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Aluminium induced damage of the lysosomes in the liver, spleen and kidneys of rats
Author(s) -
Stein Günter,
Laske Volker,
Müller Andreas,
Bräunlich Helmut,
Linß Werner,
Fleck Christian
Publication year - 1987
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550070406
Subject(s) - spleen , endocrinology , medicine , kidney , beta (programming language) , enzyme , chemistry , nephrectomy , biology , biochemistry , computer science , programming language
The influence of repeated aluminium (Al) administration (0.05 or 0.5 mg 100 g −1 b.w.t. i.p. 5 times weekly for 12 weeks) on the lysosomal enzymes N ‐acetyl‐beta‐ D ‐glucosaminidase (β‐NAG) and beta‐glucuronidase (β‐Gluc) in serum, liver, spleen and kidneys of adult female rats with intact kidneys, (NR), or following partial nephrectomy (5/6 NX) was investigated. After Al loading, at the high dose only, the β‐NAG in serum and the free β‐NAG in liver, spleen and kidneys increased. Latent β‐NAG levels decreased in all three organs the effect being dose related. Following Al loading no elevation in total enzyme activity was observed, with one exception. Depending on Al doses the spleen of the non‐operated animals, the liver of both groups of animals and the serum showed a decrease in β‐Gluc activity. No effect on β‐Gluc activity was observed in the spleen of 5/6 NX animals or in the kidneys of either group of animals. The results confirm that high doses of Al induce toxic effects and damage the lysosomes in the liver, the spleen and the kidneys. The results indicate that the extent of lysosomal damage correlates with dose and duration of Al loading. Repeated administration of Al also interferes selectively with enzyme synthesis.