Disease relevance of NSC 3977

• There is a specific sequence of events in 2-bromohydroquinone-induced toxicity [1].
• 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 in pH 7.4 and pH 6.4 buffers [2].

High impact information on NSC 3977

• Mechanism of pH amelioration of 2-bromohydroquinone-induced toxicity to rabbit renal proximal tubules [2].
• Formation of 2-bromohydroquinone by rat liver microsomes from both bromobenzene and o-bromophenol was increased by treatment of rats with either phenobarbital or 3-methylcholanthrene [3].
• Treatment of rats with AT-125 (Acivicin; NSC 163501; 10 mg/kg ip) caused a substantial inhibition of kidney gamma-glutamyl transpeptidase activity and decreased 2-bromohydroquinone-mediated elevations in blood urea nitrogen [4].

Biological context of NSC 3977

• 2-Bromohydroquinone-induced toxicity to rabbit renal proximal tubules: evidence against oxidative stress [5].

Associations of NSC 3977 with other chemical compounds

• Bromohydroquinone- or t-butylhydroperoxide-induced cell death was not decreased by any of the proteinase inhibitors [6].
• The general cysteine protease inhibitor trans-epoxysuccinyl-L-leucylamido (4-guanidino)-butane (E-64) decreased antimycin A- and tetrafluoroethyl-L-cysteine-induced cell death but had no effect on bromohydroquinone- or t-butylhydroperoxide-induced cell death [7].

References