Abstract
RPTC monolayers undergo partial regeneration following toxicant exposure (Toxicol. Appl. Pharmacol. 132:273,1995). This study investigated the recovery of RPTC functions following exposure to the oxidant t-butylhydroperoxide (TBHP). Rabbit RPTC were grown in improved culture conditions (Am. J. Physiol. 268:C1053, 1995) in the absence of glucose and the presence of 50 uM L-ascorbic acid 2-phosphate. Treatment of confluent RPTC monolayers with 0.2 mM TBHP for 40-50 min decreased monolayer DNA content by 24% after 24 hrs. Monolayer DNA content increased to control values 4 days after TBHP treatment. TBHP inhibited Na -dependent glucose uptake (using 1 mM methyl-aglucopyranoside as a marker) by 84% and 63% 4 hrs and 4 days, respectively, after treatment. Basal oxygen consumption (QOJ was decreased by 66% and 40% 4 hrs and 4 days after TBHP treatment. Ouabain-sensitive QO, was inhibited by 84% and 47% 4 hrs and 4 days after TBHP treatment. Na'-dependent glucose uptake and basal and ouabain-sensitive QO, returned to control values 6 days after TBHP treatment. y-Glutamyl transpeptidase (y-GT) activity (a brush border marker) was unaffected by TBHP exposure. These results show that: 1) TBHP decreases mitochondrial function and Na and glucose transport in the non-lethally injured RPTC, 2) monolayer regeneration (4 days) precedes the recovery of mitochondrial and transport functions (6 days), and 3) y-GT activity was not a target of TBHP. The decrease in Na'-coupled glucose transport may be secondary to a decreased Na gradient following TBHP exposure. (SupportedbyES-04410).
Original language | English (US) |
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Pages (from-to) | A348 |
Journal | FASEB Journal |
Volume | 10 |
Issue number | 3 |
State | Published - 1996 |
Externally published | Yes |
ASJC Scopus subject areas
- Biotechnology
- Biochemistry
- Molecular Biology
- Genetics