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Copper (Cu) is a vital mineral essential for many biological processes. The vast majority of all Cu in healthy humans is associated with enzyme prosthetic groups or bound to proteins. Cu homeostasis is tightly regulated through a complex system of Cu transporters and chaperone proteins. Excess or toxicity of Cu, which is associated with the pathogenesis of hepatic disorder, neurodegenerative changes and other disease conditions, can occur when Cu homeostasis is disrupted. The capacity to initiate oxidative damage is most commonly attributed to Cu-induced cellular toxicity. Recently, altered cellular events, including lipid metabolism, gene expression, alpha-synuclein aggregation, activation of acidic sphingomyelinase and release of ceramide, and temporal and spatial distribution of Cu in hepatocytes, as well as Cu-protein interaction in the nerve system, have been suggested to play a role in Cu toxicity. However, whether these changes are independent of, or secondary to, an altered cellular redox state of Cu remain to be elucidated.

After stress or trauma, the serum zinc concentration decreases. This study evaluated possible mechanisms for hypozincemia with the use of a human endotoxemia model. Two doses of endotoxin [lipopolysaccharide (LPS)] were administered on consecutive mornings to 12 healthy volunteers, and each subject was also studied after saline injection. Blood was analyzed for zinc, cytokines (tumor necrosis factor-alpha and interleukin-6), albumin, albumin-zinc binding, and C-reactive protein (CRP). Serial 24-h urine collections were analyzed for zinc. Each LPS dose briefly increased plasma cytokine concentrations and decreased the serum zinc concentration. Serum albumin, the major zinc binding protein, did not decrease, but a progressive increase in CRP was found. LPS did not alter zinc binding affinity to serum albumin. Urine zinc losses were not increased. We conclude that hypozincemia in this model cannot be explained by decreased serum albumin, changes in serum albumin-zinc binding, or increased urinary zinc excretion. Because hypozincemia was transient and followed cytokine peaks, we postulate that LPS-stimulated hypozincemia is mediated, at least partly, by a cytokine-directed internal redistribution of zinc.

The purpose of this study was to descriptively compare the physical activity and dietary intake of public school (PSC) versus home schooled children (HSC). Potential parental and home influences were also examined. Thirty six matched pairs of public school-home school children aged 7-11 years participated in this study. Each participant wore an activity monitor and recorded their dietary intake concurrently for seven consecutive days. PSC had significantly more total and weekday steps, and spent more time in moderate-to-vigorous physical activity compared with HSC. There were no differences in dietary intake between the two groups. These results suggest differences in physical activity between PSC and HSC and encourage further study of public and home school environments, in relation to the obesity epidemic.

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