Stress proteins expression in rat kidney and liver chronically exposed to aluminium sulphate

Aluminium (Al) is the third most widespread
metal in the environment. It is toxic for the brain, bone
and haematological system but unfortunately very little
data exist for other organs. Stress proteins are induced or
enhanced against metal toxicity with an essential role in
the recovery of organules and other cellular proteins.
This immunohistochemical study was performed to
analyze the distribution of three stress proteins (HSP25,
HSP72, GRP75) in rat kidney and liver orally exposed to
Al sulphate daily for 3 and 6 months. Al-induced
alterations were further studied by histopathology (H&E,
PAS, Perl’s, Masson) and ultrastructural morphometry.
In the kidney: HSP25 was enhanced in proximal tubules
after 6 months Al-exposure when abnormal brush
borders were observed; HSP72 was induced in proximal
tubules only after long Al-treatment; GRP75 was raised
in midcortical area sometimes within nuclei.
Furthermore, lysosomal and lipofuscins densities
increased in the juxtamedullary tubules after 3 months
Al exposure with respect to controls. In the liver: Perl’spositive
deposits and fibrosis became evident after Al
treatment. HSP25 was very weak; HSP72 focal in
pericentral hepatocytes at 3 months and induced also in
Kupffer cells at 6 months; GRP75 diffuse in periportal
hepatocytes and non parenchymal cells at 6 months.
Prolonged Al exposure stimulated stress proteins strictly
organ-dependently in the rat. Their distribution in kidney
and liver seems related to cumulative sublethal effects
induced by metal and could be a sensitive index of Al
susceptibility of these organs.