Haga H J, Andersen K J, Iversen B M, Ofstad J, Dobrota M, Matre R
Medical Department A, University of Bergen, Haukeland Sykehus, Norway.
Ren Physiol. 1987;10(5):249-60. doi: 10.1159/000173133.
Acute passive Heymann glomerulonephritis in rats induced heavy proteinuria and highly increased urinary activity of N-acetyl-beta-D-glucosaminidase, acid beta-galactosidase and acid phosphatase. The cortical activity of these acid hydrolases was increased essentially in the large lysosomes as demonstrated by subfractionation of the lysosome-rich mitochondrial-lysosomal fraction, by rate zonal centrifugation. Banding density of small lysosomes shifted or reduced to slightly lower value (1.225 g/ml), which is between the banding densities of small 'light' (1.20 g/ml) and small 'dense' lysosomes (1.235 g/ml) in normal rat kidney cortex. Labelled protein reabsorbed in the proximal tubule is recovered in these populations of small lysosomes as well as in the large lysosomes or 'protein droplets'. Glomerulonephritis also induced a new population of small 'light' lysosomes (density 1.185-1.195 g/ml) enriched in cathepsin D. The previously demonstrated morphological, biochemical, and physiological heterogeneity of renal lysosomes was confirmed and emphasized in the kidney cortex of glomerulonephritic rats. The main changes in the lysosomal populations appear to reflect the increased protein reabsorption as confirmed by the proteinuria.
大鼠急性被动型海曼肾小球肾炎可导致重度蛋白尿,并使尿中N - 乙酰 - β - D - 氨基葡萄糖苷酶、酸性β - 半乳糖苷酶和酸性磷酸酶的活性显著升高。通过对富含溶酶体的线粒体 - 溶酶体组分进行亚分级分离以及速率区带离心法证实,这些酸性水解酶在皮质中的活性主要在大型溶酶体中升高。小型溶酶体的条带密度发生偏移或降低至略低的值(1.225 g/ml),该值介于正常大鼠肾皮质中“轻”型小型溶酶体(1.20 g/ml)和“致密”型小型溶酶体(1.235 g/ml)的条带密度之间。在近端小管中重吸收的标记蛋白在这些小型溶酶体群体以及大型溶酶体或“蛋白滴”中均可回收。肾小球肾炎还诱导产生了一群富含组织蛋白酶D的新型“轻”型小型溶酶体(密度1.185 - 1.195 g/ml)。肾小球肾炎大鼠肾皮质中先前证实的肾溶酶体在形态、生化和生理方面的异质性得到了进一步证实和强调。溶酶体群体的主要变化似乎反映了蛋白尿所证实的蛋白质重吸收增加。