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The metabolism and intracellular recycling of methionine requires vitamin B12 as cofactor and methyltetrahydrofolate as coreactant. To examine the interrelationship between serum levels of methionine, vitamin B12 and folate, serum methionine levels were assayed in patients with reduced levels of these vitamins and in healthy subjects. Approximately half the patients with either vitamin B12 or folate deficiency, and more than half those with combined deficiency, had methionine levels below the reference range (37-136 mumol/l). There was no correlation between vitamin B12 or folate and serum methionine levels within the healthy group. There was also no correlation within the group with low folate levels. Within the vitamin B12 deficient group on the other hand, the correlation was highly significant (r = 0.547, p less than 0.001). The finding that many patients with vitamin B12 or folate deficiency have normal serum levels of methionine suggests a significant role for other factors such as betaine-dependent methionine synthesis in the maintenance of serum methionine concentrations.

Supplementation of the diet with valine or isoleucine protects the fruit bat from neurological impairment associated with experimentally induced vitamin B12 deficiency. Valine and isoleucine are precursors in the vitamin B12 dependent propionic acid pathway and it is proposed that they exert their protective effect through stimulation of this pathway. This suggests that the previously observed protective effect of methionine may be mediated also through this pathway, since methionine may be metabolised via the transsulfuration pathway to propionyl CoA. The results of this study refocus attention on the propionic acid pathway, and specifically on the methylmalonyl CoA mutase reaction, as central to the biochemical basis of the vitamin B12 neuropathy.

Ferritin levels in serum and milk were investigated in series of 15 urban and 18 rural black mothers. No mother was anaemic. Mean serum ferritin levels in the urban and rural groups were 57 +/- 55 ug/l and 25 +/- 28 ug/l (mean +/- SD). Corresponding milk ferritin concentrations were 21 +/- 22 ug/l and 29 +/- 30 ug/l respectively. The significance of ferritin in human milk is discussed.

The fruit bat Rousettus aegyptiacus develops cobalamin deficiency when exposed to the gas nitrous oxide (N2O). The effect of dietary methionine (600 mg/kg fruit) or L-3, 4-dihydroxyphenylalanine (L-dopa, 100 mg/kg body weight daily) on brain and liver S-adenosylmethionine (AdoMet) concentrations, and on the neurological impairment was studied. Methionine supplementation significantly delayed the onset of neurological impairment (p less than 0.01) and resulted in a 2.4 fold increase in liver AdoMet levels. Brain AdoMet levels were unchanged. L-dopa, which is methylated by means of AdoMet did not aggravate the N2O-induced neuropathy but did lower, albeit insignificantly, brain AdoMet levels. The results do not support the hypothesis that the neurological impairment and death in cobalamin inactivated bats is a result of a depletion of methionine or AdoMet in the nervous system.

The consumption of indigenous cereal-based fermented beer is widespread throughout Africa and other parts of the world. In some countries such beer is brewed commercially as well as at home. As evidence of beri-beri may occur in habitual consumers of the beer, the thiamin content of beer brewed commercially from a mixture of sorghum and maize was investigated. Thiamin concentration in beer averaged 0.33 mg/l, with more than 95% in the cellular fraction, mainly live yeast cells. The thiamin in the cells is not generally available for absorption and the cells take up thiamin added to the beer. At low concentrations (0.25-0.5 mg/l) up to 90% of added 14C-thiamin was taken up by the cells but with concentrations in excess of 2.5 mg/l, the uptake was less than 30%. These results indicate that fortification of sorghum beer with thiamin is feasible. The addition of 2.5 mg/l would supply up to 1.6 mg of absorbable thiamin and thus meet the recommended daily allowance in the target group of habitual consumers.

The fruit bat Rousettus aegyptiacus, when exposed to nitrous oxide (N2O) for 8-10 weeks develops cobalamin deficiency and neurological impairment leading to ataxia and death. We report the lipid composition of cerebral tissue of control animals and impaired animals following exposure to N2O, with or without dietary folic acid supplements. There were no statistically significant differences in the concentrations of total lipids, phospholipid, glycosphingolipid, plasmalogen and cholesterol between the different groups, although the ratio of choline phosphoglyceride to ethanolamine phosphoglyceride in N2O exposed animals was slightly lower than in controls. Bats exposed to N2O showed slightly higher levels of the fatty acid linoleate (18:2) in their phosphatidylethanolamine relative to arachidonate (20:4) compared with controls. This increase tended to be more pronounced in the bats receiving dietary folic acid supplements (but p greater than 0.05).

Niacin status was evaluated in groups of school children (n = 25) in Transvaal Province, South Africa, by measuring the urinary excretion of the metabolite 2-pyridone. In an urban Indian group of low socioeconomic status, and a white middle-class group, 12% and 4% respectively exhibited low or deficient levels of the metabolite. In a rural black village, 28% had evidence of low or deficient levels of niacin, even though two of the 3 locally available brands of maize meal (their dietary staple) claimed to be fortified with nicotinamide. It is concluded that external monitoring of the voluntary maize meal fortification scheme will be necessary to effectively combat deficiency of niacin in traditional maize meal consumers.