Central nervous system injury, gastrointestinal effects, and skin damage are characteristic manifestations of boron toxicity in humans. Liver and kidneys in humans and testes in animals can also be affected. Various clinical and biochemical changes associated with these effects may be measured to detect the extent of exposure to boron. There is no single biological indicator of boron exposure; consequently, several parameters must be measured including boron levels in urine and blood and biochemical changes for systemic and neurological effects.
Neurological damage has been reported in humans. Neurological effects reported in humans have focused primarily on histopathological alterations. No data were provided on biochemical changes. In animals, testicular atrophy and reduced sperm production have been demonstrated following chronic boron exposure. There are clinical and biochemical tests to detect neurological and gonadal injury, but these are not specific for boron exposure. Sparse data in animals suggest some biochemical changes; for instance, cerebral succinate dehydrogenase was increased in rats after boron exposure. Animal data further demonstrate biochemical alterations following gonadal injury. Dose-dependent reduction in hyaluronidase, sorbitol dehydrogenase, and lactic acid dehydrogenase (isoenzyme-X) were observed in rats following boron exposure.
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