Influence of bismuth on the number of neurons in cerebellum and hippocampus of normal and hypoxia-exposed mouse brain: a stereological study.

The industrial use of bismuth is increasing. In medicine, bismuth compounds have long been used in the treatment of gastrointestinal disorders, recently in combination with antibiotics for the treatment of Helicobacter pylori-associated peptic ulcers. Bismuth-induced encephalopathy is a known side-effect. One of the symptoms of bismuth encephalopathy is ataxia, suggesting possible cerebellar involvement. The introduction of autometallography (AMG) for tracing BiS/BiSe nanocrystals has provided histochemical evidence supporting the cerebellum being involved in bismuth encephalopathy, but the effect of bismuth on the neuron number in the cerebellum has never been evaluated. In vitro studies have indicated that CA1 neurons may be targets for bismuth intoxication, but results have been conflicting. Recently, the loss of dorsal root ganglion cells was reported after moderate bismuth exposure. This raises the question whether the use of another neurotoxic stimulus, such as hypoxia, amplifies the toxic effects of bismuth. Despite AMG-detectable bismuth accumulations, stereological examinations revealed no statistically significant decrease in the number of Purkinje, CA1 or CA3 neurons or in the volume of the cerebellar granule layer. Surprisingly, intermittent hypoxia led to a statistically significant loss of Purkinje cells without affecting the hippocampus. Bismuth neither ameliorated nor exacerbated the hypoxic effects on the cerebellum.