Selenium and vitamin E: Interesting biology and dashed hope
- SourceAvailable from: Alysia Mortimer
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- "However, their efficacy in vivo remains a matter of debate. Animal models have been widely used to test a number of antioxidant compounds, and though these studies have been relatively promising, clinical trials with antioxidant compounds have not always lived up to expectations (Schwedhelm et al., 2003; Kamat et al., 2008; Klein, 2009; Wojcik et al., 2010; Floyd et al., 2011). One reason why antioxidants have performed poorly in clinical trials might have to do with the fact that these compounds may only be effective in a narrow temporal window in relation to oxidative damage. "
ABSTRACT: Oxidative stress remains one of the most well studied, albeit somewhat contentious, causes of age-related changes in humans. Consequently, a large number of putative antioxidant compounds are freely available in myriad formulations that are often not tested for their efficacy or regulated for quality control. Following the development of a Drosophila model of oxidative-stress dependent aging (p38 MAP K (p38K) mutants) in our laboratory, we attempted to test the protective effect of some of these commonly available formulations against oxidative stress, in the p38K model. As environmental exposure to oxidizing toxins has been linked to a variety of human diseases, we also tested the efficacy of these supplements on chemically-induced models of oxidative stress (paraquat and hydrogen peroxide exposure). Our results suggest that when added as a dietary supplement, some of these over-the-counter compounds, notably containing açai extracts, confer significant protection for both the p38K-dependent genetic model as well as the toxin-induced model. These products were also remarkably effective at dampening stress-induced expression of the detoxifying enzyme GSTD1 and eliminating paraquat induced circadian rhythm deficits. Overall, our results suggest potential benefits of dietary supplementation with some of these compounds, especially under conditions of elevated oxidative stress. These findings should be assessed in the context of other studies that seek to identify active principles in these extracts, determine their effective dosage for human consumption and evaluate the safety of long-term prophylactic applications.Experimental gerontology 07/2012; 47(9):712-22. DOI:10.1016/j.exger.2012.06.016 · 3.53 Impact Factor
- CancerSpectrum Knowledge Environment 09/2009; 101(19):1363-4; author reply 1364. DOI:10.1093/jnci/djp272 · 15.16 Impact Factor
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ABSTRACT: Heroin use, withdrawal syndrome, and heroin-related deaths are still the most serious public health problems. Antioxidants and bio-elements are essential for metabolism in living organisms. To our knowledge, there are no data about the effect of antioxidant therapy on the levels of bio-elements and antioxidant enzymes in the naloxone (NX)-induced heroin withdrawal syndrome. Therefore, in the present study for the first time, we have investigated the role of antioxidant therapy, melatonin, and vitamin E plus Se, on the trace and major elements and antioxidant enzymes in the heroin addiction or heroin withdrawal in rats. Glutathione peroxidase levels were increased and catalase levels were decreased in the all study groups when compared to the sham group. The level of superoxide dismutase (SOD) in the fixed dose of heroin (FDH) given group was lower; however, in the variable doses of heroin (VDH) given group SOD level was higher. Furthermore, in withdrawal syndrome, Fe, Mg, Mn, and Ti levels were diminished and Al, Ca, and Cu levels were increased in the FDH+NX group. Moreover, Mg, Mn, and Se levels were also diminished and Al level was increased in the VDH+NX group. In conclusion, our results obviously indicated that heroin effected both bio-element status and antioxidant enzyme activities and, exogenous melatonin or vE+Se therapy might relieve on the element and antioxidant enzyme the destructive activity caused by heroin.Biological trace element research 02/2010; 139(1):41-54. DOI:10.1007/s12011-010-8634-0 · 1.61 Impact Factor