Glucose-6-phosphate-dehydrogenase is also increased in erythrocytes from adolescents with Down syndrome

Abstract

-For some time it has been claimed that trisomic cells are more sensitive to oxidative stress since there is an imbalance in hydrogen peroxide metabolism due to an increase in superoxide dismutase (SOD) catalytic activity. We designed the present study to assess activity levels of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glucose-6-phosphate-dehydrogenase (G6PDH)] in erythrocytes in 31 male adolescents with Down syndrome (mean age 16.3 ± 1.1). An increase of 35.2%, 15.3% and 14.9% in the catalytic activity of SOD, GPx and G6PDH respectively was observed in male adolescents with Down syndrome compared to age-matched controls. For CAT, a slight increase of 6.0% was also found. It is concluded that our data are consistent with previous evidence of the existence of oxidative stress in individuals with Down syndrome as revealed by significantly enhanced activities of SOD and GPx. The most striking feature was that G6PDH, in contrast to CAT, presented a similar behaviour. Further studies are required to identify other antioxidant enzymes in red blood cells as well as in white blood cells in order to increase the range of potential bioindicators of oxidative stress.

Case–control studies on ceruloplasmin and superoxide dismutase (SOD1) in neurodegenerative diseases: A short review

“…No significant difference was found between the individuals with DS and their age-and gender-matched controls regarding CP determinations. The activity of SOD1 was much greater in the individuals with DS than in the control group, as expected in the light of the gene-dose effect (the gene coding for SOD1 is located on chromosome 21) and earlier studies on SOD1 activity in DS [31][32][33]. CP concentration was found to increase significantly with age in the DS group (P = 0.015).…”

“…It seems likely that the excessive oxidative load caused by overproduction of SOD1, in the absence of full compensatory production of glutathione peroxidase and catalase [32,33] may be a cause of damage to the CP protein, SOD1 itself and probably other macromolecules and possibly plays a role in the early senescence observed in individuals with DS.…”

Erythrocyte phospholipid molecular species and fatty acids of Down syndrome children compared with non-affected siblings

“…Another gene located on chromosome 21 is the superoxide dismutase ( SOD-1 ) gene. Its overexpression leads to a dramatic increase in SOD-1 enzyme activity ( 7 , 8 ) . This consequence is thought to disturb the natural antioxidant enzyme balance in individuals with DS, inducing oxidative stress ( 9 , 10 ) .…”