The kidney is the main site of interferon catabolism.
The fate of human natural interferons alpha and beta and of recombinant (R) alpha 2 has been investigated by using an isolated and perfused rabbit kidney preparation with a normal physiological performance. A remarkable amount of IFN is filtrated in a monoexponential fashion, reabsorbed and very likely degraded in tubular cells with negligible excretion in the urine. The disappearance rate of HuRIFN-alpha 2 is higher than natural HuIFNs-alpha and beta and is in keeping with the lower molecular weight of RIFN-alpha 2. Differences in molecular charge or shape are probably responsible for the slightly reduced filtration of IFN-beta. Pharmacokinetic studies in animal models appear instructive and useful for devising improved dosage schedules in clinical trials.
D000818:Animals; D066298:In Vitro Techniques; D007370:Interferon Type I / Q000097:blood / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism; D008657:Metabolic Clearance Rate; D010477:Perfusion; D011817:Rabbits
D007370:Interferon Type I