2-Bromoethylamine hydrobromide, also known as 2-Aminoethyl bromide hydrobromide, is a simple, common, and harmless substance that can provide –NH2 for titanate nanotubes through intramolecular elimination of NaBr. Furthermore, it dissolves in water and can replace harmful organic solvents as excellent modification reagents. 2-Bromoethylamine hydrobromide can be used as a reactant to synthesize: Thiazolines and thiazines via tandem S-alkylation-cyclodeamination of thioamides/haloamines.; Optically active tertiary phosphines via cesium hydroxide-catalyzed P-alkylation of secondary phosphines; Secondary amines via CsOH-promoted chemoselective mono-N-alkylation of primary amines, diamines, and polyamines.

Magnetic resonance microscopy of toxic renal injury

The alkylhalide 2-bromoethylamine hydrobromide (BEA) produces renal injury in rats that mimics analgesic-related renal injury in humans. Rats (n = 48) were injected intravenously with BEA (150 mg/kg) or saline and imaged with MR 6, 48, and 336 hr later. The spin-spin relaxation time, T2, was measured from the cortex to the papilla. In other rats, we measured regional water content of the kidney. Renal injury was present 48 and 336 hr after 2-Bromoethylamine hydrobromide dosing based on increased renal organ weights, decreased urine specific gravity, and significant renal lesions (H & E). T2 was elevated in the inner stripe of the outer medulla in injured kidneys at 48 hr. The differences in T2 between cortex and outer medulla were also elevated 48 hr after BEA. MR microscopy detected damage in the outer medulla after 2-Bromoethylamine hydrobromide injury but not the damage in the inner medulla. T2 appeared to reflect the water content in the different regions of the medulla. The noninvasive in vivo capability of MR microscopy, with its high sensitivity to tissue water, allows the toxicologist to monitor the progression and regression of toxic insult in the same animal. At present the technology is complicated.[1]

Cellular mechanisms of drug-induced papillary necrosis

2-Bromoethylamine hydrobromide causes complete papillary necrosis within 24-hr of i.v. administration. The mechanism of this effect is unknown. To characterize further the effect of BEA in transporting epithelia, the urinary bladders of toads and turtles were exposed to varying concentrations of BEA in vitro.  In the toad bladder, both cyclic AMP- and vasopressin-stimulated water flow were significantly inhibited after 3 hr of exposure to 2-Bromoethylamine hydrobromide at a concentration as low as 2.5 X 10(-4) g/ml; after 1 and 2 hr no effect on water transport was observed. Serosal administration of BEA to both toad and turtle bladders significantly inhibited sodium transport to 54% of control at the end of 3 hr. The effect on sodium transport was seen as early as 10 min.Thus, in anuran membranes, 2-Bromoethylamine hydrobromide inhibits water and sodium transport but has no effect on acidification. These results suggest that its action in vivo may be related to alterations in cell volume regulation resulting from inhibition of sodium transport rather than a nonspecific toxic effect on the inner medullary epithelium.[2]

Acute cortical tubular necrosis induced by 2-bromoethylamine hydrobromide

Dose-response and sequential studies of 2-bromoethylamine hydrobromide (BEA) nephrotoxicosis were carried out using Swiss ICR mice. For the dose-response study, 150 male mice, 30 per group, were injected intraperitoneally (ip) with 100, 200, 300, 400 or 500 mg BEA/kg and ten from each group were killed 1, 3 or 5 days after treatment. The percentage of mice with tubular necrosis varied from 0 in mice given 100 mg BEA/kg to 100 in mice given 400 mg BEA/kg. The percentage of mice with renal papillary necrosis was also dose dependent and varied from 0 in the 100 mg/kg group to 72 in the 400 mg/kg group. Degeneration of proximal tubules was detected 2 hr after treatment. Three hours after treatment, grossly, the renal cortex was diffusely pale and, microscopically, there was marked acute tubular necrosis. Epithelial cells lining the cortical tubules were regenerating 3 days after treatment. By 10 days after treatment cortical interstitial fibrosis was marked with many tubules lined by regenerating epithelium and many tubules were dilated. 2-Bromoethylamine hydrobromide-induced nephrotoxicosis in the mouse was primarily an acute cortical tubular necrosis.[3]

References

[1]Hedlund, L W et al. “Magnetic resonance microscopy of toxic renal injury induced by bromoethylamine in rats.” Fundamental and applied toxicology : official journal of the Society of Toxicology vol. 16,4 (1991): 787-97. doi:10.1016/0272-0590(91)90164-y

[2]Sabatini, S. “Cellular mechanisms of drug-induced papillary necrosis.” The Journal of pharmacology and experimental therapeutics vol. 232,1 (1985): 214-9.

[3]Wolf, D C, and W W Carlton. “Acute cortical tubular necrosis in the Swiss ICR mouse induced by 2-bromoethylamine hydrobromide.” Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association vol. 28,5 (1990): 351-60. doi:10.1016/0278-6915(90)90109-z