Urinary folate loss following inactivation of vitamin B12 by nitrous oxide in rats.
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.
D000818:Animals; D002848:Chromatography, DEAE-Cellulose; D005492:Folic Acid / Q000652:urine*; D005494:Folic Acid Deficiency / Q000139:chemically induced; D008099:Liver / Q000378:metabolism; D008297:Male; D009609:Nitrous Oxide / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013763:Tetrahydrofolates / Q000652:urine; D013997:Time Factors; D014805:Vitamin B 12 / Q000037:antagonists & inhibitors*
D013763:Tetrahydrofolates; D005492:Folic Acid; D009609:Nitrous Oxide; D014805:Vitamin B 12; C005984:5-methyltetrahydrofolate