Rats were injected with [2-14C]H4PteGlu daily for 3 d and thereafter one group left in air and a second group in an atmosphere of nitrous oxide/oxygen (1/1). Nitrous oxide inactivates cobalamin. The N2O-treated rats excreted large amounts of L. casei-active folate into the urine. The urinary folate co-chromatographed with authentic 3H-labelled 5-methyltetrahydrofolate. Both groups of animals excreted 14C-labelled breakdown products in the urine but there was no evidence of increased folate catabolism in the N2O-treated rats. It was concluded that the folate deficiency that develops in the N2O-treated rat is due to massive urinary loss of folate. This appears to be secondary to impaired cellular uptake of folate which leads to a raised plasma folate level.
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Lumb et al. (1982) studied this question.
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