Retinol status and associated factors in mother-newborn pairs.

BACKGROUND: Vitamin A deficiency is still considered to be a nutritional problem during pregnancy, lactation and early childhood. The present study aimed to assess the vitamin A status of women and their newborns in the Brazilian Northeast and to determine the association between retinol in the maternal serum, umbilical cord blood and colostrum. METHODS: Vitamin A status in 65 pairs of women and newborns was assessed from samples of the mother's serum, umbilical cord serum and colostrum using high-performance liquid chromatography. The inadequacy of the vitamin A status of mothers and infants was identified if the retinol values were <0.7 µmol L- 1 in maternal serum or umbilical cord blood or <1.05 µmol L-1 in colostrum. RESULTS: The prevalence of inadequate maternal vitamin A status was 21.5% (95% CI: 11.5%-31.5%) and 13.8% [95% confidence interval (CI) = 5.4%-22.2%] based on maternal serum and colostrum, respectively. Among newborns, 41.5% (95% CI = 29.3%-53.5%) presented a low status of vitamin A based on cord serum. Multiple linear regression analysis identified that maternal serum retinol is a predictor of umbilical cord retinol (P = 0.005). Retinol in maternal serum was lower in mothers who were less educated (P = 0.04) and colostrum retinol was higher in older (P = 0.04) and multiparous (P = 0.002) mothers. CONCLUSIONS: Vitamin A deficiency is a common problem among mothers attended in public hospitals in Northeast Brazil and maternal retinol concentrations are associated with retinol status in newborns. Maternal age, parity and educational level were related to the maternal vitamin A status.

Effect of RRR-α-tocopherol supplementation on serum of breastfeeding women up to 60 days after delivery: a randomised controlled trial.

BACKGROUND: Maternal supplementation is a viable strategy to combat vitamin E deficiency in newborns, although a protocol for maternal vitamin E supplementation has not been defined. The present study assessed the effect of maternal supplementation in a single dose on the serum of postpartum women up to 60 days after delivery. METHODOLOGY: Fifty healthy breastfeeding women were recruited at two maternity hospitals both located in Natal, RN, Brazil. The participants were randomly allocated to a control group and a treatment group in a 1 : 1 ratio. Serum was collected 1, 20, 30 and 60 days after delivery. Immediately after the first collection, the treatment group received a single dose of 400 IU of RRR-α-tocopherol. α-Tocopherol was quantified by high-performance liquid chromatography. The usual dietary vitamin E intake was determined using four 24-h recalls, and intake adequacy was assessed based on the estimated average requirements for lactating women (16 mg day-1 ). RESULTS: The mean dietary vitamin E intakes of the both groups were similar (P > 0.05) and inadequate. The serum levels of α-tocopherol assessed at 1, 20, 30 and 60 days indicated adequate vitamin E status in both the control group (1194.6, 907.7, 910 and 748.6 µg dL-1 , respectively) and treatment group (1183.7, 956.0, 935.9 and 766.4 µg dL-1 , respectively). The comparison at each day showed no difference between treatments (P > 0.05). CONCLUSIONS: A single vitamin E supplement did not change the mean serum level of α-tocopherol in breastfeeding women; thus, it does not improve their vitamin E status in the first 60 days after delivery.

Maternal supplementation with a megadose of vitamin A reduces colostrum level of α-tocopherol: a randomised controlled trial.

BACKGROUND: Maternal supplementation with vitamin A is one of the strategies for controlling its deficiency in the mother-child dyad, although studies with animals showed that supplementation with high doses of vitamin A reduces the levels of α-tocopherol (vitamin E) in the mother's serum and milk. The objective of the present study was to assess the influence of maternal supplementation with vitamin A on the concentration of retinol and α-tocopherol in human milk. METHODS: Healthy puerperal women were randomly distributed into a control group (n = 44) and a supplemented group (n = 44). Blood and colostrum samples were collected after delivery, and mature milk samples were collected 30 days later. The supplemented group received 200 000 IU of retinyl palmitate after the first colostrum collection. The retinol and α-tocopherol levels in the samples were determined by high-performance liquid chromatography. RESULTS: The mean (SD) retinol and α-tocopherol levels in the maternal serum were considered adequate at 46.4 (15.9) and 1023.6 (380.4) µg dL(-1) , respectively. The colostrum retinol levels of the supplemented group increased significantly 24 h after the intervention (P < 0.001). However, the retinol levels in the mature milk of both groups did not differ (P > 0.05). Moreover, after maternal supplementation with vitamin A, the colostrum α-tocopherol level decreased by 16.4%, which is a significant reduction (P < 0.05). However, vitamin A supplementation did not affect the α-tocopherol level of mature milk (P > 0.05). CONCLUSIONS: Maternal supplementation with high doses of vitamin A increased the colostrum level of this nutrient but reduced the bioavailability of α-tocopherol, which may harm the newborn's health because newborns have limited vitamin E reserves.

Alpha-tocopherol concentration in the colostrum of nursing women supplemented with retinyl palmitate and alpha-tocopherol.

BACKGROUND: Vitamins A and E are recognisably important in the initial stages of life, and the newborn depends on nutritional adequacy of breast milk to meet their needs. These vitamins share routes of transport to the tissues and antagonistic effects have been observed in animals after supplementation with vitamin A. The present study aimed to determine the effect of maternal supplementation with a megadose of retinyl palmitate in the immediate post-partum on α-tocopherol concentration in the colostrum. METHODS: Healthy parturient women at a Brazilian public maternity were recruited for the study and divided into two groups: control (n = 37) and supplemented (n = 36). Blood and colostrum samples were collected up to 16 h post-partum. The supplemented group was administered with a retinyl palmitate capsule and, 24 h after the first collection, the second colostrum sample was obtained in the two groups for analysis of α-tocopherol. The cut-off points for deficiency are <1.05 µmol L(-1) for retinol and <11.6 µmol L(-1) for α-tocopherol. RESULTS: The mean (SD) serum concentration of 1.77 (0.50) µmol L(-1) for retinol and 30.81 (6.46) µmol L(-1) for α-tocopherol indicates an adequate biochemical status. The supplemented group showed an increase of α-tocopherol in the colostrum 24 h after supplementation (P = 0.04), and this finding was not observed in the control group. CONCLUSIONS: Supplementation with a 200,000 IU megadose of vitamin A did not negatively affect α-tocopherol levels in colostrum.

Nutritional vitamin A status in northeast Brazilian lactating mothers.

BACKGROUND: Vitamin A deficiency is the major cause of morbidity and mortality among children and in women of reproductive age in developing countries. The present study aimed to assess maternal nutritional vitamin A status, as well as analyse the association of preformed vitamin A and pro-vitamin A consumption on the nutritional status of nursing mothers, based on serum retinol and retinol colostrum concentrations coupled with dietary intake. METHODS: Serum and colostrums were collected from 86 healthy parturients, recruited within 16 h postpartum. Blood samples were obtained, the morning after an overnight fast. Retinol was analysed by high-performance liquid chromatography. Dietary vitamin A was assessed using a food frequency questionnaire and the women were separated into two groups according to the predominant dietary source of vitamin A: group A, > 50% preformed vitamin A (n = 37); and group B > 50% pro-vitamin A carotenoids, (n = 49). RESULTS: Serum retinol and total vitamin A ingestion (mean +/- SD) were higher in group A than in group B (1.4 +/- 0.4 micromol L(-1) and 2072.0 +/- 1465.9 microg retinol activity equivalent (RAE) day(-1) versus 1.2 +/- 0.6 micromol L(-1) and 1051.6 +/- 920.4 microg RAE day(-1), respectively (P < 0.05), but colostrum retinol (3.4 +/- 1.7 micromol L(-1) and 3.6 +/- 1.9 micromol L(-1)) was similar in both groups. In group B, 36.7% (n = 18) of the nursing mothers presented a risk of developing vitamin A deficiency, based on their dietary intake. CONCLUSIONS: On the basis of the intake of the pro-vitamin A carotenoids, some women may be at risk of vitamin A deficiency. However, their status is currently normal, as indicated by serum and milk retinol concentrations.

Effect of retinyl palmitate supplementation on egg yolk retinol and cholesterol concentrations in quail.

1. The purpose of this study was to assess the incorporation of retinol into quail egg yolk and cholesterol concentration in response to supplementation with different quantities of retinyl palmitate (600, 1200, 2400 and 4800 microg). 2. Supplementations were performed weekly for 4 weeks and the yolk retinol was measured using high performance liquid chromatography. 3. The results showed a progressive increase in the incorporation of retinol into the egg yolk in response to supplementation, reaching values 384% higher than control values. 4. At the end of supplementation we observed a significant decrease in egg yolk retinol concentrations with supplementations of 2400 and 4800 microg, the most enduring showing high retinol contents even after 3 weeks. 5. Supplementation increased egg weight but neither egg production nor cholesterol levels were significantly altered.

Alterations in the levels and lipid composition of plasma lipoproteins (VLDL, LDL and HDL) in Brazilian patients with hepatosplenic schistosomiasis mansoni.

1. The plasma concentrations of low- and high-density lipoproteins (LDL and HDL) were significantly reduced in Brazilian patients with compensated hepatosplenic schistosomiasis mansoni (SM) when compared with healthy individuals, but very low-density lipoprotein (VLDL) levels were unchanged. 2. All three classes of lipoproteins isolated from SM plasma had an increased content of triacylglycerol and unesterified cholesterol and decreased cholesteryl ester and phospholipid. 3. The individual phospholipid composition of patient VLDL, LDL, HDL was also altered; the amount of phosphatidylcholine was increased and that of lysophosphatidylcholine decreased. 4. The saturated and monounsaturated fatty acyl content of cholesteryl esters in patient lipoproteins was also significantly increased, and diunsaturated and polyunsaturated fatty acyl content was decreased. 5. When isolated lipoproteins were examined as negatively stained preparations by electron microscopy, the morphology of SM patient LDL was normal but the HDL fraction was abnormal and showed marked heterogeneity of size with the presence of occasional discoidal particles which resembled "nascent" HDL.

Alterations in the fatty acyl composition of plasma cholesteryl esters in Brazilian patients with hepatosplenic schistosomiasis mansoni.

1. The dyslipoproteinemia commonly occurring in the hepatosplenic forms of schistosomiasis mansoni in Brazilian patients is characterized by low plasma levels of cholesteryl esters and of the cholesterol-esterifying enzyme, lecithin:cholesterol acyltransferase (LCATase, EC.2.3.1.43). 2. In the present study, normal healthy individuals and patients suffering from hepatosplenic schistosomiasis mansoni were compared for the fatty acyl compositions of circulating plasma cholesteryl esters and of those formed in vitro by the action of LCATase on a) the endogenous plasma lipoproteins and b) an excess of lipoprotein substrate composed of heat-inactivated plasma. 3. In patient plasma the proportions of saturated and monounsaturated cholesteryl esters were higher and those of diunsaturated and polyunsaturated esters were lower than in the control group. 4. Similar differences were observed between patients and controls in the proportions of the cholesteryl ester subclasses formed in vitro by the action of LCATase on endogenous plasma lipoproteins. 5. Incubation of fresh normal or patient plasma with excess heat-inactivated plasma as substrate for LCATase produced proportions of cholesteryl ester subclasses similar to those formed during incubation of nonheated aliquots of the appropriate substrate plasma. 6. We conclude that the alterations in fatty acyl composition of plasma cholesteryl esters in patients with hepatosplenic schistosomiasis mansoni do not appear to be a direct consequence of the low levels of LCATase activity in patient plasma.

Decreased plasma lecithin:cholesterol acyltransfer and associated changes in plasma and red cell lipids in uraemia.

Plasma lipids, lecithin:cholesterol acyltransferase (LCAT) activity and erythrocyte lipid composition were compared for a group of newly diagnosed uraemic patients and a group of healthy subjects. Plasma triacylglycerol was increased and both total and high-density lipoprotein (HDL) cholesterol were decreased. A lower percentage of total cholesterol in patients' plasma was in the esterified form and plasma values of the phospholipid, lysolecithin, were also lower. The plasma LCAT activity of uraemic patients, whether expressed as nmol or percentage of cholesterol esterified per hour, was significantly lower than for normals. Both LCAT activity and lysolecithin in uraemic plasma were inversely correlated with the concentration of urea. The lipid composition of erythrocytes from patients was also abnormal, with both free cholesterol and lecithin being increased. These results are consistent with the occurrence of an acquired deficiency of LCAT in uraemia, comparable to that previously described in hepatic disease. The LCAT enzyme is secreted by the liver, and the inverse correlation noted in this study between LCAT activity and urea suggests that the increased urea in renal disease may inhibit the synthesis and secretion of the enzyme by the liver. The resulting reduction in LCAT activity may lead to the accumulation of cholesterol and lecithin in cell membranes and contribute to the overall pathophysiology of renal disease.

The phospholipase activities present in preheparin mouse plasma are inhibited by antiserum to hepatic lipase.

1. Preheparin plasma from mice, but not rats or man, contains high levels of phospholipase A and lysophospholipase activities which are distinct from lecithin:cholesterol acyltransferase (LCAT). 2. Neither the phospholipase A nor the lysophospholipase activities in preheparin plasma are inhibited by incubation in the presence of protamine sulphate or high salt concentrations. 3. When mouse plasma is incubated in the presence of an antiserum specific for rat hepatic triacylglycerol lipase (HTGL), the phospholipase activities are abolished. 4. These observations suggest that the phospholipase activities are attributable to the action of HTGL, which, in the mouse appears to be a freely circulating enzyme, whereas for other species this enzyme only appears in the blood following administration of heparin.

Influence of hypoxanthine and other purines on the lecithin:cholesterol acyltransferase reaction in the plasma of rat and other species.

1. Esterification of radiolabelled cholesterol in the plasma of rat, mouse, pig, ox and, to a lesser extent, guinea pig was partially inhibited by hypoxanthine, xanthine and guanine; esterification in human plasma and in plasma from 12 other vertebrate species was unaffected by purines. 2. Esterification of endogenous cholesterol and the formation of lysolecithin in rat plasma were decreased in the presence of purines indicating that it was the lecithin:cholesterol acyltransferase (LCAT) reaction that was inhibited rather than the isotopic equilibration of labelled cholesterol with the endogenous substrate lipoproteins. 3. Maximum inhibition of the LCAT reaction in rat plasma occurred at 1.4 mM hypoxanthine or xanthine; inhibition was not dependent upon the concentration of LCAT or plasma lipoproteins but increased with the amount of lipoprotein depleted rat plasma (LDRP) present in the incubation mixture. 4. Partial inhibition of the LCAT reaction in rat or mouse plasma by purines had no significant effect on the fatty acyl composition of the cholesteryl esters (CE) formed by LCAT. 5. In the presence of heated rat plasma, LDRP or, to a lesser extent, rat high density lipoproteins (HDL) prepared from heated plasma, the LCAT reaction in human plasma was inhibited by hypoxanthine. 6. Rat HDL and LDRP prepared from plasma pre-incubated at 37 degrees C for 4 hr before heating increased and decreased, respectively, the inhibitory effect of hypoxanthine on human plasma LCAT compared with HDL and LDRP prepared from unincubated rat plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of subadequate maternal vitamin-A status on placental transfer of retinol and beta-carotene to the human fetus.

The placental transfer of retinol and beta-carotene was assessed based on maternal serum, cord serum and placental levels at term parturition in women with adequate (n = 15; serum retinol > 20 micrograms/dl) and subadequate (n = 16; serum retinol < or = 20 micrograms/dl) vitamin-A status. There was no difference in retinol and beta-carotene levels in placenta and cord serum between these groups. However, differences in the relation of maternal, placental and cord blood components were observed between women with adequate and subadequate vitamin-A status. In women with subadequate status, circulating fetal retinol levels correlated with placental retinol levels, and maternal serum beta-carotene correlated with placental retinol. Within this group, maternal serum beta-carotene and cord serum retinol correlated significantly in women with serum retinol levels lower than 15 micrograms/dl. These results suggest that beta-carotene may be a precursor of retinol in placenta and that this conversion may depend on the nutritional status of the mother, being particularly effective in a more depleted state.

Alterations in the levels and lipid composition of plasma lipoproteins (VLDL, LDL and HDL) in Brazilian patients with hepatosplenic schistosomiasis mansoni

1. The plasma concentrations of low- and high-density lipoproteins (LDL and HDL) were significantly reduced in Brazilian patients with compensated hepatosplenic schistosomiasis mansoni (SM) when compared with healthy individuals, but very low-density lipoprotein (VLDL) levels were unchanged. 2. All three classes of lipoproteins isolated from SM plasma had an increased content of triacylglycerol and unesterified cholesterol and decreased cholesteryl ester and phospholipid. 3. The individual phospholipid composition of patient VLDL, LDL, HDL was also altered; the amount of phosphatidylcholine was increased and that of lysophosphatidylcholine decreased. 4. The saturated and monounsaturated fatty acyl content of cholesteryl esters in patient lipoproteins was also significantly increased, and diunsaturated and polyunsaturated fatty acyl content was decreased. 5. When isolated lipoproteins were examined as negatively stained preparations by electron microscopy, the morphology of SM patient LDL was normal but the HDL fraction was abnormal and showed marked heterogeneity of size with the presence of occasional discoidal particles which resembled nascent HDL

Alterations in the fatty acyl composition of plasma cholesteryl esters in brazilian patients with hepatosplenic schistosomiasis mansoni

1. The dyslipoproteinemia commonly occurring in the hepatosplenic forms of schistosomiais mansoni in Brazilian patients is characterized by low plasma levels of choleteryl esters and of the cholesterol-esterifying enzyme, lecithin:cholesterol acyltransferase (LCATase, EC.2.3.1.43). 2. In the present study, normal helathy individual and patients sufferin from hepatosplenic schistosomiasis mansoni were comapred for the fatty acyl compositons of circulating plasma cholesteryl esters and of those formed in vitro by the action of LCATase on a) the endogenous plasma lipoprotins and b) an excess of lipoprotein substrate composed of heat-inactivated plasma. 3. In patient palsma the proportions of saturated and monounsaturated cholesteryl esters were higher and those of diunsaturated and polyunsaturated esters were lower than in the control group. 4. Similar differences were observed between patients and controls in the proportions of the cholesteryl ester subclasses formed in vitro by the action of LCATase on endogenous plasma lipoprotins. 5. Incubation of fresh normal or patient plasma with escess heat-inactivated plasma as substrate for LCATase produced proportions of cholesteryl ester subclasses similar to those formed dduring incubation of nonheated aliquots of the appropriate plasma. 6. We conclude that the alterations in fatty acyl composition of palsma cholesteryl estes in patients with hepatosplenic schistosomiasis mansoni do not appear to be direct consequence of the low levels of LCATase acivity in patient plasma