(diGSyl)HQ can be emeliorated by
Anuradha Ramoji et al.
Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy, 69(3), 926-932 (2007-07-07)
Vibrational spectral measurements, namely, infrared (4000-400 cm(-1)) and Raman (3500-50 cm(-1)) spectra have been made for 2-Bromohydroquinone. Optimized geometrical structures, harmonic vibrational frequencies and intensities have been computed by the ab initio (RHF), B-based (BLYP, BP86) and B3-based (B3P86, B3LYP
D P Rodeheaver et al.
The Journal of pharmacology and experimental therapeutics, 256(3), 917-921 (1991-03-01)
The basis of extracellular acidosis amelioration of 2-bromohydroquinone (BHQ)-induced renal proximal tubular cell death was determined by comparing the metabolism, uptake and mitochondrial effects of BHQ (0.2 mM) and bromoquinone (BQ) (0.05 mM) on isolated rabbit renal proximal tubules incubated
R G Schnellmann et al.
Toxicology and applied pharmacology, 99(1), 19-27 (1989-06-01)
2-Bromohydroquinone (BHQ) is a model toxic hydroquinone and plays an important role in bromobenzene-induced nephrotoxicity. Proximal tubules isolated to contain decreased glutathione (GSH) levels were at least twice as sensitive to the GSH depleting effects of BHQ and BHQ-induced mitochondrial
Inhibition of respiration in rabbit proximal tubules by bromophenols and 2-bromohydroquinone.
R G Schnellmann et al.
Advances in experimental medicine and biology, 197, 911-917 (1986-01-01)
Hetero Diels-Alder Reactions of 1-Acetylamino-and 1-Dimethylamino-1-azadienes with Benzoquinones.
Perez JM, et al.
Tetrahedron, 56(11), 1561-1567 (2000)
S S Lau et al.
Toxicology and applied pharmacology, 103(1), 121-132 (1990-03-15)
We have previously shown that the renal necrosis observed after 2-bromohydroquinone (2-BrHQ) administration to rats is probably caused by the formation of 2-Br-(diglutathion-S-yl)HQ (2-Br-[diGSyl]HQ), since injection of this conjugate caused severe proximal tubular necrosis. In the present study we report
G W Miller et al.
Toxicology and applied pharmacology, 125(2), 192-197 (1994-04-01)
We have previously shown that strychnine mimics the cytoprotective properties of glycine in renal proximal tubule (RPT) suspensions exposed to antimycin A (AA). The aims of this study were to determine whether the cytoprotective properties of strychnine applied to various
P J Sausen et al.
The Journal of pharmacology and experimental therapeutics, 260(1), 393-401 (1992-01-01)
Because methimazole has antioxidant properties, the effects of methimazole treatment on cephaloridine, S-(1,2-dichlorovinyl)-L-cysteine (DCVC), 2-bromohydroquinone (2-BHQ) and cis-diaminedichloroplatinum (II) (cisplatin)-induced nephrotoxicity were investigated. Rats given cephaloridine (1 g/kg), cisplatin (5 mg/kg), DCVC (100 mg/kg) or 2-BHQ (157 mg/kg) i.p. exhibited
Synthesis and characterization of novel poly (aryleneethynylene) s derived from squaraines for photovoltaic applications.
Zhang W, et al.
J. Mater. Sci., 46(16), 5363-5370 (2011)
R G Schnellmann
Toxicology and applied pharmacology, 99(1), 11-18 (1989-06-01)
2-Bromohydroquinone (BHQ) plays an important role in bromobenzene-induced nephrotoxicity and is a model toxic hydroquinone. Since BHQ has a quinone nucleus and various quinones have been shown to produce cytotoxicity via oxidative stress, the goal of this study was to
J E Andrews et al.
Toxicology and applied pharmacology, 120(1), 1-7 (1993-05-01)
Glutathione conjugates of 2-bromohydroquinone (GSyl-BHQ) cause renal proximal tubular necrosis that is dependent upon the activity of gamma-glutamyl transferase (GGT). GGT is present in embryonic yolk sac and its activity increases with gestational age, suggesting that the developing embryo might
R G Schnellmann et al.
The Journal of pharmacology and experimental therapeutics, 237(2), 456-461 (1986-05-01)
An in vitro model using a suspension of rabbit renal proximal tubules was developed to investigate the mechanism of nephrotoxicity of bromobenzene. Using oxygen consumption, glutathione concentrations and retention of lactate dehydrogenase activity as markers of toxicity, the rank order
S S Lau et al.
Biochemical and biophysical research communications, 152(1), 223-230 (1988-04-15)
2-Bromo-(diglutathion-Syl)hydroquinone (2-Br-[diGSyl]HQ) is a more potent nephrotoxicant than any of three mono-substituted isomers. The reason for this differential toxicity is unknown. We now report that the rate of uptake of 2-Br-(diGSyl)HQ, 2-Br-3-(GSyl)HQ, 2-Br-5-(GSyl)-HQ and 2-Br-6(GSyl)HQ by kidney slices was 2.4
Glutathione conjugation as a mechanism of targeting latent quinones to the kidney.
S S Lau et al.
Advances in experimental medicine and biology, 283, 457-464 (1991-01-01)
T J Monks et al.
Drug metabolism and disposition: the biological fate of chemicals, 13(5), 553-559 (1985-09-01)
Incubation of either o-bromophenol or 2-bromohydroquinone with rat liver microsomes and 0.25 mM 35S-glutathione (GSH) gave rise to several isomeric 35S-GSH conjugates. A mixture of these isomeric GSH conjugates was prepared chemically and two were purified by HPLC; 1H-NMR spectroscopy
T J Monks et al.
Molecular pharmacology, 34(1), 15-22 (1988-07-01)
The formation of potentially reactive thiols has been postulated to play a role in the nephrotoxicity caused by a number of glutathione and/or cysteine conjugates. However, the inherent reactivity of such compounds has precluded both their identification in biological systems
J Zheng et al.
Chemical research in toxicology, 5(4), 561-567 (1992-07-01)
Bromobenzene is metabolized to electrophilic epoxides and quinones which covalently bind to protein sulfur nucleophiles, yet no quinone-derived mercapturic acid metabolites of bromobenzene have been reported. To search for them, phenobarbital-induced Sprague-Dawley rats were dosed (0.5-1.5 mmol/kg, ip) with either
X Yang et al.
Journal of toxicology and environmental health, 48(4), 319-332 (1996-07-01)
The role of proteinases in renal proximal tubule (RPT) cellular death was examined using specific inhibitors of proteinases. Rabbit RPT suspensions were incubated with antimycin A for 1 h or tetrafluoroethyl-L-cysteine (TFEC) for 4 h in the absence or presence
R G Schnellmann et al.
Toxicology and applied pharmacology, 90(3), 420-426 (1987-09-30)
2-Bromohydroquinone (BHQ) is a nephrotoxic metabolite of bromobenzene and a model toxic hydroquinone. The primary goal of these studies was to determine whether BHQ produces toxicity in rabbit renal proximal tubules by inhibiting mitochondrial function. BHQ induces a specific sequence
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