Recovery of cellular functions following oxidant injury

Grazyna Nowak, Michael D. Aleo, Jan A. Morgan, Rick G. Schnellmann

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

This study investigated the recovery of renal proximal tubule cellular (RPTC) functions following oxidant-induced sublethal injury. tert- Butylhydroperoxide (TBHP) treatment resulted in 24% cell death and loss 4 h following the exposure. The remaining sublethally injured RPTC proliferated, and monolayer DNA content returned to control values on day 4 following TBHP exposure. Basal oxygen consumption (QO2) and ATP content in sublethally injured RPTC were decreased 64 and 63%, respectively, at 4 h and returned to control values on day 6. Net lactate consumption decreased 71% at 4 h and returned to control values on day 4. In contrast, net glutamine consumption increased 2.7-fold at 4 h and returned to control values on day 6. Ouabain- sensitive QO2, Na+-K+-adenosinetriphosphatase (Na+-K+-ATPase) activity, and Na+-coupled glucose transport were inhibited 77, 88, and 83%, respectively, at 4 h and recovered to control values on day 6. These data show that 1) mitochondrial function, Na+-K+-ATPase activity, active Na+ transport, and Na+-coupled glucose transport are decreased in sublethally injured RPTC following oxidant exposure and are repaired over time; 2) monolayer regeneration precedes the recovery of mitochondrial and transport functions, and 3) sublethal injury and subsequent regeneration are associated with alterations in metabolic substrate utilization. These results suggest that oxidant-induced sublethal injury to RPTC may contribute to renal dysfunction and that RPTC can repair and regain cellular functions following oxidant injury.

Original languageEnglish (US)
Pages (from-to)F509-F515
JournalAmerican Journal of Physiology - Renal Physiology
Volume274
Issue number3 43-3
DOIs
StatePublished - Mar 1998
Externally publishedYes

Keywords

  • Active sodium transport
  • Amino acids
  • Ascorbic acid
  • Cell death
  • Cell repair
  • Glutamine
  • Mitochondrial functions
  • Oxygen consumption
  • Regeneration
  • Renal proximal tubular cells
  • Sodium-coupled glucose transport
  • Sodium-potassium-adenosinetriphosphatase
  • Sublethal cell injury
  • Tert-butylhydroperoxide

ASJC Scopus subject areas

  • Physiology
  • Urology

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