The Cu, Fe, and Zn contents of early milk from 102 American mothers were examined in relation to stage of lactation, intake of prenatal mineral supplements, maternal age, parity, and previous history of lactation. A total of 412 samples was collected at three stages of lactation: early transitional (4 to 7 days postpartum); transitional (10 to 14 days postpartum); and mature (30 to 45 days postpartum). For the transitional and mature stages, representative samples of late evening (PM) and early morning (AM) feedings were collected. Diurnal variation in concentration was observed only for Fe. Concentrations of all elements decreased significantly at successive stages of lactation with Zn showing the greatest decline. Cu, Fe, and Zn contents (means +/- SEM) were 104.1 +/- 5.4, 96.5 +/- 6.5, and 520 +/- 20 micrograms/100 g in early transitional milk; 93.9 +/- 3.6, 85.4 +/- 4.5, and 410 +/- 10 micrograms/100 g in transitional milk, and 84.7 +/- 3.8, 76.1 +/- 3.8, and 290 +/- 10 micrograms/100 g in mature milk, respectively. No significant relationship was found between levels of Cu and Zn in milk and whether mothers had taken dietary supplements containing these elements. In addition, no significant correlations were found between maternal age, parity, or previous history of lactation and the elemental content of milk. Based on these data, it was estimated that fully breast-fed infants would receive approximately 0.11, 0.10, and 0.50 mg/kg per day of Cu, Fe, and Zn, respectively, during the neonatal period.

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The potential effects of dietary glutathione on the metabolism of peroxidized lipid ingested in the diet were studied using everted sacs of rat small intestine and peroxidized methyl linoleate. Peroxidized methyl linoleate was added to the luminal side, and the appearance of thiobarbituric acid-reactive (TBA-reactive) material on the contraluminal side was measured. Incubation with N,N,bis(2-chloroethyl)-N-nitrosourea (BCNU) under conditions in which it inhibits the glutathione disulfide reductase/glutathione peroxidase system increased the appearance of TBA-reactive material, indicating that at least a portion of the TBA-reactive material passing through the epithelium is peroxide in nature. Adding glutathione (GSH) to the luminal side substantially decreased the appearance of TBA-reactive material on the contraluminal side, either without or with BCNU treatment. Inhibition of GSH transport and control experiments with GSH, peroxidized methyl linoleate and purified brush border membranes showed that this decrease was due primarily to uptake of luminal GSH and its use to support intracellular GSH-dependent reactions. Thus, the results indicate that exogenous GSH, which can exist in certain diets, can be taken up by the small intestine and used to protect against absorption of lipid peroxidation products.

Biosynthesis of cysteine from methionine via the hepatic transsulfuration pathway is impaired in some cirrhotic patients, who therefore might require cysteine in the diet. However, because further metabolism of cysteine also occurs primarily in the liver, the metabolic clearance of this amino acid could be impaired in cirrhosis. We administered oral loads of L-cysteine to cirrhotic patients and healthy volunteers. Plasma cyst(e)ine (free and protein-bound cysteine, and 1/2 cystine) and urinary sulfur-containing constituents were measured at various times postload. Cirrhotic subjects exhibited a greater maximal plasma cyst(e)ine concentration and plasma elimination half-life (t1/2) and a delayed excretion of metabolic end products after an oral L-cysteine load. The postload increase in total plasma cyst(e)ine was accounted for primarily by an increase in the disulfide form (cystine). These studies show that cirrhotics have an impaired ability to clear cyst(e)ine from the plasma.

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