Objectives: Free radicals are implicated in many diseases. The rise in free radicals associated with antioxidant de®ciency results in tissue damage. The pathogenesis of oedema and anaemia commonly found in children with protein-energy malnutrition (PEM) has been suggested to be caused by an imbalance between the production of toxic radicals and their safe disposal. The aim of this study was to evaluate antioxidant status in children with PEM. Design: A total of 68 children (age range: 3 months to 3 years) living in Cairo, Egypt were recruited. Forty-six of these subjects had different degrees of PEM; they were admitted at the Abo-Elrish Hospital, Cairo. Of these, 26 children had kwashiorkor (KWO) and twenty had marasmus (MAR). Twenty-two age and sex matched healthy well-nourished children were recruited from the local community, and used as controls. Methods: The antioxidant status of the study population was determined by measuring copper-zinc superoxide dismutase (Cu ± Zn, SOD) in red blood cells, glutathione peroxidase (GPX) in whole blood, and ceruloplasmin in plasma. In addition, the plasma levels of trace-elements involving antioxidant activities, such as copper (Cu), zinc (Zn), and selenium (Se) were determined, along with a select group of vitamins. The latter included vitamin A (retinol), vitamin E (a-tocopherol) and vitamin C (ascorbic acid). Results: The mean whole blood GPX activity along with plasma levels of vitamins A, E and C as well as ceruloplasmin, Cu and Se were all lower in children with either KWO or MAR than their corresponding control subjects. The erythrocyte SOD activity, on the other hand, was increased while the plasma Zn concentrations were either increased or not changed in the malnourished children. It was of interest that while haemoglobin concentrations were decreased, the plasma free iron (Fe) levels were signi®cantly increased in children with KWO. Conclusions: The signi®cant increase in red cell SOD activity associated with the decrease in plasma ceruloplasmin, antioxidant vitamins and the whole blood GPX activity in PEM children suggest that these children are potentially susceptible to high oxidative stress. An elevated plasma Fe concentrations, especially with KWO may augment the harmful effect of free radicals with a clinical consequence of oedema. Sponsorship: This study was ®nancially supported by The

Objective: To examine changes in radial bone density and biochemical status, with particular reference to calcium, over 18 months in a group of older men. Subjects: Thirty-six healthy men (aged 66 ± 76 y) were recruited to the study during July and August, 1993. These men were free-living residents of Edmonton who were recruited through local organizations for the retired and semi-retired. Data for the younger group of men (age 29 ± 60 y) were taken from a previous study conducted in our laboratory. Design: Using special-purpose computed tomography (gCT), trabecular (TBD), cortical (CBD) and integral (IBD) bone densities (gmacm 3 ) were measured in the ultra-distal radius at 6-month intervals over 18 months. At baseline, and at each subsequent study visit, serum was obtained from each subject for determinations of calcium, phosphate, 25-hydroxyvitamin D, alkaline phosphatase, and immunoreactive parathyroid hormone. A 24-h urine sample was also obtained at each study visit for determination of urinary calcium, phosphate and creatinine. Results: In repeated measures analysis of variance of the data for the older men serum 25-hydroxyvitamin D was signi®cantly decreased (P`0.001) over time, while TBD was increased ( 0.60% per year, P`0.01). Longitudinal rates of change for TBD, CBD and IBD were: 7 0.94%, 0.92% and 0.74% per year respectively when bone density data at baseline for the older men and the historical data for younger men were combined. However, separate analyses of the data for the younger and the older men indicated no signi®cant age-related changes in bone density for men aged 29 ± 60 y, or for men aged 66 ± 76 y. However, differences in TBD, CBD and IBD between the younger and older groups of men were signi®cant (P`0.001). Conclusions: In a group (n 36) of older men (mean age 71.7 y) studied longitudinally over 18 months, bone density in the distal radius did not decrease over time. Mean bone density in this group of men was, however, signi®cantly (P`0.001) lower than in a group of younger men (n 17, mean age 46.7 y). Regression analysis using cross-sectional bone density data at baseline for the older male group, and historical data for the younger male group, indicates that bone loss occurs with increasing age at a rate of about 1% per year averaged over ages 29 ± 76 y. Bone density variables were not correlated with either height or weight, or with any biochemical or hormonal variable measured in this study. Sponsor: The work was funded in part by the Dairy Bureau of Canada. Descriptors: bone density; computed tomography; 25-hydroxyvitamin D; older men

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