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Diets rich in fruits and vegetables (FV), which contain (poly)phenols, protect against age-related inflammation and chronic diseases. T-lymphocytes contribute to systemic cytokine production and are modulated by FV intake. Little is known about the relative potency of different (poly)phenols in modulating cytokine release by lymphocytes. We compared thirty-one (poly)phenols and six (poly)phenol mixtures for effects on pro-inflammatory cytokine release by Jurkat T-lymphocytes. Test compounds were incubated with Jurkat cells for 48 h at 1 and 30 µm, with or without phorbol ester treatment at 24 h to induce cytokine release. Three test compounds that reduced cytokine release were further incubated with primary lymphocytes at 0·2 and 1 µm for 24 h, with lipopolysaccharide added at 5 h. Cytokine release was measured, and generation of H2O2 by test compounds was determined to assess any potential correlations with cytokine release. A number of (poly)phenols significantly altered cytokine release from Jurkat cells (P<0·05), but H2O2 generation did not correlate with cytokine release. Resveratrol, isorhamnetin, curcumin, vanillic acid and specific (poly)phenol mixtures reduced pro-inflammatory cytokine release from T-lymphocytes, and there was evidence for interaction between (poly)phenols to further modulate cytokine release. The release of interferon-γ induced protein 10 by primary lymphocytes was significantly reduced following treatment with 1 µm isorhamnetin (P<0·05). These results suggest that (poly)phenols derived from onions, turmeric, red grapes, green tea and açai berries may help reduce the release of pro-inflammatory mediators in people at risk of chronic inflammation. [ABSTRACT FROM AUTHOR]

The workshop was organised to discuss the validity and limitations of existing functional markers of Se status in human subjects and to identify future research priorities in this area. Studies presented as part of this workshop investigated: the bioavailability of Se from different dietary sources; potential functional markers of Se status; individual variation in response to Se; the effect of marginal Se status on immune function. The workshop highlighted the need to define the relationship between functional markers of Se status and health outcomes. [ABSTRACT FROM PUBLISHER]

Dietary Se levels in the UK have fallen over the last 20 years and recent surveys indicate that average Se intakes are 30-40 microg/d, which is well below the current UK reference nutrient intake for adult men (75 microg/d) or women (60 microg/d). Functional consequences of this decline have not been recognised, although epidemiological data suggest it may contribute to increased risk of infections and incidence of some cancers. Previous data have indicated that biochemical changes in Se-dependent proteins occur in otherwise healthy UK subjects given small Se supplements. The current studies have focused on the effect of small Se supplements on the immune response since there is evidence of specific interactions between Se intake and viral replication, and since the potential anti-cancer effects of Se may be mediated by non-antioxidant effects of Se such as changes in immune function. Data indicate that subjects given small Se supplements (50 or 100 microg Se/d) have changes in the activity of Se-dependent enzymes and evidence of improved immune function and clearance of an administered live attenuated virus in the form of poliovirus vaccine. Responses of individual subjects to Se supplements are variable, and current work is evaluating potential explanations for this variability, including genetic variability and pre-existing Se status. [ABSTRACT FROM AUTHOR]

Osteoporosis is almost universal in very old age, and is a major cause of morbidity and mortality in the elderly of both sexes. Bone is lost at a rate of 0·2–0·5 %/year in both men and women after the age of 40–45 years. The causes of age-related changes in bone mass are multifactorial and include genetic predisposition, nutritional factors, endocrine changes, habitual exercise levels and body weight. Bone loss is accelerated to 2–5 % year immediately before and for up to 10 years post-menopause (Heaney, 1986). In women hormone-replacement therapy is effective in reducing the rate of bone loss caused by this peri-menopausal decrease in hormone levels (Smith & Studd, 1993); however, in men and older women (>10 years post-menopause) nutrition plays a key role in the rate of bone loss. One factor contributing to bone loss in the elderly may be a subclinical Zn and/or Cu deficiency, due to a reduced dietary intake of micronutrients and reduced absorption (Thomson & Keelan, 1986). Zn and Cu are essential cofactors for enzymes involved in the synthesis of various bone matrix constituents. Paradoxically, Ca supplementation may accentuate the problem of reduced Zn and Cu levels by impairing the absorption of simultaneously-ingested Zn and the retention of Cu (Snedeker et al. 1982; Grekas et al. 1988). The present paper will review the current literature on the potential benefits of Cu and Zn supplementation in reducing bone loss, and present new information on the effect of Ca supplementation on Zn and Cu status in post-menopausal women with osteoporosis. [ABSTRACT FROM PUBLISHER]

Assays which purport to assess free radical activity in biological systems are multiple. However, despite numerous published descriptions of new methods and modifications of methods to assess free radical activity in biological materials, there is still a lack of reliable techniques for quantification of activity in vivo. Analysis of a number of related indicators and use of a variety of approaches appears the only reliable way to evaluate these processes in vivo. In studies of free radical generation by contracting skeletal muscle we have attempted to use a variety of indicators, including measurement of endogenous antioxidant levels, measurement of indirect indicators of free radical activity (e.g. products of lipid peroxidation, DNA oxidation or protein oxidation) and, where possible, measurement of direct indicators of free radical activity by electron spin resonance techniques. In view of the relative lack of specificity of many available techniques, caution should be exerted in evaluating the numerous examples of isolated single measures of free radical activity which are present in the scientific literature. [ABSTRACT FROM PUBLISHER]

The ability of dietary supplementation with carotenoids to protect chick tissues against oxidative stress in vitro was examined. Male Leghorn chicks were fed on diets supplemented (100 mg supplement/kg diet) with either β-carotene, zeaxanthin (β,β-carotene-3,3'-diol), canthaxanthin (β,β-carotene-4,4'-dione) or α-tocopherol, or on a control diet, from 1 d old until 37 d of age. Tissues (liver, heart, skeletal muscle and plasma) were removed and assayed for total carotenoids and α-tocopherol content and portions subjected to oxidative stress by incubation of homogenates with cumene hydroperoxide and FeSO4. Animals receiving zeaxanthin and canthaxanthin had significantly greater carotenoid concentrations in liver, heart, muscle and plasma compared with untreated controls (P < 0·05); animals fed on diets supplemented with β-carotene or α-tocopherol did not have significantly different tissue carotenoid contents compared with untreated controls. α-Tocopherol supplementation elevated α-tocopherol levels in all tissues examined (P < 0·05). Supplementation with caroteuoids did not affect tissue α-tocopherol levels, but β-carotene lowered plasma α-tocopherol levels by 50% (P < 0·05). Incubation of plasma or tissue homogenates with oxidant stressors induced lipid peroxidation (production of thiobarbituric-acid reactive substances) in all tissues. Animals given α-tocopherol, β-carotene or zeaxanthin had a reduced susceptibility to oxidant stress in liver compared with unsupplemented controls (P < 0·05), and α-tocopherol-supplemented animals had reduced susceptibility in skeletal muscle compared with unsupplemented controls (P < 0·05). Canthaxanthin supplementation did not influence the susceptibility to oxidant stress in any tissue examined. These results suggest that zeaxanthin, a carotenoid present in animal and human diets, may have significant activity as an antioxidant against oxidative stress in tissues. [ABSTRACT FROM PUBLISHER]

Nitric oxide (NO) plays an important role in pathophysiology of the nervous system. Copper/zinc superoxide dismutase (SOD1) reacts with superoxide, which is also a substrate for NO, to provide antioxidative protection. NO production is greatly altered following nerve injury, therefore we hypothesised that SOD1 and NO may be involved in modulating axotomy responses in dorsal root ganglion (DRG)-spinal network. To investigate this interaction, adult Thy1.2 enhanced membrane-bound green fluorescent protein (eGFP) mice underwent sciatic nerve axotomy and received NG-nitro-