Kidney damage with Fanconi syndrome can occur frequently as side effect of chemotherapy using ifosfamide or cyclophosphamide. It is supposed that one metabolite of both, chloroacetaldehyde (CAA), is in part responsible for the observed damages of the proximal tubule. Nothing is known about transport of CAA into proximal tubule cells. Therefore, we studied the interaction of CAA with hOAT1 using Chinese hamster ovary (CHO) cells stably transfected with hOAT1 and compared it with mock-transfected CHO cells serving as control. Fluorescein net uptake (measured after 1 min. incubation) was higher in OAT1-transfected cells compared to control cells. Fluorescein net uptake was slightly and significantly increased by 1000-fold excess of CAA whereas in control cells net uptake was clearly increased. Higher CAA concentrations partially inhibited fluorescein uptake in OAT1-transfected cells but still increased net uptake in control cells. In both cell types, CAA still increased net uptake of fluorescein in the presence of probenecid. We conclude that CAA may interact with OAT1 but that CAA interacts also by inhibition of as yet unknown export mechanisms leading to increased intracellular fluorescein content. This hypothesis seems to be confirmed by efflux measurements.