Calcium, zinc, and iron bioavailabilities from a commercial human milk fortifier: a comparison study.

Adding human milk fortifiers (HMF) to human milk (HM) is one way of overcoming the nutrient deficits found in the latter. In this study, the bioavailabilities of calcium, zinc, and iron in S-26/SMA HMF added to HM were compared with those in HM fortified with various bovine milk proteins: alpha-lactalbumin, colostrum, caseinate, casein phosphopeptides, and whey protein concentrate. The bioavailability of each mineral was assessed using an in vitro digestion/Caco-2 cell culture model. Calcium and zinc uptake by the cells was traced with radioisotopes; iron uptake was assessed via cell ferritin levels. Samples were prepared on an equal protein content basis and with added calcium, but no zinc or iron was added. Results revealed that calcium uptake from HM + S-26/SMA was not different from any of the HM fortified with the bovine milk proteins, except for unfortified HM and HM + colostrum in which calcium uptake was significantly lower (-89 and -38%, respectively). Uptake of zinc and iron were significantly higher for HM + S-26/SMA than for the other HM + fortifiers.

Inactivation of human immunodeficiency virus type I in human milk: effects of intrinsic factors in human milk and of pasteurization.

Human milk was inoculated with human immunodeficiency virus type I (HIV-1) or with HIV-1-infected cells in volumes and containers typically used in human milk banks. The inoculated milk was pasteurized at 62.5 degrees C for 30 minutes in a water bath, i.e., conditions currently in use or proposed for human milk pasteurization. The process of HIV-1 inoculation and pasteurization effectively inactivated the infectivity of both cell-free HIV-1 and HIV-1-infected cells. No virus was recovered after the process, even after repeated subculturing in attempts to rescue the virus. Pasteurization reduced the infectious titer of cell-free HIV-1 and HIV-1-infected cells by more than 5 logs and 6 logs respectively. Human milk contains one or more components that inactive HIV-1 but that are not toxic for the cells used to replicate virus. These components have not been identified, but physical and solubility properties are consistent with characteristics of lipids.

Addition of the chromophore to rat rhodopsin is an early post-translational event.

Rat retinas were labeled either by intravitreal injection of [14C]leucine or by incubation with [3H]-leucine or [35S]-methionine. Subcellular fractions were prepared on linear sucrose gradients and rhodopsin was extracted with detergent and purified by chromatography on ConA-Sepharose. A fraction enriched in rough endoplasmic reticulum (RER) and substantially free of rod outer segments (ROS) was found to contain a light-sensitive protein exhibiting the properties of rhodopsin on ConA-Sepharose or Agarose chromatography and on SDS-polyacrylamide gel electrophoresis, as well as immunologically. Intravitreal injection of [3H]-retinol also labeled the rhodopsin in the RER under conditions in which the rhodopsin in the ROS was not heavily labeled. Thus the chromophore appears to be attached to opsin shortly after the apoprotein is translated in the RER.

A novel photopigment candidate in membranes of cultured chick pineal cells.

The photopigment of avian pineal which mediates light sensitivity was sought via its chromophore. Chick pineal cells in primary cultures were incubated overnight in the dark with [3H]retinol. Reduction of Schiff's bases with cyanoborohydride prior to SDS-PAGE revealed radioactivity bound to a 30 kDa component in pinealocyte membranes. All-trans-retinal, but not retinol or retinoic acid, incubated with pinealocyte homogenates prior to reduction, resulted in a loss of radioactivity from the 30 kDa region of the gel. The radioactivity was also displaced by NH2OH in the dark. Incubation of cultured cells or homogenates with retinoyl fluoride, an acylating agent specific for the retinal binding site of opsins, also displaced radioactivity from the protein. Furthermore, retinoyl fluoride, added to chick pineal cells in culture, blocked the suppressive effect of light on melatonin output by these cells. Taken together these results raise the possibility that the 30 kDa protein mediates photosensitivity in the chick pineal.

Vitamin A status needed to maintain vitamin A concentrations in nonhepatic tissues of the pregnant rat.

Vitamin A-depleted pregnant rats were fed diets containing 0, 1, 10 or 100 retinol equivalents (REq)/d during gestation. Maternal tissues of these dams, their placentas and fetuses were assayed for total vitamin A (retinol and its esters) at gestational ages 10, 13, 16 or 19 d. The vitamin A concentrations in placenta and fetuses of dams fed 10 REq/d were significantly different from those of dams fed no vitamin A. This difference was not seen in any of the six other maternal tissues assayed. We suggest that the fetus is at greater risk than other maternal tissues during severe vitamin A deprivation. For vitamin A-deprived dams, linear regression analysis indicated strong relationships between the vitamin A concentrations of nonhepatic tissues and their liver vitamin A concentrations. In contrast, among vitamin A-replete dams, these relationships were not statistically significant. An estimate was made of the minimal vitamin A status corresponding to tissue repletion by solving linear equations described by the data of the depleted dams for the vitamin A concentrations found in tissues of replete dams. This analysis revealed that a maternal vitamin A status of 3 micrograms/g liver was needed to provide the level of vitamin A found in the placenta, whole fetus and maternal tissues of vitamin A-replete dams.

Vitamin A supplementation and plasma retinol levels: a randomized trial among women.

Although dietary intake of vitamin A has little, if any, overall effect on blood retinol in generally well-nourished populations, subgroups may exist that would be responsive to supplementation. The hypothesis that vitamin A supplementation increases blood retinol in apparently well-fed individuals with lower than usual blood levels was tested in female health workers, with relatively low blood retinol values, who were randomly assigned to receive vitamin A (10,000 IU daily) or placebo. After 4 weeks the mean change in plasma retinol was -0.4 micrograms/dl for the group receiving placebo and +4.1 micrograms/dl (an increase of 9% over base-line values) for the group receiving vitamin A (P = .02). The results were similar when the base-line retinol level and several other covariates were considered. Thirteen women who had initially received placebo were then switched to vitamin A for 4 weeks. These women experienced a mean increase of 5.3 micrograms/dl in plasma retinol (P = .04). Responses to vitamin A supplementation tend to be greater among women with lower previous total vitamin A intake, as assessed by questionnaire [Spearman rank correlation coefficient (r) = 0.50; P = .01].

Vitamin A and retinol-binding protein in amniotic fluid.

Amniotic fluid and serum samples that had been obtained from mothers at 10 to 33 wk of gestation were analyzed for retinol and retinol-binding protein. No difference was found in serum retinol with advancing gestation. The concentration of retinol in amniotic fluid from 20 wk onward was significantly greater than at 16 to 18 wk. No esters of retinol and no carotenoids were detected in amniotic fluid. Serum and amniotic fluid samples from the same mothers were significantly correlated for retinol (p less than 0.02). Retinol-binding protein, detected by radial immunodiffusion, was found in amniotic fluid in molar excess of, and significantly (p less than 0.001) correlated with, retinol in amniotic fluid. Retinol in amniotic fluid obtained at 16 to 18 wk from pregnancies that ended in anencephaly or other congenital defects ranged from 2.3 to 18.0 micrograms/dl. The range of amniotic fluid values in abnormal pregnancy precludes using retinol or retinol-binding protein as a marker in prenatal diagnosis of abnormalities.

Effect of maternal protein-calorie malnutrition on fetal rat cerebellar neurogenesis.

Pregnant Sprague-Dawley rats were fed, ad libitum, diets containing either 24% (control) or 4% casein (deprived) from conception through gestation. On the 13th, 14th, 15th, 16th, 17th or the 18th day of gestation the dams of both dietary groups were injected with 2.5 mCi [3H]thymidine per gram of body weight. Pups born to these dams were reared by stock diet-fed foster mothers to insure normal postnatal nutrition and were killed on postnatal day 28. Retention of isotope in the nuclei of four types of macroneurons, as visualized in autoradiographs prepared from cerebellar tissues, was used to determine the time of final DNA synthesis in these cells. In the brains of animals malnourished in utero, the time of administration of the label which resulted in maximal retention and peak cerebellar neurogenesis had occurred as early as the 13th day of gestation.