Effects of aluminum sulfate on delta-aminolevulinate dehydratase from kidney, brain, and liver of adult mice

Abstract

The purpose of the present study was to investigate the in vitro and in vivo effects of aluminum sulfate on delta-aminolevulinic acid dehydratase (ALA-D) activity from the brain, liver and kidney of adult mice (Swiss albine). In vitro experiments showed that the aluminum sulfate concentration needed to inhibit the enzyme activity was 1.0-5.0 mM (N = 3) in brain, 4.0-5.0 mM (N = 3) in liver and 0.0-5.0 mM (N = 3) in kidney. The in vivo experiments were performed on three groups for one month: 1) control animals (N = 8); 2) animals treated with 1 g% (34 mM) sodium citrate (N = 8) and 3) animals treated with 1 g% (34 mM) sodium citrate plus 3.3 g% (49.5 mM) aluminum sulfate (N = 8). Exposure to aluminum sulfate in drinking water inhibited ALA-D activity in kidney (23.3 ± 3.7%, mean ± SEM, P<0.05 compared to control), but enhanced it in liver (31.2 ± 15.0%, mean ± SEM, P<0.05). The concentrations of aluminum in the brain, liver and kidney of adult mice were determined by graphite furnace atomic absorption spectrometry. The aluminum concentrations increased significantly in the liver (527 ± 3.9%, mean ± SEM, P<0.05) and kidney (283 ± 1.7%, mean ± SEM, P<0.05) but did not change in the brain of aluminum-exposed mice. One of the most important and striking observations was the increase in hepatic aluminum concentration in the mice treated only with 1 g% sodium citrate (34 mM) (217 ± 1.5%, mean ± SEM, P<0.05 compared to control). These results show that aluminum interferes with delta-aminolevulinate dehydratase activity in vitro and in vivo. The accumulation of this element was in the order: liver > kidney > brain. Furthermore, aluminum had only inhibitory properties in vitro, while in vivo it inhibited or stimulated the enzyme depending on the organ studied.

Effect of chronic accumulation of aluminum on renal function, cortical renal oxidative stress and cortical renal organic anion transport in rats

“…It has been reported that acute intraperitoneal administration of aluminum induces a temporal diminution of GSH in liver, increases hemooxygenase activity with reduction of cytochrome P450 and, later, an increase in LPO (Jeffery et al 1996). Other authors indicated that aluminum accumulation in liver was accompanied by a decreased GSH level and in a decrease in glutathione peroxidase (El-Maraghy et al 2001), while, in adult mice, exposure to aluminum was proved to inhibit d-aminolevulinate dehydratase activity of kidneys (Schetinger et al 1999). Data described in this work do not allow us to determine the order of development of the events studied.…”

Effect of Long-Term Exposure to Aluminum on the Acetylcholinesterase Activity in the Central Nervous System and Erythrocytes

“…The animals were euthanized 24 h after the last dose and the brains were dissected and collected immediately in beakers and maintained on ice (58C). The citrate was used to increase the aluminum absorption [22], probably by enhancing Al solubility [23]. The weight of the animals was monitored weekly, but no significant change was observed between the different groups during treatment (data not shown).…”

Acetylcholinesterase activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions

“…Citrate was used because it increases Al absorption [27,28], probably by enhancing Al solubility [22].…”