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Methionine synthetase was measured in the mucosal cells of the rat duodenum, jejunum and ileum by a previously employed method for mucosal cell isolation. No activity was found in these cells. When a dual buffer system for the isolation of villous and crypt cell population was substituted, however, methionine synthetase was found to be active in the duodenum, jejunum and ileum, both in the villous and crypt cell populations. The activity was significantly higher in the crypt cells than in the villous cells throughout the intestine, and higher levels were found in the ileum than in the duodenum or jejunum. As had been previously reported for the rat liver, nitrous oxide in vivo reduced the enzyme activity in both the villous and crypt cell populations, suggesting a role in vivo for the enzyme. We conclude that methionine synthetase is both present and active in the small intestinal mucosal cells of the rat.

1. Pigs were maintained in air or in an atmosphere of nitrous oxide which dramatically changes the S-adenosyl-L-methionine to S-adenosyl-L-homocysteine ratio in neural tissues. Samples of cerebrospinal fluid, cortex, cerebellum and spinal cord were then extracted and analysed for S-adenosyl-L-methionine and S-adenosyl-L-homocysteine. Regression analyses were carried out on values obtained in cerebrospinal fluid and in neural tissues. 2. Highly significant correlations were obtained between levels of S-adenosyl-L-homocysteine (r2 = 0.42-0.69; P less than 0.001) and S-adenosyl-L-methionine/S-adenosyl-L-homocysteine ratios (r2 = 0.56-0.65; P less than 0.001) in cerebrospinal fluid and levels and ratios in cortex, cerebellum and spinal cord. The levels of S-adenosyl-L-methionine did not show a significant correlation. 3. We conclude that the ratio of these metabolites in the cerebrospinal fluid may reflect the ratio in the central nervous system and we suggest that this may also be true in human tissues. This finding will permit the determination of the probable methylation ratio in the central nervous system in human conditions, such as vitamin B12 deficiency and acquired immune deficiency syndrome, where a similar myelopathy occurs to that seen in the nitrous oxide-treated pig. All three myelopathies may arise from an inhibition of methyltransferases involved in the synthesis of myelin that would occur when the methylation ratio is reduced.

The effect of folic acid on zinc absorption and utilization was studied in humans and in rats. Serum Zn response curves after a 25-mg oral dose of Zn was measured for 4 h with and without 10 mg folic acid. The increase in serum Zn expressed as AUC (area under the curve) was 57 mumol/L for Zn alone and 65 mumol/L with folate. Zn intragastric intubation experiments with rats showed that adding 4.4 or 176 micrograms of folate to test meals containing 13 micrograms Zn did not affect the bioavailability of Zn as measured by the retention of 65Zn by the liver and kidney. A 3-wk feeding test carried out with diets containing either 6 or 12 mg Zn/kg diet showed that adding either 2 or 160 mg of folic acid had no effect on growth or Zn uptake by the femur. These results do not indicate any inhibition of Zn utilization by folic acid.

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