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Two studies, reviewed here, have shown oxidative stress is increased in individuals with Down Syndrome (DS).
What this increase in oxidative stress means is the body does not have the full capability to cope with stress on cells from oxidation caused by free radicals. This in turn can lead to an increase in the risk of cellular damage and diseases such as atherosclerosis, Alzheimers and aging. Your body's supply of natural antioxidants may be depleted by lifestyle factors such as environmental toxins like smoking and poor diet. These oxidative stresses can reduce enzymes in the body such as gluathione and superoxide dismutase. Taking supplements such as vitamins E and C, co-enzyme Q10 and eating a det rich in foods such as tomatoes, green tea, and carrots, which are all high in antioxidants may assist the prevention of these enzyme reactions. Studies of interest: 1. Markers of oxidative stress in children with Down syndrome. Zitnanova I et al. Clin Chem Lab Med. 2006;44(3):306-10. Links Abstract: Persons with Down syndrome have increased vulnerability to oxidative stress caused by overexpression of superoxide dismutase, an antioxidant enzyme coded on chromosome 21. Increased oxidative stress may lead to oxidative damage of important macromolecules. We monitored this damage by measuring levels of different biomarkers of oxidative stress (protein carbonyls and 4-hydroxy-2-nonenal), as well as plasma antioxidant capacity, in children with Down syndrome. A total of 20 children with Down syndrome and 18 healthy individuals were recruited for this purpose. METHODS: Plasma protein carbonyls were measured using an ELISA technique, 4-hydroxy-2-nonenal was monitored by HPLC and the antioxidant capacity was evaluated using a ferric reducing ability of plasma (FRAP) assay. RESULTS: We found that children with Down syndrome had significantly elevated levels of protein carbonyls compared to healthy controls (p < 0.01). Levels of 4-hydroxy-2-nonenal and antioxidant capacity were similar in both groups. CONCLUSION: Our results on oxidative damage to proteins confirm the assumption of increased oxidative stress in individuals with Down syndrome. PMID: 16519603 [PubMed - indexed for MEDLINE]
2. Anti-oxidant gene expression imbalance, aging and Down syndrome. Sinha S. Life Sci. 2005 Feb 4;76(12):1407-26. Epub 2004 Dec 22 Links Abstract: The expression of copper zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), glutathione peroxidase (GPx), and catalase (CAT) genes have been detected in human skin fibroblast cells for 2 year normal child (control), 50 year old normal male and female and a 1 year old Down Syndrome (DS) male and female with established trisomy karyotype using the RT-PCR technique. Differential expression of these genes is quantified individually against a β-Actin gene that has been employed as an internal control. The immunoblotting of cell lysate proteins with polyclonal antibodies exhibit SOD1 (16 kD), SOD2 (40 kD), GPx (23 and 92 kD), CAT (64 kD), and Actin (43 kD) as translational products. The results demonstrate that the enhancement in the level of mRNAs encoding SOD1 in DS male and female, as well as aged male and female are 51, 21, 31 and 50% respectively compared to the normal child (control). In SOD2, DS male and female display higher (176%) and lower (26%) levels of expression whereas aged male and female exhibit enhanced levels of expression (66 and 119%) respectively compared to the control. This study demonstrates that DS affects the female less than the male whereas in the aging process, the female is more prone to oxidative damage than the male. These results not only indicate that the level of GPx mRNA is constant except in DS male, which shows a downward regulation but that even CAT mRNA is upward regulated in aged as well as in DS males and females. These disproportionate changes in anti-oxidant genes, which are incapable of coping with over expressed genes, may contribute towards the aging process, dementia and Down syndrome. |
