Abstract
AbstractFruit bats are an animal model for the neurologic damage which occurs in vitamin B12-deficient humans. Cobalamin (vitamin B12) analogs were not detected in the plasma of fruit bats treated with nitrous oxide (N2O), which inactivates cobalamin. This observation does not lend support to the suggestion that the neurological changes associated with cobalamin inactivation by N2O and/or cobalamin deficiency per se may be related to the accumulation of cobalamin analogs. However, although the plasma of control fruit bats lacked analogs, we did find analogs in their livers, at levels about 10% of total liver corrinoids, similar to human liver analog levels.
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Schedule a callMore From: Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
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