Single non-lethal doses (3 mmol/kg) of chloroform (CHCI3) , dichlorobromomethane (CHClzBr), dibromochloromethane (CHC1Br2), and bromoform (CHBr3) were administered by intraperitoneal injection to male Sprague-Dawley rats and proximal tubular secretion and reabsorption was assessed at varied times fo
Characterization of trihalomethane (THM)-induced renal dysfunction in the rat. I: Effects of THM on glomerular filtration and renal concentrating ability
โ Scribed by R. B. Kroll; G. D. Robinson; J. H. Chung
- Publisher
- Springer
- Year
- 1994
- Tongue
- English
- Weight
- 328 KB
- Volume
- 27
- Category
- Article
- ISSN
- 0090-4341
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โฆ Synopsis
Single non-lethal doses (3 mmol/kg) of chloroform (CHC13), dichlorobromomethane (CHC12Br), dibromochloromethane (CHC1Br2) , and bromoform (CHBr3) were administered by intraperitoneal injection to male Sprague-Dawley rats and glomerular filtration and renal concentrating ability were assessed at varied times (5-8 h, 21-24 h, and 45-58 h) following treatment. At this dose, each of the four trihalomethanes (THMs) elevated blood urea nitrogen (BUN) and reduced renal concentrating ability (as measured by H20 intake/output ratios, urinary total osmolality, and electrolyte levels). Three of the four THMs also significantly reduced glomerular filtration rate (GFR), with only CHC13 failing to demonstrate an effect at 3 mmol/kg. In general, CHC12Br demonstrated the greatest interference with these renal function parameters. The times of maximal THM-induced effect on BUN and glomerular filtration rate were observed to be 24 h and 21-24 h post-treatment, respectively. These data suggest that a single acute THM treatment can inhibit mammalian renal concentrating ability and glomerular filtration.
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