[Age-related changes in cell content (DNA) and glycosaminoglycan-degrading enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase of connective tissue and parenchymal organs of the rat caused by 6-methylprednisolone (enzyme induction, adaptation, acceleration of maturation and possible modification of aging].

This paper is based on previous investigations, which had shown an evident acceleration of maturation and enzyme induction in several organs, not only in the lung, due to a pre- and postnatal application of prednisolone. Applying the same dosage we now investigated whether there is a similar effect of a short-term application of prednisolone in mesenchymal and parenchymal organs of young adult and presenile rats of the same strain (Chbb: THOM/SPF) analyzing the physiological cell regeneration (DNA concentration) as well as functional parameters of the glycosaminoglycan metabolism (e.g. the lysosomal enzymes beta-glucuronidase and beta-N-acetylglucosaminidase). The results show a significant age-dependent decrease of the DNA concentration (lung, spleen, skin, and rib cartilage), a significant age-dependent decrease of the total activity of the beta-glucuronidase (kidney, rib cartilage, and skin) or a significant age-dependent increase of this enzyme activity (spleen and liver) respectively as well as a significant decrease of the beta-N-acetylglucosaminidase activity (skin and rib cartilage) or a significant increase of this enzyme activity (spleen and lung). After application of prednisolone the rats showed a significant reduction of the DNA concentration only in the skin of young adult rats, but no changes in the other organs of the young adult or presenile animals compared to untreated controls. Similar to our findings after postnatal prednisolone application, we found the greatest increases or decreases respectively of the activities of these lysosomal enzymes due to 2- to 3-fold or 4- to 5-fold prednisolone application. Again similar to our previous findings, we found the phenomena of adaptation and rebound effects including the so-called over-compensation in the young adult and especially in the presenile rats but these effects were delayed and weaker in most of the older animals compared to the young adult rats.