Disease relevance of NSC3406

• While pretreatment with aprotinin or indomethacin failed to inhibit the depressor action, 2-bromoethylamine hydrobromide (BEA), which is known to induce necrosis of the renal papilla, produced complete abolition of the depressor effect of an intrarenal injection of MK-422 in NE-induced hypertension [1].
• Binary ethylenimine at a final concentration of 0.01 M was prepared wtih 2-bromoethylamine hydrobromide in alkaline solutions, either separately from or in suspensions of rabies virus propagated in BHK cells [2].
• 1. Chemical renal medullectomy was performed in Wistar rats by intraperitoneal injection of 2-bromoethylamine hydrobromide (200 mg/kg body weight) [3].
• The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure [4].
• We used the model nephrotoxicants mercuric chloride, 2-bromoethylamine hydrobromide, hexachlorobutadiene, mitomycin, amphotericin, and puromycin to elucidate time- and dose-dependent global gene expression changes associated with proximal tubular toxicity [5].

High impact information on NSC3406

• In addition, we observed that the repair-inactive but recognition-competent Cys249 mutant (Lys249-->Cys) of hOgg1 can be functionally rescued by alkylation with 2-bromoethylamine, which functionally replaces the lysine residue by generating a gamma-thia-lysine [6].
• Nuclear magnetic resonance spectroscopy and pattern recognition analysis of the biochemical processes associated with the progression of and recovery from nephrotoxic lesions in the rat induced by mercury(II) chloride and 2-bromoethanamine [7].
• To define the role of the medulla in the mechanism of pressure-induced natriuresis, experiments were performed in a group of rats 8 to 12 days after the development of papillary necrosis induced by bromoethylamine hydrobromide [8].
• Dextrans with average molecular weights of 5,000, 10,000, and 17,500 and inulin were rendered cationic by amination with 2-bromoethylamine hydrobromide [9].
• 2-Bromoethylamine as a potent selective suicide inhibitor for semicarbazide-sensitive amine oxidase [10].

Chemical compound and disease context of NSC3406

• The rat renal papilla was selectively destroyed by 2-bromoethylamine hydrobromide; increasing doses produced a graded severity of histological damage, polyuria and a reduction in urinary prostaglandin E2 excretion [11].
• Different models of site-specific ERF have been developed in the rat; proximal tubular necrosis (induced by cisplatin), papillary necrosis (induced by 2-bromoethylamine), and glomerulonephritis (induced by sodium aurothiomalate or by antiglomerular basement membrane antibodies) [12].

Biological context of NSC3406

• The final blood pressure was similar to that observed in normal rats treated with 2-bromoethylamine compared with their respective controls [11].
• In order to examine the contribution of renal papilla to atrial natriuretic factor (ANF)-induced diuresis, clearance studies were done in rats with intact papillae and bromoethylamine hydrobromide (BEA)-induced papillary necrosis [13].
• Male MF1-nu/nu/Ola/Hsd nude mice, maintained in a gnotobiotic environment, were dosed i.p. with either 50, 100 or 200 mg/kg 2-bromoethanamine (BEA) hydrobromide to induce a model papillary necrosis [14].
• Effect of bromoethylamine hydrobromide on systemic acid-base balance [15].
• The renal responses to acute expansion of the blood volume (20%), acute saline loading (5% body wt), or administration of atrial natriuretic peptide (ANP) were investigated in rats 7-10 days after inducing experimental renal papillary necrosis by the injection of bromoethylamine hydrobromide [16].

Anatomical context of NSC3406

• These data suggest that changes in the medullary matrix might play a previously unrecognized role in the development of 2-bromoethanamine hydrobromide-induced renal papillary necrosis, and these changes may give rise to loss of the material that supports the medullary capillaries [17].
• Hexachlorobutadiene-N-acetylcysteine (HCBD-NAC), adriamycin and 2-bromoethanamine hydrobromide are three renal toxins that have shown in vivo a highly selective target cell toxicity--to the proximal tubules, the glomerular epithelial cells and the medullary interstitial cells, respectively [18].

Associations of NSC3406 with other chemical compounds

• All mutants of Lys76 display reduced activity with large effects on the K(m) for phosphite, and Lys76Cys could be chemically rescued by alkylation with 2-bromoethylamine [19].
• Renal cortical and medullary spin-lattice (T1) relaxation times were measured at various time points over a period of 56 days following the administration of a single i.p. injection of 100 mg/kg 2-bromoethanamine hydrobromide (BEA), 200 mg/kg hexachloro-1,3-butadiene (HCBD) or 100 mg/kg puromycin aminonucleoside (PAN) to male Wistar rats [20].
• In the present study, inhibitory properties of 2-bromoethylamine (2-BEA) and 3-bromopropylamine (3-BPA) toward rat lung-bound SSAO have been studied [21].
• Arachidonic-acid-dependent metabolism of 2-bromoethanamine to a toxic metabolite in rat medullary interstitial cell cultures [22].
• Effects of reserpine and L-cysteine and glutathione depletion on 2-bromoethylamine hydrobromide-induced tubular necrosis in Swiss ICR mice [23].

Gene context of NSC3406

• 2-bromoethylamine has been recently developed with a potent, selective and suicide SSAO inhibitor without any inhibitory effect on MAO activity Using this inhibitor, it is possible to study the role of the enzyme in mammalian tissues [24].
• A keratin sponge was chemically modified to obtain carboxyl and amino sponges by the alkylation of a large amount of active SH group on keratin proteins with iodoacetic acid and 2-bromoethylamine, respectively [25].

Analytical, diagnostic and therapeutic context of NSC3406

• Pretreatment of the rabbits with 2-bromoethylamine hydrobromide, which destroyed the renal medulla, abolished the fall in arterial pressure (-0.08 +/- 0.08 mm Hg/min) in response to increased renal perfusion pressure [26].
• METHODS: Renomedullectomy was produced by single intraperitoneal injection of 2-bromoethylamine (BEA) at 400 mg/kg [27].
• The authors studied these mechanisms in bromoethylamine hydrobromide-induced RPN in rats by microvascular and tubular micropuncture injection studies [28].
• Thirty-two male Swiss ICR mice were injected intraperitoneally with 300 mg 2-bromoethylamine hydrobromide/kg body weight, anesthetized, and perfused with glutaraldehyde-paraformaldehyde solution at 5, 15, 30, 60, 90, 120, 150, and 180 minutes after treatment [29].
• Papillary necrosis was induced in female rats by intravenous infusion of 2-bromoethylamine hydrobromide (BEA) 48 h prior to clearance experiments; untreated (UNT) animals served as controls [30].

References