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A well-studied aminoglycoside ; and nephrotoxicity. Indeed, gentamycin-induced PLD has been observed in conjunction with renal toxicity Laurent et al., 1990 ; and the inhibition of the development of PLD inhibits nephrotoxicity Samadian et al., 1993 ; . The possible toxicological consequences of PLD are an area of great interest both to the Food and Drug Administration FDA ; and the pharmaceutical industry. In 2004, the FDA established a PLD working group whose objective is to determine whether compounds-inducing PLD pose a potential clinical risk. Consequently, a PLD database is being populated with clinical and preclinical data on compounds from in-house FDA reviews. The results will hopefully enable to come to a decision resulting in a PLD guidance that will be useful to the pharmaceutical industry. Nevertheless, very recently, Reasor et al. 2006 ; indicated that from a regulatory perspective and consistent with the task of determining drug safety, PLD has been considered as an adverse finding, whether justified or not. The presence of foamy cells as detected by histopathological analyses only suggests that PLD may have occurred. The standard confirmatory method for the detection of PLD on ex vivo samples is electron microscopy Drenckhahn et al., 1976 ; . However, the method is expensive, time consuming, and not dedicated to medium and high-throughput screenings. In addition, drug-induced PLD detected by electron microscopy could be discovered only after subchronic to chronic intake of compounds. In silico approaches have been successfully used to predict drug-induced PLD. For instance, the data presented by Ploemen et al. 2004 ; support the use of simple physicochemical calculations of ClogP and pKa to discriminate rapidly between compounds suspected of being PLD inducers. Nevertheless, there is a clear need to develop in vitro methodologies to enable rapid assessment during the drug development and help in the selection of the best candidates. PLD can be rapidly assessed by measuring the binding of dyes to the phospholipids. For instance, different cellular models e.g., primary hepatocytes, HepG2, U-937, CHO-K1, and CHL IU cell lines, spleen macrophages ; , dyes e.g., nile red, NBD-PC ; , and methodologies e.g., flow cytometry, fluorescence microscopy, gene expression ; have been successfully used to detect PLD under in vitro conditions Casartelli et al., 2003; Gum et al., 2001; Kasahara et al., 2006; Morelli et al., 2006; Sawada et al., 2005; Ulrich et al., 1991 ; . Recently, Sawada et al. 2005 ; , who developed a rapid and sensitive in vitro screening test for druginduced PLD based on gene expression analysis in HepG2 cells, identified 17 genes as potential markers of PLD. To increase the throughput of the assay, the PCR-based assay was transferred into a 96-well microplate-based multiple mRNAs measuring assay Sawada et al., 2006 ; . In a previous study, we showed that gene expression analysis generated with an array containing a restricted set of genes chosen as relevant markers of toxicity and metabolism allowed us to cluster 11 different hepatotoxicants de Longueville et al., 2003 ; . In the same spirit, the present study was undertaken to.

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