Marcadores de estrés oxidativo en el síndrome de Down

Abstract

Introduction Oxidative stress results from an imbalance between formation and neutralization of pro-oxidants. Oxidation of biomolecules can damage them, disturbing normal functions and may contribute to a variety of disease states and aging. Objective We analysed activities of Cu/Zn superoxide dismutase (Cu/ZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR), which form the main enzyme protection mechanism against harmful effects of reactive oxygen species, and the levels of malondialdehyde (MDA), an end product of lipid peroxidation, in order to develop a better knowledge of a new aspect in this syndrome's pathology. Material and Methods 100 individuals with Down syndrome, aged from newborns to 29 years (34 males and 66 females) were analysed: 90 individuals with regular trisomy 21, 6 with mosaic trisomy 21 and 4 with trisomy 21 by Robertsonian translocation. A group of individuals without pathology was also included (40 males, 60 females) with similar ages to the DS individuals. In all cases we determined: 1) antioxidant enzymes activity: Cu/ZnSOD, CAT, GPx and GR, 2) levels of MDA. Results We observed: a) an increase in the oxidative stress in DS individuals caused by an excess in Cu/Zn SOD, which they try to compensate mainly by increasing the activity of GPx and CAT; b) high levels of lipid peroxidation; c) no significant differences between male and female in DS individuals; d) lower oxidative stress in individuals with DS mosaic. Conclusions Trisomic cells are more sensitive to oxidative stress. This sensitivity could be caused by an imbalance in the hydrogen peroxide metabolism.