RÉSUMÉ
In a prospective study, the riboflavin nutritional status was evaluated in pregnant women to whom varied vitamin doses were given and in women who did not receive any vitamin supplementation during gestation. Riboflavin nutritional determination was assessed by means of glutathione reductase activation coefficient (GR-AC), and the value higher than 1.5 was considered as indicative of riboflavin deficiency. The pregnant women were divided into four groups: 123 pregnant women to whom any vitamin supplementation were not given, 25 who daily received 2.5 to 3.5mg of riboflavin, 53 who were daily supplemented with 1.0 to 1.7mg of riboflavin, and 22 to whom were daily given 0.85mg of riboflavin. The women group daily supplemented with 2.5 to 3.5mg riboflavin showed the lowest riboflavin deficiency, and the other groups (64.5%) presented vitamin deficiency with GR-AC higher than 1.5. These data suggest that the vitamin concentrations found in the commercially available vitamin supplemented preparations, as well as those found in ingested food were insufficient to provide a good nutritional status for pregnant women. These findings strongly suggest that riboflavin deficiency has in fact been a relevant public health problem in São Paulo city.
Neste estudo prospectivo foi avaliado o estado nutricional em riboflavina nas parturientes que faziam uso da suplementação vitamínica de variadas concentrações de riboflavina, bem como naquelas que não fizeram uso de qualquer suplementação durante o período gestacional. O recurso utilizado para a avaliação nutricional foi a determinação do coeficiente de ativação da glutationa redutase (CA-GRE). Os valores de CA-GRE acima de 1,5 foram considerados como indicativos de deficiência de riboflavina. Foram analisados quatro grupos de gestantes: 123 parturientes sem suplementação vitamínica; 25 que utilizaram formulação contendo de 2,5 a 3,5mg de riboflavina; 63 parturientes que utilizaram fármacos contendo 1,0 a 1,7mg de riboflavina e o quarto grupo constituído de 22 mulheres que receberam formulação contendo 0,85mg de riboflavina. O grupo de parturientes que apresentou menor índice de deficiência de riboflavina foi aquele que fez o uso da suplementação vitamínica com as taxas entre 2,5 a 3,5mg de vitamina B2. Os demais grupos, com a inclusão daquele que não complementou a dieta com suplementação vitamínica, apresentaram índices de deficiências bem maiores. Esses achados indicam que as quantidades de riboflavina apresentadas nesses fármacos, bem como na dieta alimentar, foram insuficientes para atingir níveis bioquímicos semelhantes ao do grupo controle. No geral, foi encontrada
RÉSUMÉ
To elucidate the biochemical basis of impaired skin collagen maturity in pyridoxine-or riboflavin-deficient rats the following two mechanistic possibilities were tested: (i) Reduction in the activity of skin lysyl oxidase (EC 1·4·3·13) which initiates the cross-linking of collagen and (ii) putative rise in homocysteine level leading to neutralization of allysine (α-aminoadipic acid δ-5-semialdehyde)or hydroxyallysine (hydroxy α-aminoadepic acid (δ-semialdehyde) in collagen by the formation of thiazine complexes. Skin lysyl oxidase activity was not affected in pyridoxine deficiency suggesting that pyridoxal phosphate may not be its cofactor. In riboflavin deficiency, lysyl oxidase activity was not altered in the newly regenerated rat skin but a slight reduction was observed in the skin of 18-day-old rat pups. This could be related to the body weight deficit rather than deficiency per se. Aldehyde content of purified salt soluble collagen of regenerated skin was significantly reduced in both the deficiencies. A 2 to 4-fold increase in the concentration of skin homocysteine was observed in both the deficiencies. The results suggest that increase in skin homocysteine level may be responsible for the impaired skin collagen maturity in riboflavin or pyridoxine deficiency.
RÉSUMÉ
A cross sectional investigation among 190 children aged 17-58 months showed: the incidences of riboflavin deficiency, anemia, and iron-lack were 62.4%, 19.6%, and 51.4% respectively. The average concentrations of Hb and SF were lower in riboflavin deficiency(RD) children than those in riboflavin normal(RN) children. The incidences of anemia and iron-lack were 23.8% and 68.8% respectively in RD children, while 6.3% and 17.4% in RN children (P
RÉSUMÉ
The effect of riboflavin deficiency on the fluidity of erythrocyte (RBC) membrane, the level of membrane MDA, the activity of RBC SOD and lipid peroxidation were studied. Growing male rats were fed with an experimental (riboflavin-deficient, RD) or a control (riboflavin-supplemented, RS, 22mg/ kg) diet for 7 weeks.The RBC membrane of RD rats contained higher level of MDA (0.6868?0.1732 nmol/mg protein) compared with the control (0.5548?0.0980 nmol/mg protein), while the activity of RBC SOD (7.745210.6101 nU/mg protein) of RD rats were significantly decreared compared with the control (8.2685?0.3010 nU/mg protein), which indicated the lipid peroxidation was elevated.Membrane fluidity was studied with fluorescence polarization (P) and mean microviscosity (?) using DPH as probe. The value of P and? of RD rats (0.2976 ? 0.0198, 3.9483? 0.3680, respectively) were significantly higher than the RS rats (0.2760 ? 0.0207, 2.875310.4634, respectively), which showed the membrane fluidity in RD rats was decreased according with the increase in lipid peroxidation. This study demonstrated that the RBC membrane fluidity was dicrcased in riboflovin deficient rats. It was relative to the increasing lipid peroxidation and decreasing RBC SOD activity.