作者: N. Ozaki , K.A. Matheis , M. Gamber , T. Feidl , T. Nolte
DOI: 10.1016/J.ETP.2009.07.004
关键词:
摘要: For the application of microarray technology as an additional endpoint in toxicological studies, there is a need to understand associations between pathological processes and gene expression alterations. In current study, we investigated gentamicin nephrotoxic model compound. Gene changes kidney response dose 80 mg/kg were analyzed by using DNA alterations associated with results from conventional histopathological investigations described pathomechanisms gentamicin. Under conditions our experiment, mRNA level 211 genes found be deregulated The gentamicin-induced affection proximal convoluted tubules was strong up-regulation mRNAs encoding for proteins which are used nephrotoxicity markers urine plasma such Kim-1, Osteopontin TIMP1. Candidate marker GATM deregulated. Gentamicin-induced lysosomal phospholipidosis indicated deregulation located products ATP6V1D, subunit H+ transporting ATPase. Effects on glucose transport metabolism down-regulation SGLT-2 glucose-6-phoshatase. Renal cell apoptosis up-regulated TP53 BAX. role oxidative stress toxicity reflected transferrin receptor heme oxygenase. study show potential complex mechanism single study.