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Background: When consumed as whole grain, wheat has a high nutrient density that contributes to a healthy diet. However, products labeled as whole wheat can still contain a substantial amount of non-whole grain wheat, leading to confusion for consumers trying to maximize their whole grain intake. A biomarker of whole grain is needed to reveal the whole grain status within wheat-based foods.Objective: Wheat germ agglutinin (WGA), a lectin found predominantly in the germ tissue of wheat kernels, was evaluated as a biomarker of whole grain in commercial wheat products. Methods: The levels of WGA within wheat flour and pasta were assessed by an immunoblot method and compared to a whole grain standard. WGA content was also compared to other biomarkers including starch, minerals, phytate, and total protein content.Results: WGA content tightly correlated with the percentage of whole grain in pre-made mixtures of whole wheat and refined (white) flours. Several commercial flours labeled as whole wheat were then tested for WGA content and found to contain up to 40% less WGA compared to a whole grain standard. Several commercial pasta products labeled as whole wheat were also tested for WGA content and found to contain up to 90% less WGA compared to a whole grain standard. The discrepancies in WGA content were unlikely due to wheat varietial differences alone, as the WGA content measured in common varieties used in domestic wheat flour production varied less than 25%. Other wheat constituents including starch, mineral, phytate, and total protein were less consistent and did not discriminate between the commercial whole wheat flours and pasta products. Conclusions: The WGA content within wheat flour and pasta correlated with the levels of whole grain and identified discrepancies when tested in commercial wheat products compared to a whole wheat standard. WGA is a unique biomarker that could help identify which wheat products have the greatest amount of whole grain wheat.

Age-related macular degeneration (AMD) is the leading cause of severe visual impairment in the elderly in developed countries. AMD patients have elevated levels of iron within the retinal pigment epithelia (RPE), which may lead to oxidative damage to mitochondria, disruption of retinal metabolism, and vision impairment or loss. As a possible model for iron-induced AMD, we investigated the effects of excess iron in cultured human fetal RPE cells on oxidant levels and mitochondrial cytochrome c oxidase (complex IV) function and tested for protection by N-tert-butyl hydroxylamine (Nt-BHA), a known mitochondrial antioxidant. RPE exposure to ferric ammonium citrate resulted in a time- and dose-dependent increase in intracellular iron, which increased oxidant production and decreased glutathione (GSH) levels and mitochondrial complex IV activity. NtBHA addition to iron-overloaded RPE cells led to a reduction of intracellular iron content, oxidative stress, and partial restoration of complex IV activity and GSH content. NtBHA might be useful in AMD due to its potential to reduce oxidative stress, mitochondrial damage, and age-related iron accumulation, which may damage normal RPE function and lead to loss of vision.

Blood transfusion therapy is life-saving for patients with beta-thalassaemia and sickle cell disease (SCD), but often results in severe iron overload. This pilot study examined whether the biomarkers of tissue injury or inflammation differ in these two diseases. Plasma malondialdehyde (MDA) was significantly increased 1.8-fold in thalassaemia relative to control patients. In contrast, MDA in SCD was not significantly different from controls. In multivariate analysis, the strongest predictors of elevated MDA were liver iron concentration (P < 0.001) and specific diagnosis (P = 0.019). A significant 2-fold elevation of non-transferrin bound iron (NTBI) was observed in thalassaemia relative to SCD. NTBI was not a significant predictor of high MDA in multivariate analysis. SCD patients showed a significant 2.2-fold elevation of the inflammatory marker interleukin (IL)-6 relative to controls, and a 3.6- and 1.7-fold increase in IL-5 and IL-10 relative to thalassaemia. Although alpha-tocopherol was significantly decreased by at least 32% in both thalassaemia and SCD, indicating ongoing oxidant stress and antioxidant consumption, gamma-tocopherol, a nitric oxide-selective antioxidant, was increased 36% in SCD relative to thalassaemia. These results demonstrate that thalassaemia patients have increased MDA and circulating NTBI relative to SCD patients and lower levels of some cytokines and gamma-tocopherol. This supports the hypothesis that the biology of SCD may show increased inflammation and increased levels of protective antioxidants compared with thalassaemia.

Zinc deficiency continues to be a major concern of international nutrition, yet there are still few sensitive and reliable biomarkers for identifying moderate zinc deficiency or monitoring changes ...

Iron accumulates as a function of age and is associated with the pathology of numerous age-related diseases. These changes may be caused by altered iron homeostasis at the cellular level, yet this is poorly understood. Therefore, changes in iron content in primary human fibroblasts were studied in culture models of cellular senescence. Total iron content increased exponentially during cellular senescence, reaching approximately 10-fold higher levels than young cells. Increasing intracellular iron levels through iron-citrate supplementation or decreasing intracellular iron levels using iron-selective chelators had little effect on cellular life span and markers of cellular senescence when used at subtoxic doses. However, accelerating cellular senescence with low-dose H(2)O(2) also accelerated senescence-associated iron accumulation. Delaying cellular senescence with N-tert-butyl-hydroxylamine (NtBHA) attenuated senescence-associated iron accumulation. Furthermore, H(2)O(2) or NtBHA had no effect on iron intracellular levels in immortalized fibroblasts. Thus, iron accumulation is not a cause, but a consequence of normal cellular senescence in vitro. Senescence-associated iron accumulation may contribute to the increased oxidative stress and cellular dysfunction seen in senescent cells.

Diet-induced Obesity Decreases Liver Iron Stores in Mice Fed Iron Deficient, Adequate, or Excessive Diets