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Pre-administration of L-tryptophan improved ADR-induced early renal failure in mice

Yuko Arioka1, Yasuko Yamamoto, Masato Hoshi

  • 1Human Health Sciences, Graduate School of Medicine and Faculty of Medicine, Kyoto University, Japan.

Life Sciences
|July 4, 2012
PubMed
Abstract

Insights

Adriamycin-induced renal failure in mice activates indoleamine 2,3-dioxygenase (IDO) in kidney tubules. Early L-tryptophan (Trp) supplementation shows protective effects against kidney injury and reduces TNF-alpha.

Area of Science:

  • Nephrology
  • Biochemistry
  • Immunology

Background:

  • Adriamycin (ADR) is a nephrotoxic agent used to induce kidney failure in research models.
  • Indoleamine 2,3-dioxygenase (IDO) is an enzyme involved in tryptophan metabolism, with potential roles in inflammation and tissue injury.
  • Understanding the role of IDO in acute kidney injury is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the localization and expression of IDO and its metabolite, L-kynurenine (Kyn), in the kidney following ADR-induced renal failure.
  • To evaluate the therapeutic potential of L-tryptophan (Trp) administration in mitigating ADR-induced kidney damage.

Main Methods:

  • BALB/c mice were administered ADR (15 mg/kg) to induce renal failure.
  • Immunohistochemistry (IHC) with HE and PAS staining was used to assess morphological changes and IDO localization.
  • High-performance liquid chromatography (HPLC) measured L-Kyn concentrations.
  • The impact of L-Trp supplementation on renal function and inflammatory markers (TNF-alpha, TGF-beta, IL1-beta) was examined.

Main Results:

  • IDO expression was significantly upregulated in tubular cells starting from Day 4 post-ADR injection.
  • L-Trp administration reduced the incidence of renal failure at Day 4 but not at Day 7 after ADR treatment.
  • L-Trp treatment effectively suppressed the ADR-induced increase in TNF-alpha mRNA levels, while TGF-beta and IL1-beta remained unaffected.

Conclusions:

  • Adriamycin-induced renal failure triggers a notable local expression of IDO within kidney tubules.
  • Early administration of L-tryptophan demonstrates efficacy in ameliorating ADR-induced renal failure, particularly in the initial stages.
  • IDO pathway modulation presents a potential therapeutic target for acute kidney injury.

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