Abstract
It is well known that an acute or subacute exposure to p-dichlorobenzene (p-DCB) is capable of inducing α2u-globulin-mediated nephropathy and that its continuous administration accelerates the development of age-associated chronic progressive nephrosis (CPN). In the present study, in order to investigate the necessity of continued p-DCB exposure for CPN induction, kidneys of male F344 rats maintained for a 6 month-recovery period after cessation of 9 months exposure at concentrations of 600, 300 or 75 ppm by inhalation were histologically examined. Development of CPN lesions was accelerated as compared to the control in spite of the lack of any persisting α2u-globulin-mediated nephropathy. Therefore, the present results support the hypothesis that the induced CPN is a secondary effect of kidney tubule damage.
