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HERO ID
1238539
Reference Type
Journal Article
Subtype
Abstract
Title
Protective effect of alpha-tocopherol on renal injury caused by chromate exposure
Author(s)
Arreola-Mendoza, L; Reyes, JL; Namorado, MC; Martin, D; Del Razo, LM
Year
2005
Is Peer Reviewed?
1
Journal
Toxicologist
ISSN:
0731-9193
Report Number
TOX/5001266
Volume
84
Issue
1-S
Page Numbers
232
Language
English
Abstract
Chromate Cr(VI) is a common industrial waste product and environmental pollutant. It is also a recognized human carcinogen. Some toxic effects of Cr(VI) exposure have been related with its oxidative capacity. In the kidney, exposure to Cr(VI) has been associated with proximal tubular necrosis, although its mechanism remains unclear. Our aim was to examine acute renal damage caused by the exposure of Cr(VI), to disclose the degree of lipid peroxidation (LPO) cause by this metal and the functional consequences on different nephron segments (glomeruli, proximal and distal tubules). We also assessed the segmental selectivity of the protective effect of alpha-tocopherol on these alterations. Wistar female rats (200 g bw) received potassium dichromate (15 mg/kg, sc, single dose). LPO and renal function were monitored on days 0, 1, 2, 3, 7, 10 y 14 after Cr(VI) administration. A second group received alpha-tocopherol (125 mg/kg/day, gavage), 5 days before and 7 days after Cr(VI), and were monitored on 0, 2 and 7 days of Cr(VI) exposure. LPO was quantified in renal tissue; creatinine clearance, glucose and sodium fractional excretions, free-water and osmolal clearances were also measured. Results showed oxidative damage 48 h after exposure to Cr(VI) with spontaneous recovery after day 7. Renal function was maximally altered on day 3 and thereafter recovery ensued. Glomerular filtration decreased, glucose and sodium fractional excretions increased and free water and osmolal were affected. These changes showed a similar timecourse to that of the oxidative damage. alpha-tocopherol-treated group showed less oxidative damage and preservation of proximal tubule function. In contrast, glomerular and distal function did not show difference with the group that received Cr(VI) alone. These results suggest that Cr(VI) causes alterations along different segments of the nephron and the antioxidant treatment had protective effect only on the injury caused by Cr(VI) on the proximal tubular function.
Conference Name
44th Annual Meeting of the Society of Toxicology
Conference Location
New Orleans, LA
Conference Dates
March 6-10, 2005
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Chromium VI
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