Does vitamin C act as a pro-oxidant under physiological conditions?

Vitamin C readily scavenges reactive oxygen and nitrogen species and may thereby prevent oxidative damage to important biological macromolecules such as DNA, lipids, and proteins. Vitamin C also reduces redox active transition metal ions in the active sites of specific biosynthetic enzymes. The interaction of vitamin C with 'free', catalytically active metal ions could contribute to oxidative damage through the production of hydroxyl and alkoxyl radicals; whether these mechanisms occur in vivo, however, is uncertain. To examine this issue, we reviewed studies that investigated the role of vitamin C, both in the presence and absence of metal ions, in oxidative DNA, lipid, and protein damage. We found compelling evidence for antioxidant protection of lipids by vitamin C in biological fluids, animals, and humans, both with and without iron cosupplementation. Although the data on protein oxidation in humans are sparse and inconclusive, the available data in animals consistently show an antioxidant role of vitamin C. The data on vitamin C and DNA oxidation in vivo are inconsistent and conflicting, but some of the discrepancies can be explained by flaws in experimental design and methodology. These and other important issues discussed here need to be addressed in future studies of the role of vitamin C in oxidative damage.     

Is there a vitamin E paradox?

In addition to epidemiologic studies that suggest a benefit for high intakes of alpha-tocopherol, studies of supplementation in humans have clearly shown that alpha-tocopherol decreases lipid peroxidation, platelet aggregation, and functions as a potent anti-inflammatory agent. In the five large prospective clinical trials with alpha-tocopherol therapy, four have shown a beneficial effect on cardiovascular end-points (two studies on a primary end-point and two studies on other cardiovascular end-points). Thus, the totality of evidence based on the epidemiologic data, in-vitro studies and animal models, and the clinical trials appears to support a benefit for alpha-tocopherol supplementation in patients with pre-existing cardiovascular disease. However, definitive recommendations must await ongoing clinical trials.     

Does vitamin D protect against DNA damage?

Vitamin D is a secosteroid best known for its role in maintaining bone and muscle health. Adequate levels of vitamin D may also be beneficial in maintaining DNA integrity. This role of vitamin D can be divided into a primary function that prevents damage from DNA and a secondary function that regulates the growth rate of cells. The potential for vitamin D to reduce oxidative damage to DNA in a human has been suggested by clinical trial where vitamin D supplementation reduced 8-hydroxy-2'-deoxyguanosine, a marker of oxidative damage, in colorectal epithelial crypt cells. Studies in animal models and in different cell types have also shown marked reduction in oxidative stress damage and chromosomal aberrations, prevention of telomere shortening and inhibition of telomerase activity following treatment with vitamin D. The secondary function of vitamin D in preventing DNA damage includes regulation of the poly-ADP-ribose polymerase activity in the DNA damage response pathway involved in the detection of DNA lesions. It is also able to regulate the cell cycle to prevent the propagation of damaged DNA, and to regulate apoptosis to promote cell death. Vitamin D may contribute to prevention of human colorectal cancer, though there is little evidence to suggest that prevention of DNA damage mediates this effect, if real. Very limited human data mean that the intake of vitamin D required to minimise DNA damage remains uncertain.     

Does Reproductive Investment Decrease Telomere Length in Menidia menidia?

Given finite resources, intense investment in one life history trait is expected to reduce investment in others. Although telomere length appears to be strongly tied to age in many taxa, telomere maintenance requires energy. We therefore hypothesize that telomere maintenance may trade off against other life history characters. We used natural variation in laboratory populations of Atlantic silversides (Menidia menidia) to study the relationship between growth, fecundity, life expectancy, and relative telomere length. In keeping with several other studies on fishes, we found no clear dependence of telomere length on age. However, we did find that more fecund fish tended to have both reduced life expectancy and shorter telomeres. This result is consistent with the hypothesis that there is a trade-off between telomere maintenance and reproductive output.     

Is there a potential therapeutic role for vitamin E or other antioxidants in atherosclerosis?

In-vitro studies and animal model studies provide an ever-growing body of evidence, direct and indirect, that oxidation of low-density lipoprotein and/or related oxidative mechanisms play a role in atherogenesis. However, two recent, very large, carefully conducted clinical intervention trials using adequate doses of vitamin E demonstrated no effect on a composite end-point of non-fatal infarction, stroke or death from cardiovascular causes. Why the unexpected negative results? Possibly because the animal intervention evidence on which these trials were based deals primarily with very early lesions (fatty streaks). That evidence does not necessarily provide a basis for predicting what antioxidant intervention will do in patients with advanced lesions, particularly when the end-points used relate to unstable plaques and fatal thrombosis, events for which we have no adequate animal models. Nor does it necessarily follow that the same antioxidants used successfully in animals will be effective in humans. The strength of the evidence for the oxidative modification hypothesis is such that negative clinical trials with one particular antioxidant, in patients with very advanced coronary heart disease and lasting only 3-5 years, should not be taken as refutation of the hypothesis. Perhaps different kinds of human trials are needed, trials in which the development of new lesions is measured, in order to test whether antioxidants can decrease the rate of initiation and early progression of atherosclerosis as they do in animals. The answer to the title query is 'Probably, but it is too soon to say'.     

Anti‐atherosclerotic effects of vitamin E – myth or reality?

Atherosclerosis and its complications such as coronary heart disease, myocardial infarction and stroke are the leading causes of death in the developed world. High blood pressure, diabetes, smoking and a diet high in cholesterol and lipids clearly increase the likelihood of premature atherosclerosis, albeit other factors, such as the individual genetic makeup, may play an additional role. Several epidemiological studies and intervention trials have been performed with vitamin E, and some of them showed that it prevents atherosclerosis. For a long time, vitamin E was assumed to act by decreasing the oxidation of LDL, a key step in atherosclerosis initiation. However, at the cellular level, vitamin E acts by inhibition of smooth muscle cell proliferation, platelet aggregation, monocyte adhesion, oxLDL uptake and cytokine production, all reactions implied in the progression of atherosclerosis. Recent research revealed that these effects are not the result of the antioxidant activity of vitamin E, but rather of precise molecular actions of this compound. It is assumed that specific interactions of vitamin E with enzymes and proteins are at the basis of its non-antioxidant effects. Vitamin E influences the activity of several enzymes (e.g. PKC, PP2A, COX-2, 5-lipooxygenase, nitric oxide synthase, NADPH-oxidase, superoxide dismutase, phopholipase A2) and modulates the expression of genes that are involved in atherosclerosis (e.g. scavenger receptors, integrins, selectins, cytokines, cyclins). These interactions promise to reveal the biological properties of vitamin E and allow designing better strategies for the protection against atherosclerosis progression.     

Yolk androgens and embryo sex: maternal effects or confounding factors?

Maternal effects occur when offspring phenotype is affected by environmental factors experienced by the mother and, in egg-laying species, are often mediated via egg resources. There is currently great interest among behavioural ecologists in maternally allocated yolk androgens, especially their relationship with offspring sex and development. Such studies need embryonic tissue for sexing, however, requiring eggs to be incubated (usually for 3 days). Therefore, there are concerns about whether the androgen concentrations assayed reflect those allocated by the mother. In addition, studies showing sex biases in maternal allocation of androgens could be confounded if male and female embryos uptake or metabolise androgens at different rates. We ran a series of experiments using zebra finch (Taeniopygia guttata) eggs to address these potential confounding factors. First we showed, using eggs naturally incubated for up to 5 days, that eggs containing embryos had lower yolk androgen concentrations than eggs that had failed to form embryos. We then tested various hypotheses for this difference using controlled incubation treatments. Our results suggested that (a) embryo development causes the yolk to become progressively more diluted with albumin; and (b) between 3 and 5 days of incubation embryos start uptaking or metabolising androgens. Crucially, we found no decline in yolk androgen concentration at 3 days incubation, and no evidence for sex-specific rates of uptake or metabolism of androgens. This strongly suggests that yolk androgen levels up to 3 days incubation do reflect those allocated by the mother, and that studies of sex biased maternal allocation of yolk androgens are not confounded by sex differences in embryo development.     

Does Inbreeding and Loss of Genetic Diversity Decrease Disease Resistance?

Inbreeding and loss of genetic diversity are predicted to decrease the resistance of species to disease. However, this issue is controversial and there is limited rigorous scientific evidence available. To test whether inbreeding and loss of genetic diversity affect a host's resistance to disease, Drosophila melanogasterpopulations with different levels of inbreeding and genetic diversity were exposed separately to (a) thuringiensin, an insecticidal toxin produced by some strains of Bacillus thuringiensis, and (b) live Serratia marcescensbacteria. Inbreeding and loss of genetic diversity significantly reduced resistance of D. melanogasterto both the thuringiensin toxin and live Serratia marcescens. For both, the best fitting relationships between resistance and inbreeding were curvilinear. As expected, there was wide variation among replicate inbred populations in disease resistance. Lowered resistances to both the toxin and the pathogen in inbred populations were due to specific resistance alleles, rather than generalized inbreeding effects, as correlations between resistance and population fitness were low or negative. Wildlife managers should strive to minimise inbreeding and loss of genetic diversity within threatened populations and to minimise exposure of inbred populations to disease.     

Dietary vitamin E affects α-TTP mRNA levels in different tissues of the Tan sheep

The α-tocopherol transfer protein (α-TTP) is a ~ 32 kDa cytosolic protein that plays an important role in the efficient circulation of plasma α-tocopherol in the body, a factor with great relevance in reproduction. The α-TTP gene has been studied in a number of tissues; however, its expression and function in some ovine tissues remain unclear. A previous study from our laboratory has demonstrated α-TTP expression in sheep liver. In the present study we determined whether α-TTP is expressed in non-liver tissues and investigated the effects of dietary vitamin E on the α-TTP mRNA levels. Thirty-five male Tan sheep with similar body weight were randomly allocated into five groups and supplemented 0, 20, 100, 200 and 2000 IU sheep^− 1 day^− 1 vitamin E, for four months, respectively. At the end of the study, the animals were slaughtered and tissue samples from the heart, spleen, lung, kidney, longissimus dorsi muscle and gluteus muscle were immediately collected. We found that the α-TTP gene is expressed in sheep tissues other than the liver. Moreover, dietary vitamin E levels had influenced the expression levels of α-TTP gene in these tissues in a tissue-specific way. The technique of immunohistochemistry was used to detect α-TTP in tissues of the heart, spleen, lung, and kidney and we found that α-TTP was mainly located in the cytoplasm while no α-TTP immunoreactivity was detected in the cytoplasm of longissimus dorsi and gluteus muscle samples. Importantly, our findings lay the foundation for additional experiments focusing on the absorption and metabolism of vitamin E in tissues other than the liver.     

Does Land-Use Intensification Decrease Plant Phylogenetic Diversity in Local Grasslands?

Phylogenetic diversity (PD) has been successfully used as a complement to classical measures of biological diversity such as species richness or functional diversity. By considering the phylogenetic history of species, PD broadly summarizes the trait space within a community. This covers amongst others complex physiological or biochemical traits that are often not considered in estimates of functional diversity, but may be important for the understanding of community assembly and the relationship between diversity and ecosystem functions. In this study we analyzed the relationship between PD of plant communities and land-use intensification in 150 local grassland plots in three regions in Germany. Specifically we asked whether PD decreases with land-use intensification and if so, whether the relationship is robust across different regions. Overall, we found that species richness decreased along land-use gradients the results however differed for common and rare species assemblages. PD only weakly decreased with increasing land-use intensity. The strength of the relationship thereby varied among regions and PD metrics used. From our results we suggest that there is no general relationship between PD and land-use intensification probably due to lack of phylogenetic conservatism in land-use sensitive traits. Nevertheless, we suggest that depending on specific regional idiosyncrasies the consideration of PD as a complement to other measures of diversity can be useful.     

Does It Sink or Float?

ABSTRACT

This activity is designed to teach prekindergarten to second grade students about the concept of sink or float through an inquiry activity. Students will use familiar objects to predict and test the properties of sink and float. Background information is offered to teachers to assist them with this activity. This lesson begins with an engaging story, Who Sank the Boat? by Pamela Allen.     

Does Chi Give or Take?

In lytic cycle crosses with Red-Gam-lambda phage, particles were examined that had undergone an Int-mediated exchange. It was assumed that this exchange dimerized the circular lambda, making it packageable. Among these Int-mediated recombinants, particles were identified that had, in addition, enjoyed a close double exchange mediated by the RecBC pathway. Such close double exchanges indicate localized negative interference and are analogous to eukaryotic conversions that have retained parental configuration of flanking markers. These events are stimulated by Chi, a recombinator specific to the RecBC pathway. When Chi is present in only one parent in the cross, the complementary double exchange recombinants are Chi stimulated to the same degree. This behavior of Chi contrasts with that of characterized eukaryotic recombinators.     

Passive smoking reduces and vitamin C increases exercise-induced oxidative stress: Does this make passive smoking an anti-oxidant and vitamin C a pro-oxidant stimulus?

The current interpretative framework states that, for a certain experimental treatment (usually a chemical substance) to be classified as “anti-oxidant”, it must possess the property of reducing (or even nullifying) exercise-induced oxidative stress. The aim of the study was to compare side by side, in the same experimental setup, redox biomarkers responses to an identical acute eccentric exercise session, before and after chronic passive smoking (considered a pro-oxidant stimulus) or vitamin C supplementation (considered an anti-oxidant stimulus). Twenty men were randomly assigned into either passive smoking or vitamin C group. All participants performed two acute eccentric exercise sessions, one before and one after either exposure to passive smoking or vitamin C supplementation for 12 days. Vitamin C, oxidant biomarkers (F₂-isoprostanes and protein carbonyls) and the non-enzymatic antioxidant (glutathione) were measured, before and after passive smoking, vitamin C supplementation or exercise. It was found that chronic exposure to passive smoking increased the level of F₂-isoprostanes and decreased the level of glutathione at rest, resulting in minimal increase or absence of oxidative stress after exercise. Conversely, chronic supplementation with vitamin C decreased the level of F₂-isoprostanes and increased the level of glutathione at rest, resulting in marked exercise-induced oxidative stress. Contrary to the current scientific consensus, our results show that, when a pro-oxidant stimulus is chronically delivered, it is more likely that oxidative stress induced by subsequent exercise is decreased and not increased. Reversely, it is more likely to find greater exercise-induced oxidative stress after previous exposure to an anti-oxidant stimulus. We believe that the proposed framework will be a useful tool to reach more pragmatic explanations of redox biology phenomena.     

Why don't we use vitamin E in dermatology?

OBJECTIVE: To review the possible uses of topical and systemic tocopherols as therapy for skin conditions in light of the widespread use of vitamin E by patients. DATA SOURCES: Index Medicus was searched for articles published from 1922 (when vitamin E was discovered) to 1966 (the beginning of MEDLINE). MEDLINE was searched for articles in English and French on vitamin E or tocopherol in relation to dermatology. Additional original articles were identified from the reference lists of the review articles. STUDY SELECTION: Only well-designed controlled studies were accepted; anecdotes and open studies are cited for completeness and as direction for future research. DATA SYNTHESIS: There was some weak or conflicting evidence that vitamin E is of value in yellow nail syndrome, vibration disease, epidermolysis bullosa, cancer prevention, claudication, cutaneous ulcers, and collagen synthesis and wound healing. It was of no use in atopic dermatitis, dermatitis herpetiformis, psoriasis, subcorneal pustular dermatosis, porphyrias and skin damage induced by ultraviolet light. CONCLUSIONS: After 44 years of research there is still scant proof of vitamin E''s effectiveness in treating certain dermatologic conditions. Further research in well-designed controlled trials is needed to clarify vitamin E''s role.     

Copper status in rats fed diets supplemented with either vitamin E,vitamin A,or β-carotene

Copper status was measured in rats fed copper-adequate, purified diets supplemented with either vitamin E (250 IU/kg), vitamin A (40,000 IU/kg), or β-carotene (2 g/kg). It was hypothesized that the extra intake of the antioxidants would spare vitamin C resulting in a decreased copper status as shown previously after supplementation with vitamin C. A significant increase in plasma ascorbate concentration was observed after β-carotene supplementation, but not after supplemental vitamin E or vitamin A. Extra intake of either β-carotene or vitamin A slightly, but significantly, raised plasma copper concentrations. β-carotene also slightly raised liver copper concentration. Supplemental vitamin E had no effect on plasma and liver copper concentrations. It is concluded that the observed relatively small effects of supplemental vitamin A and β-carotene on copper status in rats are not mediated by changes in plasma vitamin C concentration.     

Simultaneous production of β-carotene, vitamin E and vitamin C by the aerial microalga Trentepohlia aurea

The biomass production and antioxidant accumulation of the aerial microalga Trentepohlia aurea were examined. Using ammonium chloride as nitrogen source for growth in liquid medium, the growth rate was exponential and accompanied by a marked fall in the pH of the medium. The highest growth rate of 152 mg L^-1 day^-1 (logarithmic phase) was attained when T. aurea was cultured with aeration of 5% CO₂-enriched air in medium buffered with HEPES. The growth rate and antioxidant content were enhanced under 5% CO₂ by switching the light intensity from 43 to 143 μmol photon m^-2 s^-1 for the two-stage culture. As a result, T. aurea cells accumulated 2.1 mg β-carotene, 0.3 mg L-ascorbic acid and 2.4 mg tocopherols, respectively, per g dry cell. The simultaneous production of useful materials, such as β-carotene, vitamin E and vitamin C, was demonstrated. This revised version was published online in June 2006 with corrections to the Cover Date.