[Relation between mental deficiency and vitamin C deficiency].
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Plasma ascorbic acid is decreased in women with the pregnancy disorder preeclampsia. We used a mutant strain of rats (Osteogenic Disorder Shionogi), dependent on dietary sources of vitamin C, to investigate whether reduced intake of the vitamin would differentially affect vascular function in late-pregnant (day 19) and age-matched virgin rats. The animals were given either 1 mg/mL of ascorbic acid ad libitum in drinking water [fully supplemented (FS)] or 0.25 mg/mL [marginally supplemented (MS)]. Fetal weights were 21% lower in MS than FS rats, whereas mean maternal weights and pup numbers did not differ. Small mesenteric arteries (diameter, 268+/-7 microm) were mounted in a pressurized arteriograph. Myogenic reactivity (contractile response to step increases in intraluminal pressure) was increased in arteries from MS pregnant compared with FS pregnant rats to levels observed in virgin rats. Ascorbic acid intake did not affect myogenic responses of arteries from virgin rats. Hence, the normal pregnancy-induced reduction in myogenic reactivity was abrogated in MS pregnant animals. Inhibition of nitric oxide synthase had no effect on the myogenicity of arteries from virgin or MS pregnant rats but increased myogenicity of FS pregnant rats to the level of MS pregnant rats. Free radical scavengers reversed the accentuated myogenicity of MS pregnant rats without affecting FS pregnant or virgin rat arteries. These data indicate that moderate ascorbate deprivation increases mesenteric artery myogenic responsiveness during pregnancy. This increase may result from a decrease in nitric oxide-mediated modulation of the myogenic contractile response.
BACKGROUND: Although ascorbic acid (AA) increases dietary iron bioavailability, there has been no food-based community trial of its efficacy in improving iron status. OBJECTIVE: The objective was to assess the efficacy of 25 mg AA as agua de limón (limeade), consumed with each of 2 daily meals, in improving the iron status of iron-deficient women. DESIGN: Two rural Mexican populations were randomly assigned to an AA or a placebo group, each with 18 iron-deficient women. The AA group was given 500 mL limeade containing 25 mg AA twice a day, 6 d/wk, for 8 mo. The placebo group was given a lime-flavored beverage free of AA or citric acid. Beverages were consumed within 30 min of 2 main daily meals. Data were collected on morbidity (3 times/wk), dietary intake (on 6 d), socioeconomic status, parasites (twice), medical history, and response to treatment. Blood samples at 0, 2, 4, 6, and 8 mo were analyzed for hemoglobin, plasma AA, plasma ferritin, transferrin receptors, and C-reactive protein. RESULTS: AA intake was significantly (P < 0.0001) higher in the AA group, but nonheme iron, heme iron, and phytic acid intakes did not differ significantly. Plasma AA was significantly (P < 0.01) higher in the AA group at 2, 4, 6, and 8 mo. There were no final differences between groups in hemoglobin, plasma ferritin, or transferrin receptor concentrations or in the ratio of transferrin receptors to plasma ferritin after control for initial concentrations. CONCLUSION: Increasing dietary AA by 25 mg at each of 2 meals/d did not improve iron status in iron-deficient women consuming diets high in phytate and nonheme iron.
The structure of the familiar antioxidant L-ascorbic acid (vitamin C) was described in 1933 yet remarkably, its biosynthesis in plants remained elusive until only recently. It became clear from radioisotopic labeling studies in the 1950s that plant ascorbic acid biosynthesis does not proceed in toto via a route similar to that in mammals. The description in 1996 of an Arabidopsis thaliana mutant deficient in ascorbic acid prompted renewed research effort in this area, and subsequently in 1998 a new pathway was discovered that is backed by strong biochemical and molecular genetic evidence. This pathway proceeds through the intermediates GDP-D-mannose, L-galactose, and L-galactono-1,4-lactone. Much research has focused on the properties of the terminal enzyme responsible for conversion of the aldonolactone to ascorbate, and on related enzymes in both mammals and fungi. Two of the plant biosynthetic genes have been studied at the molecular level and additional ascorbate-deficient A. thaliana mutants may hold the key to other proteins involved in plant ascorbate metabolism. An analysis of the biosynthesis of ascorbate and its analogues in algae and fungi as well as the study of alternative proposed pathways should broaden our understanding of ascorbate metabolism in plants. With a biosynthetic pathway in hand, research on areas such as the control of ascorbate biosynthesis and the physiological roles of ascorbate should progress rapidly.
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