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D-Serine-induced nephrotoxicity: a HPLC-TOF/MS-based metabonomics approach.

R E Williams¹, H Major, E A Lock

¹Department of Drug Metabolism and Pharmacokinetics, AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, UK.

|December 15, 2004

Summary

This summary is machine-generated.

D-serine causes kidney damage, leading to aminoaciduria, proteinuria, and glucosuria. HPLC-MS metabonomics revealed specific urinary metabolite changes, aiding in understanding D-serine-induced renal injury mechanisms.

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Area of Science:

Toxicology
Metabonomics
Renal Physiology

Background:

D-serine is known to induce selective necrosis in rat proximal straight tubules.
This nephrotoxicity is characterized by aminoaciduria, proteinuria, and glucosuria.

Purpose of the Study:

To investigate urinary metabolic perturbations associated with D-serine-induced nephrotoxicity using HPLC-MS.
To elucidate the mechanism of D-serine-induced renal injury.

Main Methods:

HPLC-MS-based metabonomic analysis of rat urine samples.
Rats were dosed with D-serine (250 mg/kg ip) or vehicle.
Urine collected at 0-12, 12-24, 24-36, and 36-48 h post-dosing and analyzed in positive and negative ion modes.

Main Results:

Significant changes in urinary profiles were detected compared to controls.
Increased levels of serine, hydroxypyruvate, glycerate, tryptophan, phenylalanine, lactate, and acetyl carnitine were observed.
Decreased levels of methylsuccinic acid, sebacic acid, and xanthurenic acid were noted, along with general aminoaciduria.

Conclusions:

HPLC-MS metabonomics successfully identified urinary metabolic alterations linked to D-serine nephrotoxicity.
The study provides insights into the biochemical pathways affected by D-serine exposure.
Further investigation is ongoing to identify additional affected metabolites.