L. Delacruz et al., URINARY MARKERS OF NEPHROTOXICITY FOLLOWING ADMINISTRATION OF 2-BROMOETHANAMINE HYDROBROMIDE - A COMPARISON WITH HEXACHLOROBUTADIENE, Biomarkers, 2(3), 1997, pp. 169-174
2-bromoethanamine hydrobromide (BEA) has been widely considered to be
a target selective nephrotoxin that causes necrosis of the medulla in
24-48 h, but recent reports suggest that early cortical injury is also
associated with this lesion. In order to assess the cortical effects
of BEA (100 mg kg(-1) bw single ip injection), several urinary markers
of renal injury were evaluated over a 7-day period in male Wistar Alb
ino rats. Hexachlorobutadiene (HCBD-150 mg kg(-1) bw in peanut oil ip)
, a renal toxin which targets selectively for the proximal tubule, was
used as a comparison. After BEA treatment, urinary levels of alanine
aminopeptidase, gammaglutamyl-transpeptidase, alkaline phosphatase and
glucose increased transiently. Each of the proximal tubule marker enz
ymes peaked earlier following HCBD treatment and elevation of alanine
aminopeptidase and gamma-glutamyl-transpeptidase was sustained for lon
ger periods than for BEA. Following BEA treatment, lactate dehydrogena
se rose prominently on day 1 followed by a return to control values on
day 2 and a further rise on day 3 and remained high until the end of
the study. BEA also increased the urinary excretion of total protein a
nd albumin. After HCBD treatment, lactate dehydrogenase showed a trans
ient elevation and glucose levels were slightly increased. Based on th
e present observations the changes induced by BEA administration on ur
inary markers of renal injury are different from those observed follow
ing HCBD treatment. These findings suggest that BEA toxicity also invo
lves other parts of the kidney besides the papilla.