Browsing by Subject "Aluminium"

Now showing 1 - 4 of 4
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    Histopathological changes in gerbil liver and kidney after aluminium subchronic intoxication
    (F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Garrosa, Manuel; Llanes, Felipe; Gayoso, Manuel J.
    Young gerbil livers and kidneys were analyzed by means of light and electron microscope to assess the histopathological changes caused by prolonged systemic aluminum (Al) administration. The experimental group was injected with AlCl3 i.p. for 5 weeks, while litter mates received PBS as sham-injected controls or served as untouched controls. Mortality occurred in 33% of experimental and 12.5% of sham-injected groups. The animals were perfused intracardially with 1% glutaraldehyde plus 1% paraformaldehyde and samples of liver and kidneys were processed for aluminum and iron histochemistry and conventional light- and transmission electron microscopy. White deposits composed of cellular debris appeared on the surface of liver and kidneys and in the mesentery as a consequence of Al treatment. Adherences of Glisson capsule to the diaphragm, as well as scattered small foci of hepatocyte necrosis with non-caseificant microgranulomas and mild portal inflammation, developed in the experimental group. Sham-injected animals also exhibited these granulomas but to a lesser degree. Al deposits were found in experimental animal granulomas and inside macrophages cytoplasm scattered throughout the liver. Iron deposition appeared in pericentral hepatocytes of experimental animals, in granulomas and in portal spaces of the three groups of animals. Ultrastructurally, hepatocytes of experimental animals showed mitochondria hyalinization, disintegration of endoplasmic reticulum and clustering of ribosomes. Phagolysosomes appeared larger and occurred more frequently in both hepatocytes and Kupffer cells of experimental animals. In 2 out of the 6 experimental animals studied, tubular atrophy was present in the renal cortical region, the kidneys of the remaining animals appearing normal. Al and iron were found very occasionally in the kidney parenchyma of experimental animals, while isolated mesangial cells showed iron deposits in a few glomeruli of both experimental and the two groups of control animals.
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    Neurofibrillary pathology and aluminum in Alzheimer's disease
    (Murcia : F. Hernández, 1995) Shin, R. W.; Lee, V. M. Y; Trojanowski, J. Q.
    Since the first reports of aluminum-induced neurofibrillary degeneration in experimental animals, extensive studies have been performed to clarify the role played by aluminum in the pathogenesis of Alzheimer's disease (AD). Additional evidence implicating aluminum in AD includes elevated levels of aluminum in the AD brain, epidemiological data linking aluminum exposure to AD, and interactions between aluminum and protein components in the pathological lesions of AD, ¡.e., neurofibrillary tangles (NFTs) and senile plaques (SPs). As most of this evidence is circumstantial and some of it is not consistent in al1 reports, the role of aluminum in the pathogenesis of AD has remained controversial. However, the interaction of aluminum with altered forms of t in the paired helical filaments (PHFs) of neurofibrillary lesions is highly likely to contribute to the formation of NFTs because (1) aluminum and abnormally phosphorylated t (known as PHFt) are colocalized in NFTs, and (2) aluminum is known to preferentially interact with such phosphorylated proteins. Recently, we demonstrated that aluminum binds selectively to PHFt, induces PHFt to aggregate, and retards the in vivo proteolysis of PHFt. These data suggest that aluminum could serve as cofactor in the formation of NFTs by interacting with PHFt. This review summarizes current understanding of how aluminum might contribute to the formation of neurofibrillary lesions from PHFt in neurons of the AD brain.
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    Regular consumption of a silicic acid-rich water prevents aluminium-induced alterations of nitrergic neurons in mouse brain: histochemical and immunohistochemical studies
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Foglio, E.; Buffoli, B.; Exley, C.; Rezzani, R.; Rodella, L.F.
    Silicon is not generally considered an essential nutrient for mammals and, to date, whether it has a biological role or beneficial effects in humans is not known. The results of a number of studies suggest that dietary silicon supplementation might have a protective effect both for limiting aluminium absorption across the gut and for the removal of systemic aluminium via the urine, hence, preventing potential accumulation of aluminium in the brain. Since our previous studies demonstrated that aluminium exposure reduces the number of nitrergic neurons, the aim of the present study was to compare the distribution and the morphology of NO-containing neurons in brain cortex of mice exposed to aluminium sulphate dissolved in silicic acid-rich or poor drinking water to assess the potential protective role of silicon against aluminium toxicity in the brain. NADPH-d histochemistry and nNOS immunohistochemistry showed that high concentrations of silicon in drinking water were able to minimize the impairment of the function of nitrergic neurons induced by aluminium administration. We found that silicon protected against aluminium-induced damage to the nitrergic system: in particular, we demonstrated that silicon maintains the number of nitrergic neurons and their expression of nitrergic enzymes at physiological levels, even after a 12 and 15 month exposure to aluminium
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    Stress proteins expression in rat kidney and liver chronically exposed to aluminium sulphate
    (Murcia : F. Hernández, 2006) Stacchiotti, A.; Rodella, L.F.; Ricci, F.; Rezzani, R.; Lavazza, A.; Bianchi, R.
    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.