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The aim of the present work was to study the nephrotoxicity of aluminum lactate administered for 3 months (0.57 mg/100 g bodyweight aluminum, i.p., three times per week) to male Wistar rats. Renal function was studied after 6 weeks of treatment (urine was obtained from rats in metabolic cages) and at the end of the treatment using clearance techniques. Another group of rats was used as kidneys donors at the end of treatment. The renal cortex was separated and homogenized to determine glutathione (GSH) level, glutathione S-transferase (GST) activity and lipid peroxidation (LPO) level. Renal cortex slices were also used to study the p-aminohippuric acid (PAH) accumulation during steady-state conditions and the kinetics of uptake process. Clearance results, at the end of the treatment, indicated that renal functions in treated-rats were not different from those measured in control rats, although the renal concentration parameters differ when they were measured in treated rats after 24 h of food and water deprivation. Balances of water and sodium were also modified at both 1.5 and 3 months of treatment. The activity of alkaline phosphatase (AP) relative to inulin excreted in urine was significantly impaired: controls 2.2+/-0.6 IUI/mg, Al-treated 5.1+/-0.5 IU/mg, P<0.05. These data indicated that proximal tubular cells were loosing apical brush border membranes. Data obtained in cortex homogenates indicated that both GSH and GST activity were significantly decreased, and a significant increase of LPO was noted simultaneously in Al-treated rats. Renal accumulation of PAH, estimated as slice-to-medium ratio, decreased significantly in the Al-treated rats: control rats 3.06+/-0.02 ( n=12), Al-treated rats 2.26+/-0.04 ( n=12), P<0.0001. The maximal rate of uptake was also diminished in treated rats, while the apparent affinity remained unchanged. All these results indicate that aluminum accumulation in renal tissue affects cellular metabolism, promotes oxidative stress and induces alterations in renal tubular PAH transport, together with an impairment in sodium and water balance only detected under conditions of water deprivation, without other evident changes in glomerular filtration rate or other global functions measured by clearance techniques at least at this time of chronic toxicity.

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The chronic exposure to Aluminum (Al) may compromise different liver functions, mainly during the hepatic regeneration. The aim of this study is to investigate the interactions between the chronic i.p. exposure to Al and hepatic regeneration (HR) on bile flow and organic anion transport in experimental animals. For this purpose, we studied bile flow and fractional transfer rates for the transport of hepatic organic anions (hepatic uptake, sinusoidal efflux, and canalicular excretion), as well as parameters related with the oxidative stress (OS), on rats chronically treated with Al at 0 and 2 days of HR. The Al treatment and time of HR caused a decrease in the biliary flow and in the hepatic uptake and canalicular excretion constants. In addition, Al and HR increased the lipoperoxidation associated with a reduction of the glutathione content and glutathione peroxidase and catalase enzyme's activities. Since the effects of Al and HR on biliary flow and transport systems were additive, but not on the oxidative status, different mechanisms might be involved on these alterations. Even though the OS may play a key role on the hepatic deleterious effects, there is no unique cause-effect relationship between OS and liver dysfunction in this experimental animal model.