Abstract
Aluminium (Al) exposure may affect the liver of experimental animals. This investigation aimed at evaluating morphological changes in rat liver after a single high dose of Al (as metallic powder suspension). A total of forty female Wistar rats were divided in one exposed and one control group, 20 rats each. The exposed rats received 0.5 mL of sterile physiological suspension of fine Al powder in the concentration of 100 mg mL-1 intraperitoneally (50 mg Al per rat). After 7 weeks all animals were killed (by exsanguination from the abdominal aorta in ether anaesthesia). Liver aluminium was analysed using electrothermal atomic absorption spectrometry. For light microscopy the liver tissue was stained with hematoxylin and eosin, and for histochemical analysis with aurin threecarbocsillic acid (aluminon). Liver Al level was markedly higher in the exposed (37.1 microg g-1) than in control rats (0.71 microg g-1). The exposed rats showed crystalloid Al inclusions in the capsular, subcapsular, and portal liver tissue. The basic liver structure remained intact. Slightly multiplied bile ductuli were found in 16 of 20 exposed and in 8 of 20 control rats. Three exposed rats had mycrovesicular steatosis. The peritoneum and Glisson's capsule showed strong macrophage infiltration and a foreign-body-like reaction with multiple giant macrophages containing Al crystalloid inclusions. Although this reaction was a defense against the metal, some Al passed this barrier and entered the liver tissue, exerting toxic effects in bile ductuli and hepatocytes.
Highlights
Aluminium (Al) exposure may affect the liver of experimental animals
Light microscopy showed that the basic liver structure remained intact
Portal areas, which were of standard dimensions, had several gently pigmented, Al-positive macrophages
Summary
Aluminium (Al) exposure may affect the liver of experimental animals This investigation aimed at evaluating morphological changes in rat liver after a single high dose of Al (as metallic powder suspension). The peritoneum and Glisson’s capsule showed strong macrophage infiltration and a foreign-body-like reaction with multiple giant macrophages containing Al crystalloid inclusions This reaction was a defense against the metal, some Al passed this barrier and entered the liver tissue, exerting toxic effects in bile ductuli and hepatocytes. Exposure to Al is almost inevitable, since it is present in water, air, and food, as well as in drugs, as an active substance or an additive It was not until 1975 that Al attracted attention, when the first case of encephalopathy was associated with high quantities of Al in brain cells [1]. This research provided additional evidence to our clinical findings in workers occupationally exposed to Al
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